Mycotoxins in Food and Feed

Mycotoxins in Food and Feed: Present Status and Future Concerns
Rajeev Bhat, Ravishankar V. Rai, and A.A. Karim
ABSTRACT: Disease outbreaks due to the consumption of contaminated food and feedstuff are a recurring problem worldwide. The major factor contributing to contamination are microorganisms, especially fungi, which produce low-molecular-weight compounds as secondary metabolites, with confirmed toxic properties referred to as mycotoxins. Several mycotoxins reported to date are cosmopolitan in distribution and incur severe health-associated risks (including cancer and neurological disorders). Hence, creating awareness among consumers, as well as developing new methods for detection and inactivation is of great importance for food safety. In this review, the focus is on the occurrence of various types of mycotoxins in food and feed associated with risks to humans and livestock, as well as legislation put forth by various authorities, and on presently practiced detoxification methods. Brief descriptions on recent developments in mycotoxin detection methodology are also inlcuded. This review is meant to be informative not only for health-conscious consumers but also for experts in the field to pave the way for future research to fill the existing gaps in our knowledge with regard to mycotoxins and food safety.
Introduction
Contamination of food and agricultural commodities by various types of toxigenic molds (fungi) is a serious and a widely neglected problem. Regardless of decades of extensive research, mold infection still remains a challenging problem (Munkvold 2003). It has been estimated by FAO that worldwide approximately 25% of the crops get contaminated by molds and are affected by mycotoxins (CAST 1989; Rice and Ross 1994), and the estimated loss extends to billions of dollars (Trail and others 1995). Molds have been designated to rank second only to insect pests as a cause of damage during the storage of grains (CAST 1989). Poor harvesting practices, improper drying, handling, packaging, storage, and transport conditions contribute to fungal growth and increase the risk of mycotoxin production. Major loss of fresh harvest that renders it to be an impediment for safe consumption can be attributed mainly to 3 factors: biological (storage pests), microbial (bacteria, fungi), and chemical (insecticide, fungicide residues). These 3 factors, singly or in combination, can readily react with the substrate or the raw material leading to the production of off-avors, discoloration of the product, and reduction in nutritional value. Today, in most of the cases, chemical fumigants or chemical-based protective agents are used for the safe preservation of fresh produce. HowMS 20090721 Submitted 7/28/2009, Accepted 8/27/2009 . Authors Bhat and Karim are with Food Technology Div., School of Industrial Technology, Univ. Sains Malaysia, 11800 Penang, Malaysia. Author Rai is with Dept. of Microbiology, Univ. of Mysore, Manasagangotri, Mysore 570 006, India. Direct inquiries to author Bhat (E-mail: rajeevbhat1304@gmail.com).
ever, increasing concern and demand by consumers for safe and high-quality foods have made it mandatory to look for better alternatives to chemicals. In this regard, it has been a major challenge for the scientic community around the world, as some of the chemical fumigants (like ethylene dioxide, methyl bromide), which are routinely used for postharvest preservation purposes, have been reported to be highly toxic. Some of these chemicals are either banned in developed countries or are likely to be banned in developing countries (by 2015) (Anonymous 1995; FAO 2005). Worldwide, it is generally claimed that natural products are safe. However, contamination of human or animal food (or feed) via natural biotoxins produced by microbes might result in outbreaks of several diseases. Among the microbes, fungal toxins assume more importance due to their worldwide distribution. The colonizing fungi are capable of producing toxins, and can cause deleterious health effects in humans or in livestock consuming the contaminated products. Such cases of fungal poisoning may cause death in animals, but are rarely fatal to humans (PfohlLeszkowicz 2000). As there is an increasing concern among consumers regarding food safety, as well as demand for high-quality foods with minimal bio or chemical contaminants, frequent occurrence of these toxins will denitely have a negative impact on the economy of the affected region/country. Fungal toxins have been detected in various food commodities from many parts of the world and have been recognized to be one of the most dangerous contaminants of food and feed (CAST 1989). The production of toxins by a fungus does not correlate directly with its growth, but is also dependent on the fungistatic and fungicidal compounds that might affect the invasion and
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CRFSFS: Comprehensive Reviews in Food Science and Food Safety

colonization. Even though research papers, reviews, monographs, and reports are available on the contamination of food and feed by fungal toxins, most of the information available is either restricted to one type of mycotoxin or the data are scattered. Hence, keeping this in mind, in the present review, we have aimed at providing a detailed overview on the mycotoxigenic fungi, diversity of mycotoxins, associated health risks to humans and livestock, and on the formal governmental regulations/ legislation put in place. A brief input on the various types of detection methods (see Table 1) has been included to provide baseline information for future research, as well as to create awareness among the general population and health-conscious consumers. species can grow at low aw and at higher temperatures than Fusarium species, which generally require higher aw and low temperature range. However, this growth condition can vary during storage and transportation, wherein a rapid change in relative humidity can occur. Even though swift growth of a particular mold can occur on a substrate, it is not a prerequisite that the mold should produce a mycotoxin. This fact indicates that the production of mycotoxin from a particular species depends entirely on the availability of optimum conditions. As reported by Joffe (1986), Fusarium molds associated with alimentary toxic aleukia can grow prolically at temperatures of 25 to 30 C without producing any mycotoxin, but at near-freezing temperatures, large quantities of mycotoxins are produced without much mold growth. Figure 1 shows a few of the mycotoxin-producing fungi growing on legume seeds. Some of the secondary metabolites produced by a fungus might possess high biological activity and can be toxic to other microorganisms (antibiotics), plants (phytotoxins), or animals. A few of the secondary metabolites like fumagillin, fusaric acid, and mycophenolic acid produced by fungi have been used as therapeutic agents, while other metabolites are considered to be potent toxins (Osweiler 2000; CAST 2003). According to Wicklow and others (1994), mycotoxin production in fungi might have evolved as an effective anti-insect or as an anti-rodent agent. Moss and Frank (1987) have opined that the secondary metabolism of molds might be inuenced by the presence of inhibitory compounds such as agricultural biocides. The nature and quantity of mycotoxins produced is entirely inuenced by interactions of several factors: types of substrate, moisture content, available nutrition, temperature, humidity in the surrounding environment, maturity of the fungal colony, cooccurrence with other fungi, competition from other microorganisms, stress factors, physical damage of the substrate due to insect activity, and other associated factors (Anonymous 1983; Coulumbe 1993; Hendry and Cole 1993; Viquez and others 1994; Rao 2001). Once produced, mycotoxins might be present on all parts of the fungal colony, including the hyphae, mycelia, on spores, and on or in the substrate on which the colony grows. Diversity in the toxic effects and the synergetic properties of mycotoxins has made it mandatory to consider them as risk factor to humans and in livestock health (Yiannikouris and Jonany 2002; D az-Llano and Smith 2006). Concerns over health effects of mycotoxins are being seriously considered worldwide. For example; after the hurricane Katrina, the Centers for Disease Control and Prevention (CDCP, U.S.A.) issued new revised warnings with regard to severe health effects from exposure to mycotoxins produced due to mold growth (Anonymous 2006). Reports are available wherein consumption of mycotoxin-contaminated food/feed is responsible for toxic syndromes in humans and livestock (Smith and others 1995; Berry 1998; Peraica and others 1999; MAFRI 2006). Apart from being highly toxic, some mycotoxins are also linked to the incidence of certain types of cancer and neurological disorders. This feature has induced global concern over safety aspects on the consumption of contaminated food and feed, especially in the case of milk and milk products (Egmond and Paulsch 1986; Dmello and Macdonald 1997; Castegnaro and Mcgregor 1998). Mycotoxins are normally metabolized in the liver, in the kidneys, and by microorganisms in the digestive tract. As a consequence, it is very difcult to derive the chemical structure and associated toxicity of the toxin residues excreted by animals or found in their tissues as they are different from the parent molecules (Ratcliff 2002). Mycotoxicosis is the general term given for the disease that is caused by mycotoxins (Nelson and others 1993). The severity of a mycotoxicosis depends on the toxicity of the mycotoxin, dose involved, extent of exposure, and age and nutritional status of the
Fungi, Conditions Promoting Their Growth, and Production of Mycotoxins

Fungi are eukaryotic, single-celled, multinucleated organisms that are heterotrophic in nature and characterized by a chitinous cell wall. In a majority of the cases fungi occur as lamentous growth and grow in multicellular colonies (grouped together as a mycelium) as compared with yeasts, which are single cells. Nearly 70000 fungal species have been reported and described, but it is estimated that nearly 1.5 million species might still exist (Hawksworth 1991; Hawksworth and others 1995). Details pertaining to ssion fungi (bacteria) are not dealt in this review. The colonizing molds (fungi that reproduce by releasing tiny spores into the air) might live as parasites, symbionts, or as saprophytes on a substrate. Since time immemorial, most of the molds have played a signicant role in human life and welfare (as natural bio-degraders in the environment, in the preparation of certain foods and beverages, as antibiotic preparations, and as sources of industrially important chemicals like alcohols, acetone, and enzymes). Fungi can invade, colonize, and produce mycotoxins either during preharvest (at the eld level) or postharvest stages (storage, transport, and processing). However, lamentous fungi (fungi imperfecti) that are adapted to the terrestrial environment are usually recognized as mycotoxin producers. These fungi colonize and utilize solid substrates by penetrating deep into their matrices by secreting enzymes to break down complex products. In most of the cases, the colonizing fungi produce and secrete lowmolecular-weight compounds (with conrmed toxic properties), generally referred to as secondary metabolites or mycotoxins, which are usually not required for normal growth and survival. The word mycotoxin is derived from 2 words: mukes referring to fungi (Greek) and toxicum referring to poison (Latin). Mycotoxins are relatively large molecules that are not signicantly volatile (WHO 1978; Schiefer 1990). Mycotoxins are produced by some of the specic strains of lamentous fungi belonging to species of the genera Aspergillus, Penicillium, and Fusarium that invade crops at the eld level and may grow on foods during storage under favorable conditions (temperature, moisture, water activity, relative humidity). Fungi normally grow between 10 and 40 C, over a pH range of 4 to 8, and at water activity (aw) levels above 0.70 (sometimes can grow on a very dry surface also) (Lacey 1991). The minimal aw requirements of some of the common toxigenic molds may also vary. For example, for Aspergillus avus it is between 0.78 and 0.80 aw, A. fumigatus 0.85 and 0.94 aw, A. parasiticus 0.78 and 0.82 aw, Eurotium spp. 0.71 and 0.81 aw, Fusarium spp. 0.85 and 0.87 aw, and Penicillium chrysogenum 0.78 and 0.81 aw. Mycotoxin-producing molds, under favorable environmental conditions, may thrive in almost all the climatic conditions of the world and on any solid or liquid support. The growth conditions of a specic fungal species might vary in the eld compared to postharvest stages. For example, Aspergillus and Penicillium
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Table 1 --- Some of the recent methods developed/adapted for the detection of mycotoxins. Raw material Groundnut Peanut Raw and pasteurized sheep, cow and goat milk, egg, and beef samples Chilli Red chilli powder Rice Corn Maize and barley Nuts, cereals, dried fruits, and spices Milk Egg Immunoafnity pre-concentration combined with on-column visual detection LCMS/MS Vicam immunoafnity column for the clean-up procedure and with bromine derivatizaton with an electrochemical cell Rapid FT-NIR method Signal-amplied electrochemical immunosensor ELIME-array (based on an indirect competitive ELISA format) Near-infrared spectroscopy (NIR) In-tube solid-phase micro-extraction (SPME) coupled with LC-MS. Tripathi and Mishra (2009) Tan and others (2009) Piermarini and others (2009) Fernandez-Iba nez and others (2009) Nonaka and others (2009) Goryacheva and others (2009) Jestoi and others (2009) HPLC using UV and uorescent detectors Herzallah (2009) Class-specic monoclonal antibody-based ELISA Li and others (2009) Adsorptive cathodic stripping voltammetry Hajian and Ensa (2009) Detection method Reference
Mycotoxin
Aatoxin (B1, B2) Aatoxin (B1, B2,G1, G2, M1) Aatoxin (B1, B2, G1, G2, M1, M2) O Riordan and Wilkinson (2009)
Mycotoxins in food and feed . . .
Aatoxin (B1, B2, G1, G2) Aatoxin B1 Aatoxin B1 Aatoxin B1
Aatoxin B1 Aatoxin (B1, B2, G1, G2) Aatoxin M1
Fusarium toxins (beauvericin and enniatins [A, A1, B, B1]) Fumonisin B1 DON Bovine milk --Cereals, fruit, and coffee products Tunisian foods Cheese --Corn breakfast and infant cereals Sweet pepper LC-MS/MS Molecular imprint polymer technology
Gazzotti and others (2009) Weiss and others (2003) Tabata and others (2008) Ghali and others (2009) Zhang and others (2009b) Huang and others (2009) Shim and others (2009) Zinedine and others (2009) Monbaliu and others (2009)
Ochratoxin A (OTA) and citrinin OTA
OTA
OTA and aatoxins
High-performance liquid chromatography with uorescence detection (HPLC-FL) using LC/MS/MS HPLC technique preceded by an immunoafnity clean-up step Solid-phase micro extraction coupled to liquid chromatography-tandem mass spectrometry. Dual-label time-resolved uoroimmunoassay One-step simultaneous immunochromatographic strip test Pressurized liquid extraction coupled to liquid chromatography Multi-mycotoxin liquid chromatography/tandem mass spectrometry method
OTA and ZEN OTA Multi mycotoxinstrichothecenes, aatoxin (B1,B2, G1, G2), Alternaria toxins, fumonisins (B1, B2, B3), ochratoxin A, ZEN, beauvericin, and sterigmatocystin ZEN ZEN and fumonisins Patulin
Fluorescence polarization immunoassay (FPIA) Immunoafnity clean-up and detection by liquid chromatography GC-MS
Chun and others (2009) Manova and Mladenova (2009) Cunha and others (2009)
Patulin
Corn Cereals Apple fruit and apple products including juice, cider, and baby food, and also in quince fruit and quince jam Apple juice Fruit juice and dried fruit
Iha and others (2009) Kataoka and others (2009)
Patulin
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Single-laboratory validation of a liquid chromatography liquid chromatograph (with a C18 column and diode array detector) In-tube solid-phase microextraction coupled with liquid chromatographymass spectrometry

Figure 1 --- Various toxigenic molds. (a) Different fungi contaminating legume seeds, (b) Aspergillus avus, (c) Aspergillus niger , (d) Fusarium spp., (e) Pure culture of Fusarium sp., (f) micro and macro conidia of a Fusarium sp., (g) Alternaria alternata, and (h) Alternaria tenuissima.
individual. Populations residing in developed countries are generally considered to be less exposed to mycotoxins than those in developing countries. This might be attributed to various factors: execution and practice of modern food handling/preservation technology, as well as successful governmental regulation and commercial control over food quality and safety. The presence of mycotoxin-producing fungi in a substrate (cereals, grains, and other sources) has been well dened and accepted as a natural bio-contaminant in many of the EU countries, the U.S., Canada, Russia, and in most of the Asian countries (Smith and Moss 1985). However, even monitoring and exercising of good agricultural and manufacturing practices (GAP and GMP) along with an effective Hazard Analysis and Critical Control Point (HACCP) approach might not completely avoid or eliminate mycotoxins in the food chain. Mycotoxins can enter the food chain directly via plant products such as cereal grains, coffee, oil seeds, spices, fruit
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juices, and beverages (wine and beer), and indirectly from animal diets (pastures, feeds) contaminated with mycotoxins, which can leave residues in milk, meat, and other products.
Mycotoxins and Associated Health Risks

Nearly 400 types of mycotoxins have been discovered, most of them since the 1960s, and are generally being categorized into groups based on structural similarities (Bennet and Klich 2003) and their major toxic effects. Mycotoxins are classied into cyclopeptides, polycetoacids, terpenes, and nitrogenous metabolites, depending on their biological origin and structure. Devegowda and others (1998) have comprehensively reported on the worldwide distribution of dominant mycotoxins. According to them, in Africa and the Asian subcontinents, aatoxins are the major toxins; in Australia, it is aatoxins and fumonisins; in

North America, it is aatoxins, ochratoxin, zearalenone (ZEN), and vomitoxin; in South America, it is aatoxins, fumonisins, ochratoxin, vomitoxin (DON), and T-2 toxin; in Eastern European countries, it is ZEN and vomitoxin; and in Western European regions it is ochratoxin, ZEN, and vomitoxin. However, with the increase of international trade and relaxation of quarantine barriers, the time is not too far away when these mycotoxins might also be detected in all areas of the world. From a health point of view, the important mycotoxins in food and feed include: aatoxins, ochratoxin, trichothecenes, fumonisins, ZEN, and patulin. Aaatoxins, fumonisins, and ergot alkaloids are associated with acute mycotoxicoses in both humans and livestock. However, on the positive side, mycotoxinassociated diseases are not contagious. Human health risks are usually associated with the direct consumption of food products contaminated with mycotoxins like aatoxins, deoxynivalenol (DON), fumonisins, ochratoxin, and ergot alkaloids. Several of these toxins might be produced before harvest (aatoxins, DON, ergot toxin), while others are produced mainly during postharvest stages (fumonisin, ochratoxin). The general symptoms of mycotoxicoses in humans are vomiting, diarrhea, and other associated gastro-intestinal problems (discussed in detail later). In general, mycotoxins are known to suppress the immune system. The effects of mycotoxins on immunity have been excellently reviewed earlier by Sharma (1993). Some of the mycotoxins that can suppress the immune system include mainly the trichothecenes (such as DON and T-2 toxin), which can reduce immunity by inhibiting protein synthesis and cell proliferation. Compared to the individual effects, mycotoxins in combination have been reported to exert even greater negative impact on health and productivity, especially in livestock (Smith and Seddon 1998). In animals, mycotoxins produce a broad range of harmful effects such as reduction in animal productivity, increased incidence of disease due to immuno-suppression, damage to vital organs, and interference with reproductive capacity; and in some extreme cases, death might occur. Mycotoxins produced in animal feeds generally cause irritation to the digestive tract and are capable of reducing nutrient absorption. When contaminated feeds are ingested by an animal, they usually interfere with the endocrine and exocrine systems. For example, ZEN affects the reproductive performance due to its estrogenic effect. ZENs estrogenic effect results from the afnity of ZEN and its derivatives to bind with an animals estrogen receptors (Klang and others 1978). Also, growth and proliferation of molds in animal feeds have been reportedly known to reduce the available nutrients like vitamins and amino acids (lysine) (Kao and Robinson 1972). Animal feeds, especially hay and straw, gets contaminated by fungi during preharvest stages itself, and subsequently from mycelial dust (fungal spores) during the drying stages. Such dust is believed to cause chronic diseases especially related to lungs in cattle and horses. Laan and others (2006) have considered certain dust fractions to be the major cause for chronic and recurrent airway diseases in horses. Pulmonary mycosis, abortion, or mastitis has been reported in animals feeding on contaminated silage and hay (dos Santos and others 2003). Contaminated hay has been shown to result in impaired semen quality in bulls (Alm and others 2002). The details on the health effects related to consumption of contaminated feeds in animals are discussed later in the text. (Schoental 1984), and the decline of the Etruscan civilization has been ascribed to fusariotoxins (T-2 toxin and ZEN) (Schoental 1991). Also, some of the Egyptian tombs, found to contain ochratoxin A, were held responsible for the mysterious deaths of several archaeologists (Pittet 1998). However, historically, the longest known mycotoxicosis is ergotism. This disease is also referred to as St. Anthonys re or sacred re/ignis sacer or re sickness. It was considered, during earlier periods, that a pilgrimage by affected people to the shrine of St. Anthony would bring relief in the head from the intense burning sensation experienced, hence the name. Several such epidemics occurred between the 8th and 16th centuries and the possible reason has been attributed to poor dietary conditions, particularly the consumption of our contaminated by ergots. People affected with ergotism were exposed to lysergic acid diethylamide (LSD), a hallucinogen, produced during the baking of bread made out of ergot-contaminated wheat. In modern times, the 1st recognized acute intoxication was reported from France during 1954, when a large number of persons were victims of ergotism (Van Dongen and De Groot 1995). It was during 1977 to 1978 that Ethiopia saw the last recorded major outbreak of gangrenous ergotism affecting nearly 140 individuals of whom 34% died (King 1979). The cause of this outbreak was attributed to a long wet season which favored the growth of wild oats susceptible to Claviceps purpurea. In 1966, a case of attempted suicide was reported from the U.S. after consumption of pure aatoxin B1 (Willis and others 1980). During the 1960s, in the U.K., nearly 100000 young turkeys died due to aatoxicosis and thousands of other animals and humans were affected (Rodricks and Stoloff 1977). During 1972 to1988, a total of 884 persons were affected when outbreaks of food poisoning occurred described as moldy sugarcane poisoning (MSP) caused by an Arthrinium species (3nitropropionic acid) (Liu and others 1988, 1992). Today, some of the mycotoxins have disappeared owing to stringent sanitary and quality measures. For example, citreoviridin-related malignant acute cardiac beriberi, also known as yellow rice disease has not been reported for several decades (the causative mold is Penicillium citreonigrum). Another mycotoxicosis not seen for decades is alimentary toxic aleukia, which was common during the 1930s and 40s (1932 to 1947) in the USSR. This disease was caused by trichothecenes produced by Fusarium species and was held responsible for the death of nearly 100000 human beings (Gajdusek 1953; Joffe 1978). However, with increasing knowledge and available databases, a relationship is being tried worldwide to correlate the presence and occurrence of recently detected mycotoxins with historical outbreaks, which might assume future importance when exploring and studying newer mycotoxins.
Types of Mycotoxins
Aatoxins
Aatoxins are highly toxic, mutagenic, teratogenic, and carcinogenic compounds that are produced as secondary metabolites by fungi belonging to several Aspergillus species, mainly A. avus and A. parasiticus (Groopman and others 1988; Massey and others 1995; Romagnoli and others 2007; ORiordan and Wilkinson 2008). Aatoxins have a high presence in tropical and subtropical regions where humidity and temperature conditions are optimal for toxin production. The name aatoxin has Historical Perspectives been derived from the combination of a for the Aspergillus Earlier reports have clearly indicated the devastating risks as- genus and a for the species avus, and toxin meaning poison sociated with the consumption of mold-contaminated products. (Ellis and others 1991). Discovery of aatoxins dates back to the Death due to ergotism has been described in the Old Testament 1960s following the severe outbreak of turkey X disease (in the
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U.K.) that resulted in the death of more than 100000 turkeys and other farm animals. The cause was attributed to feed (Brazilian peanuts) contaminated with A. avus. Aatoxins are encountered in a wide range of important agricultural commodities, including cereals (maize, sorghum, pearl millet, rice, wheat), spices (chillies, black pepper, coriander, turmeric, ginger), oilseeds (groundnut, soybean, sunower, cottonseed), tree nuts (almond, pistachio, walnut, coconut), milk (human and animal), and butter. Until now, nearly 18 different types of aatoxins have been identied wherein the major ones include aatoxin B1, B2, G1, G2, and M1. Fungal species belonging to Aspergillus avus typically produce AFB1 and AFB2, whereas A. parasiticus produces AFG1 and AFG2 as well as AFB1 and AFB2. The 4 major aatoxins (aatoxin B1, B2, G1, and G2) are based on their uorescence under blue or green light and their relative mobility during separation by thin-layer chromatography (TLC) (Stroka and Anklam 2000; Bennett and Klich 2003). Four other types of aatoxins, M1, M2, B2A, G2A, that are produced in minor amounts, have been isolated from cultures of A. avus and A. parasiticus. A number of closely related compounds, aatoxin GM1, parasiticol, and aatoxicol are produced by A. avus. Aatoxin-producing fungi show wide variations in their growth requirements. For example, the minimum temperature range for growth of A. parasiticus is 6 to 8 C and maximum is 44 to 66 C, optimum being 25 to 35 C (Diener and others 1982), while A. avus can produce toxin between 12 and 42 C and its optimum is 28 to 30 C (Brackett 1989). Presently, it is estimated that human consumption of aatoxins ranges between 0 and 30,000 ng/kg/d with an average intake of 10 to 200 ng/kg/d (Revankar 2003). The maximum acceptable levels of AFB1 in cereals, peanuts, and dried fruits, either for direct human consumption or as an ingredient in foods, has been set by the European Committee Regulations (ECR) as 4 ppb for total aatoxins (AFB1, AFG1, AFB2, and AFG2) and 2 ppb for AFB1 alone (Moss 2002; Stroka and Anklam 2002). Out of the nearly 18 different types of aatoxins identied to date, the Intl. Agency for Research on Cancer (IARC) has classied 4 aatoxins (AFB1, AFG1, AFB2, AFG2) as Group 1 carcinogens (Chiavaro and others 2001). Aatoxins in milk. Aatoxin contamination in milk and its products is of extreme importance and is a serious problem, as most of the human species as well as animals, particularly the young nurturing ones, are dependent on milk as a part of complete basal nutrition. Infants are particularly more sensitive to toxins than adults. The IARC (1993a) categorizes AFM1 as a possible human carcinogen. The European Communities and the Codex Alimentarius have xed the limit of AFM1 intake to a maximum of 50 ng/kg (Anonymous 2001). Compared to AFB1, AFM1 is rather less carcinogenic and mutagenic; however, it has been reported to exhibit a high level of genotoxic activity in animals (JECFA 2001). Several reports are available wherein AFM1 has been found in milk. It has been detected in breast milk and in cord blood and maternal blood in African countries (like in Sudan, Ghana, and Kenya), the Guangi Xi region of China (Galvano and others 1996), UAE (Abdulrazzaq and others 2003), Turkey (Keskin and others 2009), Australia, and Thailand (El Nezami and others 1995). Also, reports are available on the high contamination of AFM1 in milk in a few EU countries (between 28 and 1012 ng/kg; Markaki and Melissari 1997; Martin and Martin 2000). Recently, AFM1 has also been detected in powdered milk, pasteurized milk, ultrahigh-treated milk, and in other milk-based products (Montagna and others 2008; Ghazani 2009; Shundo and others 2009). Contamination of milk by AM1 might occur in 2 ways, directly due to intake of contaminated feeds by animals that might pass into the milk, or indirectly following contamination of milk and milk products with fungi (Applebaum and others 1982; Blanco
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and others 1993; Barrios and others 1997; Sarimehmetoolu and others 2003; Driehuis and others 2008; Sugiyama and others 2008). However, it should be noted that aatoxin M1 is a metabolite of aatoxin B1, and therefore the possibilities of any direct carryover of AFM1 from feed to milk could be ruled out. It is generally recognized that contamination of milk and milk products with AFM1 varies according to geographical location (dry or wet) and season (hot or cold). Lafont and others (1980) reported that the carryover of aatoxins from animal feed to milk is less than 1% in cows and varies between 0.14% and 0.95%, which is dependent not only on the individual animal but also on the lactation stage of the animal. Aatoxins in raw drugs. Even though considerable advances have been achieved in modern medicine, there has been a renewed interest in the use of traditional plant-based products for a variety of therapeutic purposes (Rates 2001). Currently, a large share in the health care market has been taken over by products based on the popularity of health foods (nutraceuticals/functional foods) of plant origin (Johnson 1997). Contamination of crude drugs of plant origin (as in Ayurvedic and Chinese medicine, and others) incurs heavy economic losses in the tropics and subtropics. The conventional methods of collection, storage, and marketing usually promote the association with several toxigenic molds (Roy and others 1987). Several reports are available on aatoxins contaminating raw drugs of plant origin. The potential of producing aatoxins (AFB1) by some 20 strains of Aspergillus avus contaminating raw drugs has been reported by Chourasia (1990) who reported levels ranging between 0.09 and 0.88 g/mL of the culture ltrate. Roy and others (1988) analyzed common drug plants to detect aatoxin contamination. Out of 15 samples analyzed, 14 were positive for aatoxins ranging between 0.09 g/g in Acacia catechu and 1.20 g/g in Piper nigrum. The researchers also reported that out of 158 isolates of A. avus from the drugyielding plants 49 were toxigenic in nature and the amount of AFB1 produced by the toxigenic isolates ranged between 0.86 and 5.24 g/mL. Similar observations on the contamination of medicinal plant samples have been reported by Aziz and others (1998). They examined a total of 84 medicinal plants and spices and reported 17 samples to be contaminated by AFB1 which ranged between 10 and 160 g/kg. Ali and others (2005) evaluated 23 commercial samples of traditional herbal medicines from Malaysia and Indonesia and found the presence of aatoxin in most of the samples. The mean levels of AFB1, AFB2, and AFG1 in positive samples were 0.26 (70%), 0.07 (61%), and 0.10 (30%) g/kg, respectively, and one of the samples was positive for AFG2 at a level of 0.03 (4%) g/kg. Though these are just a few of the examples to cite, an alarming increase among consumers relying on food of plant origin, renders it a necessity to undertake safety measures against fungal contamination and mycotoxins that might be present in raw materials possessing nutraceutical value. Aatoxins in eggs. Consumption of egg as a rich source of protein is well known. Reports available on aatoxin contamination in eggs are scarce (Micco and others 1987; Pandey and Chauhan 2007; Aly and Anwer 2009; Herzallah 2009). Micco and others (1987) reported that AFB1 bio-transformation in the liver of hens could generate a variety of toxic hydroxylated metabolites that can be transferred to eggs. Hens that are fed with contaminated feeds with more than 3300 mg/kg of AFB1 over a period of 28 d were reported to produce contaminated eggs (Wolzak and others 1985). Also, reports are available on the presence of aatoxin residues transmitted into eggs (Qureshi and others 1998). However, since 1974 the EC has set a limit of 20 g AFB1/kg of layer feed. A study by Pietri and others (2001a) indicated that if this ofcial limit is respected, then no trace of AFB1 or its metabolites can be detected in eggs.

Aatoxin poisoning (aatoxicosis). Consumption of foods/feeds contaminated with high levels of aatoxins may lead to acute aatoxicosis and regular intake, even at low levels (ppb), is reported to be responsible for stunting and loss of weight among children, and in some cases has led to the development of hepatocellular cancer (Bhat and Vasanthi 2003; Hall and Wild 2003). Aatoxins have also been linked with kwashiorkor, a protein-energy malnutrition disease (Adhikari and others 1994). Reports are available wherein AFB1 and aatoxicol (a metabolic product of AFB1) were detected more frequently in the serum, liver, urine, and stools of children suffering from kwashiorkor (Apeagyei and others 1986; Hendrickse and Maxwell 1989; De Vries and others 1990). The role of aatoxins in the development of Reyes syndrome (encephalopathy with severe lesions in kidney and liver following inuenza or varicella) has never been proved, regardless of the frequent detection of aatoxins in the liver of children who have died of this disease (Dvorackova and others 1977; Hogan and others 1978; Casteels-van Daele and Eggermont 1994). Egal and others (2005) have reported that 90% of children in West Africa (Benin and Togo) are exposed to aatoxins due to consumption of contaminated maize and groundnuts, which leads to a measurable impairment of child growth. Severe liver lesions in malnourished adults during the 1970s, with fatal outcome have been reported after severe cases of acute aatoxicosis in parts of Asia and Africa (Krishnamachari and others 1975; Bhat and Krishnamachari 1977). Aatoxins are perceived to be co-factors in the higher incidence of liver cancer (hepatocellular carcinoma) along with hepatitis-B virus in tropical Africa (FAO 1997). Hepatitis-B virus (HBV) interferes with the ability of hepatocytes to metabolize aatoxins, and an aatoxin M1-DNA conjugate exists for a longer time in the liver, increasing the probability of damage to tumor suppressor genes. This effect is synergistic with the resulting damage far greater than just the sum of aatoxins or HBV individually (Williams and others 2004). Among the animals, monogastric farm animals such as poultry and swine are at particular high risk, as a large part of their basal diet consists of cereals. Also, these animals lack the ruminal reservoir of a multitude of microorganisms which can degrade the toxins before they are absorbed by the intestine. The susceptibility of these animals to toxin contamination depends on species, age, and diet. Bonomi and others (1994) have reported that ingestion of aatoxins-contaminated feeds in farm animals can lead to substantial losses in productivity and meat quality. The major symptoms of acute aatoxicosis in mammals include lethargy, ataxia, rough hair coat, and enlarged fatty liver. With chronic exposures, early symptoms of aatoxin poisoning include reduced feed efciency and milk production and decreased appetite (Nibbelink 1986). The FDA tolerance level for aatoxin in human food is 20 g/kg; for breeding livestock feed 100 g/kg; breeding cattle feed 20 g/kg; and poultry feed 300 g/kg (Park and Liang 1993). According to the FAO/WHO expert committee recommendations (1990) the tolerance limit for AFB1 is 5 g/kg food products, for AFM1 it is 0.05 g/kg milk products, and for B1+G1+B2+G2 it is 15 g/k, as for example in raw peanuts.
Ochratoxin-A (OTA) Health risks associated with aatoxin consumption
Ochratoxin-A (OTA; molecular weight 403.8) is the 2nd most important mycotoxin; it is produced by the fungi Aspergillus ochraceus and Penicillium verrucosum. It has also been reported that isolates of Aspergillus niger as well as A. carbonarius are capable of producing OTA (Varga and others 1996; Heenan and others 1998). OTA generally appears during storage of fresh produce (in cereals, coffee, cocoa, dried fruit, spices, and also in
pork) and occasionally in the eld on grapes. It may also be present in some of the internal organs (particularly blood and kidneys) of animals that have been fed on contaminated feeds. In temperate climates OTA is produced by Penicillium verrucosum, while a number of Aspergillus spp. (A. ochraceous, A. niger, A. sulphureus, A. sclerotiorum, and A. melleus) are known to be responsible for its production in tropical and pan-tropical regions of the world. Moss (1996) isolated Petromyces alliaceus from onion and has shown it to be a good OTA producer under laboratory conditions. OTA has also been shown to be biosynthesized by Aspergillus carbonarius in apple and grape juices (Pitt 2000). OTA in milk. OTA contaminations in human milk are common in the temperate and cool areas of the world, including Italy (Micco and others 1995; Miraglia and others 1995; Galvano and others 2001), Switzerland (Zimmerli and Dick 1995), Germany (Gareis and others 1988), and France (Boudra and others 2007). OTA levels in milk from cows in Norway were sufcient to cause a higher intake of OTA than the suggested tolerable daily intake of 5 ng/kg body weight/d (Skaug 1999). OTA contamination in milk from tropical/ hot regions have also been reported in India (Rastogi and others 2004), Egypt (El-Sayed Abd Alla and others 2000), and Brazil (Shundo and others 2009). High levels of OTA in human milk have been reported by Jonsyn and others (1995) wherein, in some instances, infants in Sierra Leone were being exposed to OTA levels that exceeded the permissible limits in animal feed in some of the developed countries. In Norway, Skaug and others (1998, 2001) examined the relationship between OTA contamination of human milk and dietary intake and concluded that the risk of OTA was related to dietary intakes (cereals, processed meat products, cheese, cakes, cookies, and juices). OTA in wine, coffee, tea, cocoa, and herbs. Zimmerli and Dick (1996) in a survey of 133 wines obtained from retail outlets in Switzerland reported, for the 1st time, the occurrence of OTA in wine. OTA was higher in red wines than in white and rose wines. Also, Otteneder and Majerus (2000) have shown OTA to be more common in red wines than in rose and white wines and attributed this to the differences in the winemaking procedure. Impact of geographical effects on the occurrence of OTA in red wines has been reported by Otteneder and Majerus (2000) in Germany; Pietri and others (2001b) in Italy; Stefanaki and others (2003) in Greece; Ratola and others (2004) in Portuguese wines; and in Chilean vineyards (D az and other 2009). The occurrence and the concerns pertaining to OTA in grapes and wine have been extensively reviewed (Battilani and others 2006; Leong and others 2006; Hocking and others 2007). Recently, Flajs and others (2009) employed the enzyme-linked immunosorbent assay (ELISA) and high-performance liquid chromatography (HPLC) for OTA analysis in must and in wine samples collected in Croatia. Their results revealed that OTA concentrations in must (range 19 to 50 ng/L) were higher than in the wines (range 0 to 21 ng/L). The CEC (2002) has xed an OTA limit of 10 g/kg in dried wine fruits. Except for Italian red wines, the mean concentration of OTA in wine in the EU countries does not exceed 100 ng/L (Varga and Kozakiewicz 2006). With regard to coffee and cocoa, the occurrence of OTA is of main concern as the populations dependent on these products are present worldwide. In one of the recent reports, both the wet and dry methods of coffee processing have been reported to represent high levels of OTA (up to 5 g/kg) (Batista and others 2009). Contamination of cocoa beans by OTA has been reported (Jrgensen 2005; Vecchio and Finoli 2007; Am ezqueta and others 2008a). Cocoa bean powder is also known to contain OTA wherein it was in lower levels in cocoa butter than in the nonfat fraction (powder or cake) (Beckett 1994). A 1998 survey in
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the U.K. on exposure of consumers to OTA in cocoa powder and chocolate produced low results which were of little concern (Britannia Foods, http://www.britanniafood.com). With regard to tea, except for one SCOOP report (Miraglia and Brera 2002) not much information is avaible on OTA contamination. Based on this report on a survey (between 1995 and 1998, for 131 samples) in Germany, 8 tea samples showed OTA contamination (0.28 to 10.3 g/kg). OTA contamination of medicinal herbs has also been reported to occur under inadequate storage conditions (Petzinger and Ziegler 2000; Rizzo and others 2004). Associated health risks of OTA. OTA is deemed to be nephrotoxic, immuno-suppressive, carcinogenic, and teratogenic. The IARC has classied ochratoxin A as a compound possibly carcinogenic to humans (Group 2B) (IARC 1987). OTA is also the causal agent for both endemic nephropathy and urothelial tumors (Castegnaro and others 1990). OTA as a causative agent of endemic nephropathy has been reported to occur in rural populations of some regions of Bosnia, Bulgaria, Croatia, Herzegovina, Romania, and Yugoslavia (Krogh 1974). Worldwide, nearly 20,000 people are either suffering from or are suspect of having endemic nephropathy (Ple stina 1992), and the main symptoms include bilateral, primarily chronic, lesions of the renal cortex (tubular degeneration, interstitial brosis, and hyalinization of the glomeruli) (Vukeli c and others 1992). Recently, Zhang and others (2009a) have reported induction of apoptosis in neuronal cells that might be a contributing factor to the pathogenesis of neurodegenerative diseases like Alzheimers disease and Parkinsons disease. OTA has been detected in blood samples and was found to be more frequent and in higher concentrations in inhabitants from endemic regions (Petkova-Bocharova and Castegnaro 1991; Maarou and others 1995). In Italy, signicantly higher OTA concentrations were found in patients treated with dialysis than in transplanted ones and in patients with chronic glomerulonephritis, renal calculus, cysts, chronic renal failure, and healthy subjects (Breitholtz-Emanuelsson and others 1994). In endemic regions of Bulgaria, Croatia, and Yugoslavia the incidence of urothelial tumors of the pelvis and urethra was 50, 90, and 100 times greater than in nonendemic regions (Chernozemsky 1991). Studer-Rohr and others (2000) have reported that, in the human body, OTA has a long half-life of 35 d after a single oral dosage attributed mainly to adverse elimination by toxicokinetics. In the human body, OTA is neither stored nor deposited; however, laboratory studies have conrmed that it is distributed via the blood mainly to the kidneys (Hult and Fuchs 1986). In animals, OTA levels in pigs are of major concern especially in northern European countries. Available reports, as an outcome of several surveys, indicated low levels of OTA. Some of these surveys were performed in Germany (pork sausages) (Frank 1991), in France (pig liver) (Dragacci and others 1999), Denmark (pork meat) (Jorgensen and Petersen 2002), and in Italy (ham) (Chiavaro and others 2002). As OTA is fat-soluble, it is not readily excreted and accumulates in the tissues of animals, particularly pigs. Lower concentrations of OTA are considered to be nephrotoxic in most mammals. Even though several epidemiological studies have been conducted, a relationship between OTA exposures with human nephropathies has never been established (WHO 2001). Recently, the toxicity and carcinogenicity of OTA in animals and humans have been reviewed by Annie and Manderville (2007). They detailed that OTA is nephrotoxic and is suspected of being the main etiological agent responsible for human Balkan endemic nephropathy (BEN) and associated urinary tract tumors. Fungi belonging to Penicillium viridicatum and P. verrucosum play a major role in porcine nephropathy and are an important etiological agent in Balkan endemic nephropathy (Krogh 1987).
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Fusariotoxins (Fusarium toxins)
Fungi belonging to the genus Fusarium are associated with the production of fusariotoxins. There are 2 types of toxins produced by these fungi, namely, metabolites that have properties similar to the hormone estrogen such as ZEN (F-2 toxin) and other ones that are the nonestrogenic trichothecenes. There are several synonyms related to fusariotoxin poisoning: fusario-mycotoxicosis, trichothecene mycotoxicosis, T-2 toxicosis, vomitoxicosis, and ZEN toxicosis.
Fumonisins
Fumonisins (synonym: Macrofusine, molecular weight 721.8) are the most recently isolated mycotoxins (rst discovered in 1988) that are known to possess high cancer-inducing properties (Gelderblom and others 1988; Bennett and Klich 2003). This toxin was originally isolated from Fusarium moniliforme (present name: F. verticillioides Sheldon.) and from Fusarium proliferatum, a common fungal contaminant of corn (maize) throughout the world (Gelderblom and others 1988; Castelo and others 1998). Of late, 6 different types of fumonisins (FA1, FA2, FB1, FB2, FB3, and FB4) have been reported, wherein the A series is the amides and the B series possesses a free amine (Gelderblom and others 1992). Even FC1 has also been reported in the C series. Fumonisins are also known to be produced by F. proliferatum and other related species, especially on maize that has been previously infected during its preharvest stages. Reports are available on the presence of fumonisins in several agricultural products like corn, cornour, dried milled maize fractions, dried gs, herbal tea, medicinal plants, bovine milk, and others (Omurtag and Yazi and cio glu 2004; Gazzotti and others 2009; Karbancioglu-Guler Heperkan 2009; Pietri and others 2009; Seo and others 2009), indicating high risks to public health. It has been estimated that consumption of fumonisin B1 (FB1) by humans in the U.S. is about 80 ng/kg/d (WHO 2002). Occurrence of fusarial toxins in ensiled grass or hay, originating mainly from preharvest contamination, has been reported by Baath and others (1990). Associated health risks of fumonisins. Consumption of fumonisin-contaminated foods by humans has been correlated with increased incidence of esophageal cancer in various parts of South Africa, Central America, Asia (Chelule and others 2001; Marasas and others 2004), and among the black population in Charleston, South Carolina (Sydenham and others 1991). Similar observations have been reported from China (Abnet and others 2001), Italy (Franceschi and others 1990), and Brazil (Van der Westhuizen and others 2003). This toxin has also been reported to be immunosuppressive (WHO 2002). The IARC (International Agency for Research on Cancer 1993c) has classied fumonisins under group 2B (possibly carcinogenic to humans). Among the various types, FB1 is known as a cancer promoter and plays an important role in carcinogenesis in humans (Chu and Li 1994). Fumonisin consumption has also been related to neural tube defects in human babies as they (especially FB1) reduce the uptake of folate in different cell lines (Marasas and others 2004). In the concluding report of the recent task force of the U.S. Council for Agricultural Sciences and Technology (CAST 2003), additional research into the relationship between fumonisin, sphingolipid metabolism disruption, and apoptosis has been asked for to understand the potential carcinogenicity of fumonisins in human health. In a preliminary evaluation report, experts from Nordic countries (Denmark, Norway, Sweden, Finland, and Iceland) have concluded that human daily intake of fumonisins should be less than 1 g/kg body weight/d (Petersen and Thorup 2001). According to Miller and others (1996), the recommended levels of fumonisin concentration in animal feed is: 5 g/g for horses and other equine species, 10 g/g for porcine species, 50 g/g for cattle, and 50 g/g for poultry.

Among the animals, in almost all the species tested, FB1 has been shown to be hepatotoxic and nephrotoxic. In most of the animal species, fumonisins are poorly absorbed from the digestive tract and are rapidly distributed and eliminated (WHO 2002). Primary symptoms observed are changes in histology, either in the liver or kidney of fumonisin-treated animals, wherein increased apoptosis followed by regenerative cell proliferation occur. Even though the toxicity of fumonisin is low, it has been linked with several diseases in domestic animals: equine leukoencephalomalacia (ELEM) in horses, toxic feed syndrome in poultry, and porcine pulmonary edema syndrome (PPE) in swine (Ross and others 1992, 1993; Norred and Voss 1994). These diseases involve disturbed sphingolipid metabolism and cardiovascular malfunction. In animals, fumonisin is also known to impair the basic immune function, to cause liver and kidney damage, to be a heart risk, and to reduce weight gains, and thereby augmenting the mortality rates (Casteel and others 1994; Norred and others 1998). Jones and others (1994) have shown that consumption of FB1 causes respiratory difculties in swine. Fusarium moniliforme that produces mutagenic fusarins and fumonisins has been reported to be responsible for disease symptoms in horses and donkeys (Wilson and others 1991). In dairy cattle, reduction in milk production has been reported, even at low levels of 100 ppm (Diaz and others 2000). However, a detailed survey on the health effects on long-term consumption of Fumonisin-contaminated feedstuffs might give a broader insight on the same. Some of the Fusarium species (F. avenaceum, F. poae, and F. tricinctum) are also known to produce the mycotoxins beauvericin (BEA) and enniatins (ENNs) (Logrieco and others 2002; Thrane and others 2004), which are the cyclic hexadepsipeptides consisting of alternating hydroxyl-acid and N-methylamino acid residues. These 2 types of toxins have been isolated from grains obtained from Scandinavia (Uhlig and others 2007). Jestoi (2008) has reported the occurrence of BEA contamination in cereals obtained from other locations.
Zearalenone and associated health risks
swine and mink, but rather acted as an estrogen agonist. Enlarged mammae and atrophied testes were exhibited due to ZEN intake in boars (Flannigan 1991). Consumption of contaminated feed by dairy cows did not result in any of the health hazards to humans (Wood 1992). The Joint FAO/WHO Expert Committee on Food Additives (JECFA) has established a provisional maximum tolerable daily intake for ZEN to be 0.5 g/kg of body weight (JECFA 2000).
Vomitoxin (DON) and associated risks
ZEN (molecular weight: 318.4) and zearalenol are estrogenic resorcylic acid lactone compounds produced by Fusarium species (Diekman and Green 1992). Among the human population, children are the most affected due to consumption of ZEN-contaminated foods (mainly cereals and cereal-based food products). This toxin has worldwide distribution and can contaminate most of the cereals like barley, maize, oats, sorghum, and others. ZEN has also been detected in wheat and in bread (Tanaka and others 1988; Aziz and others 1997). Associated health risks. This toxin has been implicated in several incidents of precocious pubertal changes (Kuiper-Goodman and others 1987). In domestic animals, ZEN poisoning has been associated with hyperestrogenic or feminizing syndromes. Pigs are generally the most affected and it causes genital/urinary prob lems (Zollner and others 2002; D anicke and others 2005). The major symptoms of ZEN poisoning include hyperemia and edematous swelling of the vulva in prepubertal gilts and in severe cases prolapse of the vagina and rectum. In some cases, atrophy of the testes in male pigs occurred with decreased libido and hypertrophy of the mammary glands (Marasas and others 1984). In general, poultry are the least affected after ingestion of ZEN. However, swine showed acute symptoms in prepubertal gilts that included enlarged mammae, swelling of uterus and vulva, and atrophy of the ovaries. In severe cases, prolapse of the vulva and rectum have occurred. Effects of ZEN and/or tamoxifen (TAM) on swine and mink reproduction have been studied by Yang and others (1995). Results of their study indicated that TAM was not effective in ameliorating the hyperestrogenic effects of ZEN in
DON (12, 13-epoxy-3,4,15-trihydroxytrichothec-9-en-8-one; molecular weight: 240.26) is commonly known as alphamethyl phenethylamine, amphetamine deoxynivalenol, 4deoxynivalenol (DON), or as RD-toxin. Vomitoxin is commonly encountered in food products and feeds prepared from contaminated corn and wheat (Rotter and others 1996). This toxin is the most frequently detected Fusarium toxin produced by Fusarium graminearum. DON has been reported in most parts of the world (Canady and others 2001) and in the U.S. alone computer simulations have shown annual costs for DON to be 637 million dollars in crop losses of wheat and corn and 18 million in feed losses (CAST 2003). Vomitoxin is considered to be highly stable and can survive various food processing methods (such as milling, powdering). DON and its metabolite de-epoxyDON have also been reported to be present in low amounts in eggs (Sypecka and others 2004; Valenta and Danicke 2005) and in beer at low levels (Scott 1996). Recently, low levels of deoxynivalenol (2.6 to 17.9 ng/g) and its metabolite deepoxy-DON (2.4 to 23.7 ng/g) have been reported in 20 homeproduced egg samples collected in Belgium (Tangnia and others 2008). Consumption of vomitoxin-contaminated products has been correlated with reduced milk production in dairy cattle, vomiting in swine, inhibition of reproductive performance and immune function in several animal species, along with induction of apoptosis in mice (Jones and others 1994; Zhou and others 2000). Maximum limit of 1 ppm of DON for bran, our, and germ meant to be used for human consumption has been set by the U.S. Food and Drug Administration (FDA) (Proctor and others 1995). Maximum tolerated levels in the range of 500 to 1000 g/kg (0.05 to 0.1 ppm) for DON in most other food products have also been set (van Egmond and Jonker 2004). The maximum level of DON in raw cereals allowed by the European Union is 1250 g/kg (Food Safety Authority of Ireland, http://www.fsai.ie). In humans, the effects of DON on health are not completely understood. However, some toxicity information after consumption of DON-contaminated cereals, grains, and other products has been reported (Yoshizawa 1983; Luo 1994; Meky and others 2001; Sun and others 2002).
Trichothecenes and associated health risks
Similar to ZEN and vomitoxin, trichothecenes are also produced by Fusarium species. Trichothecenes are also known to be produced by other fungal genera like Trichoderma, Trichotecium, Myrothecium, and Stachybotrys (IPCS 1990). Trichothecenes are sesquiterpenoid mycotoxins that accumulate in kernels of infected spikelets rendering the grain unsuitable for human or animal consumption (Harris and others 1999; Langevin and others 2004). Trichothecenes are usually found to be contaminants of cereals and their derivatives (Foroud and Eudes 2009). Nearly 160 trichothecenes have been identied and are classied into 4 groups depending on their chemical structure. The major ones are T-2 and HT-2 toxins (group A) and nivalenol (NIV) (group B).
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Associated health risks of trichothecenes. Trichothecene mycotoxicosis (scabby grain toxicosis) has been reported to occur within hours after ingestion of contaminated foods (wheat, corn, rice). Reports available indicate that poisonings have occurred in Japan (Ueno 1971), China (Wang and others 1993), and India (Ramakrishna and others 1989). Fusarium head blight, one of the serious epidemics in North America during the 1990s, caused an estimated economic loss of 3 billion dollars in the U.S. alone (McMullen and others 1997). The main symptoms of trichothecene mycotoxicosis are abdominal pain, nausea, vomiting, diarrhea, dizziness, and headache. Trichothecenes have strong impacts on the health of animals and humans due to their immunosuppressive effects. GroupA trichothecenes are of major concern as they are more toxic than the type B trichothecenes. In animals, these mycotoxins are held responsible for reduced feed uptake, vomiting, and immuno-suppression. In instances of chronic poisoning, GroupA trichothecenes produce signicant changes in the blood cell count and in immune function. Among the group A, T-2 toxin is the most important one. It is readily metabolized by the gut microora of mammals into a number of other metabolites. HT2 toxin is a primary metabolite in the gut and is absorbed into the blood after ingestion of T-2 toxin. Metabolism continues in the liver along with biliary excretion, resulting in a substantial combined rst-pass effect in the gut and liver (WHO 2002). The principal effects of perturbed protein synthesis from T-2 toxin are usually observed in the immune system and include changes in leukocyte counts, delayed hypersensitivity, depletion of selective blood cell progenitors, and depressed antibody formation (WHO 2002). Compounds of the other group of trichothecenes (Group B) generally cause a reduction in dietary consumption, especially in pigs. The joint FAO/WHO expert committee on food and additives (JECFA 2001) has established a permissible limit of 1 g/kg body weight and 0.061 g/kg body weight for T-2 toxin and HT-2 toxin, respectively.
Patulin and associated health risks
sic environmental factors as variations in temperature and water activity (Northolt and others 1996). Associated health risks of Patulin. Patulin toxin is reported to affect the functions of gastrointestinal tissue, kidney, liver, and the overall immune system (Escoula and others 1988; Speijers and others 1988; Wichmann and others 2002). This toxin is regarded to be genotoxic, carcinogenic, can induce oxidative stress response in mammalian cells, generate reactive oxygen species (ROS), and induce apoptosis in human leukemia cells (HL-60) (Barhoumi and Burghardt 1996; Schumacher and others 2006; Liu and others 2007; Wu and others 2008). Contradictorily, Wouters and Speijers (1996) have reported patulin to be noncarcinogenic. However, the IARC has classied patulin as category 3; not classiable as to its carcinogenicity in humans (IARC 1993b). The permissible limit for patulin in apples and their products in the U.S. and EU has been set at 50 ppb (FDA, http://www.fda.gov/ora/compliance ref/cpg; EUROPA, http://europa.eu.int/eur-lex/en/archive/2004). A permissible limit of patulin content in apple juice, and as juice ingredients in other beverages, has been set at 50 g/kg, in solid apple products at 25 g/kg, and in baby food of 10 g/kg (Mycotoxin Certication Standard 2008, www.mycotoxin-certication.eu).
Citrinin
Generally, fruits and vegetables are easily contaminated by toxigenic molds leading to quality deterioration (Drusch and Ragab 2003; Moss 2008). Agronomic practices employed during fruit cultivation and juice making have been reported to signicantly inuence the occurrence and production of patulin and citrinin (Martins and others 2002). Patulin (molecular weight: 145.1) is a mycotoxin that forms the smallest group of toxic metabolites referred to as polyketides, and is reported to be produced by fungi belonging to Aspergillus spp., Penicillium expansum, and Paecilomyces and Byssochlamys spp. (Byssochlamys nivea, B. fulva) (Dutton and others 1984; Fuchs and others 2008; Moss 2008; Cunha and others 2009). Patulin is being considered as a possible toxin in Europe and New Zealand (Lacey 1991) and is regarded as the most dangerous mycotoxin in fruits, particularly apples, pears, and their products (Frisvad and Thrane 1996; Kabak and others 2006; Murillo-Arbizu and others 2009). Patulin is mainly associated with surface-injured fruits, which renders them vulnerable to fungal infection, mainly by Penicillium spp. (Sewram and others 2000). Patulin is also reported to be present in silage/feeds intended for ruminants; and it has been reported to be responsible for the deaths of cattle in France (Moreau 1979). Schneweis and others (2000) reported that lower concentrations of patulin found in silage will rarely cause the typical neurotoxic signs in animals, but might exert detrimental effects on the rumen microora, mainly because of its antimicrobial activity. The occurrence of patulin in a raw material has been directly related to some of such extrin66
Citrinin (molecular weight: 250.25) is the secondary metabolite produced by Penicillium expansum and some of the Aspergillus and Monascus spp. (Kurata 1990; Vinas and others 1993; Li and others 2003; Kim and others 2007; Abramson and others 2009). Citrinin often occurs as a common contaminant of food and feed (fruits, barley, maize, cheese, dietary supplements) (Manabe 2001; Schneweis and others 2001; Bailly and others 2002; Bennett and Klich 2003; Meister 2004). Barley, as well as other cereals employed for producing beer, has been reported to be a good substrate for the growth of many toxigenic fungi capable of producing citrinin (Galvano and others 2005). Associated health risks of citrinin. In humans, reported health risks due to citrinin are scarce. Some reports do indicate citrinins association with mycotoxic nephropathy in swine and Balkan endemic nephropathy in humans (IARC 1986; Chernozemsky 1991; Hald 1991). However, details available on the toxic effects of citrinin in animals show its nephrotoxic nature as well as teratogenic effects in rabbits, poultry, dogs, and rats and mice along with induction of apoptosis (Kogika and others 1993; Bennett and Klich 2003; Yu and others 2006; Chan 2007; Kumar and others 2007; Singh and others 2007).
Alternaria toxins
Mycotoxins produced by fungi belonging to Alternaria species are referred to as Alternaria toxins. Alternaria species commonly occur during the pre- and postharvest stages of fruits and vegetables. These fungi are capable of producing a range of mycotoxins and other less toxic metabolites. The most important toxinproducing species is Alternaria alternate, which usually contaminates cereals, sunower seeds, rapeseed, olives, and fruits. Among the various Alternaria toxins, alternariol (AOH) and alternariol monomethyl ether (AME) are reported to be the most toxic (Combe and others 1970; Pero and others 1973). The toxins AOH and AME have been detected in sorghum (Ansari and Shrivastava 1990), sunower seeds (Chulze and others 1995), barley, wheat, oats (Gruber-Schley and Thalmann 1988; Azcarate and others 2008), olives, tomatoes, mandarin oranges, peppers, and melons (Logrieco and others 1988). Also, apart from AOH and AME, other naturally occurring Alternaria toxins include tenuazonic acid, altenuene, and altertoxin. The signicance of tenuazonic acid in fresh tomatoes used for the production of tomato sauce has been detailed by

Mislivic and others (1987). The other fungal species producing these toxins include A. alternata, A. dauci, A. cucumerina, A. solani, and A. tenuissima (Montemurro and Visconti 1992). Associated health risks of Alternaria toxins. Alternaria toxins have been implicated in humans and animal health disorders. AME is reported to be cytotoxic and along with AOH has been shown to possess synergistic effects. AOH is lethal to unborn mice at levels of 100 mg/kg body weight (Pero and others 1973). Presently, no limits are set for Alternaria mycotoxins as various surveys conducted have shown their natural occurrence in foods to be very low and the prospects for direct human exposure are limited.
Claviceps purpurea /ergot toxins and associated health risks
Sclerotia of fungi belonging to the genus Claviceps produce ergot alkaloids. A sclerotium is a dark-colored, hard mycelial mass that establishes itself on the seed or kernel of the plant. Usually, wild grass species are considered to favor the crosscontamination of C. purpurea onto the cultivated grass (Poo and Araya 1989). Apart from Claviceps, ergot alkaloids are also produced as secondary metabolites by fungal species belonging to Penicillium, Aspergillus, and Rhizopus (Flieger and others 1997). The human disease ergotism is entirely inuenced by the type of alkaloids present (Burfening 1973) (The term ergotism has occassionally also been used to denote the plant disease). Associated health risks of ergot toxins. The Claviceps purpurea toxin is of not much signicance today and human ergotism is extremely rare, which might be attributed to 2 reasons: primarily, due to the recent improvements in the cleaning and milling processes that are able to remove most of the ergots leaving very low levels of the alkaloids in the our, and, second, these alkaloids might be relatively unstable and can be destroyed easily by conventional processing (baking, cooking, milling). However, it is necessary to cover a few aspects on C. purpurea toxins. Earlier reports are available on ergot poisoning of domestic animals by ingestion of feeds containing Claviceps purpurea sclerotia (Groger 1972; van Rensburg and Altenkirk 1974). Ergot alkaloids have been reported in sleepy grass (Stipa robusta) which is common in the South-Western parts of the U.S. (Cheeke 1995). The most common intoxications associated with ergot alkaloids is fescue toxicosis wherein the tall fescue (Festuca arundinacea) pasture grass common to the U.S. was infected by Claviceps spp. that produced ergovaline (an alkaloid), which proved to be toxic to animals (Botha and others 2004). These ergot alkaloids have also been reported in pasture grasses of Northern Europe (FinkGremmels 2005). Toxicity symptoms of Claviceps toxins include delirium, prostration, violent head pain, abscesses, and gangrene of the extremities. The toxin most likely acts as a vasoconstrictor. Some of the secondary metabolites of fungi that were used as antibiotics in earlier years are now considered toxins (Peraica and others 1999). However, with regard to ergot alkaloids, they are still being used in the treatment of Parkinsons disease, as prolactin inhibitors, in cerebrovascular insufciency, and in migraine treatments. Ergotamine, a major alkaloid involved, possesses greater biological activity than the other components of ergot and is used in human medicine (mainly as a vasoconstrictor and an oxytoxic) (van Rensburg and Altenkirk 1974).
Cyclopiazonic acid and associated health risks
Cyclopiazonic acid (CPA) (molecular weight: 336.4) is a toxic secondary metabolite that was originally isolated from Penicillium cyclopium and later on from other fungal species like: P. griseofulvum, Aspergillus avus, A. versicolor, and A. tamarii. Chemically, it is an indole tetramic acid. The signicance of CPA is obscure;
however, it is reported to naturally occur in peanuts (Urano and others 1992), corn (Lee and Hagler 1991), and in cheese (LeBars 1979). The health risks associated with CPA is very minimal, but in high concentrations it may be acutely toxic, especially to animals. This toxin is usually encountered on consumption of contaminated cereals. It is generally claimed to be a co-contaminant with AFB1 in North America. However, due to its co-occurrence, it is believed to reduce the danger of aatoxins by contributing towards their metabolic inhibition. Morrissey and others (1984) have assessed the potential effects of CPA on pregnancy and fetal development in Fischer-344 rats, which were given daily doses of CPA (0, 1, 5, or 10 mg CPA/kg body weight). The researchers reported a signicant decrease in feed consumption (at high dose) and the animals that died had histologic lesions in the liver, spleen, kidney, and other organs. Signicant differences in skeletal development were also observed that showed retardation of ossication of cervical centra and caudal vertebrae. Toxic effects of CPA in broiler chicks have been reported earlier (Cullen and others 1988; Kubena and others 1994; Balachandran and Parthasarathy 1996). CPA is also being assumed to induce mycotoxicoses in quail in Indonesia (Stoltz and others 1988). Only a few signicant ndings are discussed in the subsequent text. Smith and others (1992) evaluated the individual and combined effects of aatoxins and CPA in day-old Petersen x Hubbard broiler chickens to 3 wk of age. The treatments included supplementation with levels of 0 and 3.5 mg aatoxins/kg of feed, and 0 and 50 mg CPA/kg of feed. They recorded a signicant reduction in the body weight by aatoxins, CPA, and the aatoxins-CPA combination at the end of 3 wk. Toxicity of CPA indicated increase in weights of the liver, kidney, and proventriculus with enhancement in the levels of uric acid and cholesterol. A signicant decrease in serum phosphorus was also recorded. Activities of aatoxins and CPA combination showed an increase in weight of the liver, kidney, pancreas, and proventriculus with a decrease in concentrations of serum albumin and phosphorus. An increase in concentrations of serum glutamic oxalacetic transaminase and blood urea nitrogen, and decreases in the relative weight of the bursa of Fabricius were also observed. The postmortem results showed that chickens fed with CPA and the aatoxin-CPA combination had thickened mucosa and dilated proventricular lumens, hard brotic spleen, and atrophy of the gizzard. Kubena and others (1994) studied the effects of feeding 6 mg T-2 toxin and 34 mg CPA/kg of diet singly and in combination in male broiler chicks from 1 d to 3 wk of age. They found that the body weights were depressed by T-2 or CPA singly or after the combination of T-2 and CPA. A signicant synergistic interaction between T-2 and CPA with regard to liver and kidney weights and serum cholesterol and triglyceride concentrations was recorded. However, the efciency of feed utilization or mortality was not affected by dietary treatments. Oral lesions were observed in chicks fed diets containing CPA. Gentles and others (1999) evaluated the individual and combined effects of OTA and CPA in Petersen x Hubbard broiler chickens from 1 d to 3 wk of age, wherein treatments of 0 and 2.5 mg OTA/kg feed and 0 and 34 mg CPA/kg feed were administered. Results showed a decrease in the body weight gain by OTA, CPA, and OA-CPA in combination at the end of 3 wk. Increased relative weights of the proventriculus and activity of creatine kinase were the main toxic symptoms of CPA. The researchers reported that exposure to OA-CPA was characterized by increased relative weights of the liver, kidney, pancreas, and proventriculus, decreased concentrations of serum albumin, total protein, and cholesterol, and with increased activity of creatine kinase and
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disease. Jensen (2005) has reported N. lolii to be capable of providing the host plant with resistance to several pests along with enhancing the growth of the plant. However, the fungus was also observed to trigger the production of toxic metabolites with severe effects on livestock. No reports are available on the associated health risks to huMycotoxins encountered in animal feeds mans and hence further research is a necessity to provide sufSporidesmins, slaframine, stachybotryotoxins, lolitrem, and pho- cient information on the possible transfer of these toxins from mopsins animal products to the human food chain. Sporidesmins. These are hepatotoxins (to which sheep are very sensitive) produced by Pithomyces chartarum, a sapro- Phomopsins. Phomopsins A and B are the 2 secondary metabophytic fungus that grows on dead grass. Sporidesmins include lites isolated from extracts of lupin seed cultures of Phomopsis epidithiopiperazine-2,5-dione (ETP), a fungal toxin that can dis- leptostromiformis (a parasite of eld lupin Lupinus luteus), known rupt the cellular functions via oxidative alteration of cysteine to cause lupinosis (Culvenor and others 1977). Phomopsins are residues on key proteins (Srinivasan and others 2006). In France, linear hexapeptide compounds having an ether-linked macropastures have been shown to harbor fungi like Pithomyces pro- cycle between amino acids 1 and 3 in the linear chain (Edgar ducing sporidesmin, which causes facial eczema (a hepatoge- 1991). The fungus Phomopsis leptostromiformis can also grow nous photosensitization) (Le Bars and Le Bars 1996). Outbreaks saprophytically on other species such as Lupinus albus and L. of pithomycotoxicosis (facial eczema) have also been reported angustifolius. Poisoning, known as lupinosis, occurs after ingesfor ruminants in the Azores Islands of Portugal after warm, humid tion of contaminated lupins. This toxin commonly affects sheep, periods during late summer and autumn (Pinto and others 2005). cattle, horses, pigs, and rats. Common symptoms include high Death of a captive Eastern Grey kangaroo due to consumption hepatotoxicity. Typical characteristic features in affected animals of feed contaminated with Pithomyces chartarum is believed to would be: in cattle, excessive salivation and watering eyes (with have been induced by sporidesmins (Hum 2005). atrophic arthrosis in chronic cases); in horses, sluggishness or ataxia with production of reddish-brown colored urine; and in Slaframine (1-acetoxy-8-aminooctahydroindolizidine). Slafra- sheep and cattle transudation. mine (or slobber factor) is a mycotoxin produced by fungi Among the 2 groups, phomopsin A is of high clinical signibelonging to the genus Rhizoctonia that usually attack cattle and cance. Phomopsin A, a macrocyclic heptapeptide isolated from produce drooling. Slaframine poisoning is common during cool the fungus Phomopsis leptostromiformis is a potent inhibitor of and wet seasons, which provide ideal environmental conditions microtubule assembly and of vinblastine binding to tubulin. In 1 for the proliferation and growth of Rhizoctonia leguminicola, of the studies by George and others (1979) it was shown that a commonly called black patch indicating bronze to black crystalline mixture of phomopsins A and B (about 4:1) produced spots or rings observed on leaves and stems (Burrows and Tyril clinical, biochemical, and histological changes characteristic of 2001). This fungus infects red clover (Trifolium pratense), white lupinosis when administered to sheep by intraperitoneal route. clover (Trifolium repens), alsike clover (Trifolium hybridum), When separately administered by the same route to nursing rats, alfalfa, and can also be present on pastures and in stored dry the 2 compounds caused typical mitosis-arresting effects in the hay. Slaframine is generally claimed to be active in stored hay parenchymal cells of the liver. Phomopsin A was the more imthroughout the year. Slaframine is not an active compound but portant of these 2 agents. is considered to be converted to an active metabolite by liver Effects of different doses of pure phomopsins administered to microsomal enzymes. Slaframine concentrations above the 10 sheep have been reported by Peterson and others (1987). From ppm level in feed are usually associated with clinical signs their study, a dose of 1000 /kg administered at daily rates of (Osweiler 1996). 50 or 200 /kg killed all sheep, while a single dose of 500 /kg Common clinical symptoms observed in horses due to caused signicant liver damage, without being fatal. Single doses slaframine poisoning include excessive salivation, lacrimation, of 125 and 250 /kg and repeated daily doses of 12.5 /kg over colic, and diarrhea. The 1st symptom of slaframine poisoning 16 wk caused no detectable tissue damage. develops after about 1 to 3 h of consumption of contaminated However, no risks have been reported to humans due to forage. Even a case of abortion in a mare has been reported (Smith phomopsins. A maximum contamination limit of 5 ng/g of phoand Henderson 1991). Osweiler (1996) suggested that atropine mopsins in lupin-based food has been recommended in Australia may provide symptomatic relief of salivation and diarrhea as a and Great Britain (Anonymous 1996). preliminary treatment. 3-Nitropropionic Acid. Arthrinium spp. produce a secondary Lolitrem toxin. Lolitrem toxin is produced by Acremonium lolii metabolite known as 3-nitropropionic acid (3-NPA), reportedly on perennial ryegrass, which produces staggers in sheep (Moss known to cause acute food poisoning referred to as moldy sugar1995). The toxic syndrome involves muscle tremors, muscle cane poisoning (Liu and others 1988; Ming 1995). The common weakness and spasms, and takes nearly 14 d for the 1st symptoms symptoms of poisoning include vomiting, dystonia, convulsions, to develop in livestock after consuming infected perennial rye- carpopedal spasm, and in certain cases coma. The incubation grass. Neurological disease in horses due to lolitrem intoxications period for the symptoms to develop is 2 to 3 h after ingeshas been reported (Goehring and others 2005). Intoxications have tion of contaminated sugarcane. In adults, the main symptom also been reported in bulls fed on rye-grass straw that had high is associated with gastrointestinal problems, whereas signs of selevels of lolitrem B (between 2.9 and 4.8 ppm) (Benkhelil and vere encephalopathy are not common (Ludolph and others 1991). others 2004). As a result of bilateral symmetric necrosis of the basal ganglia, in Generally, a mutual association occurs between perennial rye- certain cases delayed dystonia develops (10% to 50% of patients) grass (Lolium perenne L.) and the endophytic fungus Neoty- and the development of delayed symptoms has been predicted by phodium lolii. These endophytic fungal species produce indole abnormal basal ganglia that are visible on cranial computerized terpenoids among which the lolitrem B toxin is present in am- tomography scans (Ming 1995). ple amounts. These toxins are able to act as antagonists of the Production of hypothermia and inhibition of histochemical laGAB-aergic neurotransmission, leading to the cause of staggers beling of succinate dehydrogenase in rat brain by 3-NPA have in concentrations of triglycerides and uric acid. Postmortem examination showed thickened mucosa and dilated proventricular lumen in chickens fed CPA or OA-CPA. It was concluded that OA, CPA, and the OA-CPA combination can limit broiler performance and adversely affect broiler health.
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Table 2 --- Some of the recent postharvest methods adapted for removal of mycotoxins in human food. Mycotoxin Aatoxin Treatments Chemical agents like ammonia, caustic soda, hydrogen peroxide, bisultes, chlorinated agents, formaldehyde Radiation processing (gamma rays) Ozone Roasting Natural botanicals/herbs Scott (1998) Reference
AFB1 AFB1 and G1 AFB1 AFB1
Aatoxin M1
Organic mycotoxin binders (glucomannans), bentonite clay, hydrogen peroxide, pasteurization
Bhat and others (2007), Ogbadu (1980), Temcharoen and Thilly (1982) McKenzie and others (1997) Staron and others (1980) Alderman and Marth (1976), Kensler and others (2004), Peterson and others (2006), Reddy and others (2009) Doyle and others (1982), Devegowda (2000),
Citrinin DON, ZEN, and FB1 and FB2 Fumonisin (FB1)
phosphateethanol extraction Fermentative bacteria, thermal treatments Alkaline treatments, thermal treatments, genetic modication of plant Radiation processing Thermal treatments Polishing and milling By use of bentonite, modied bentonites, and chitosan Lactic acid bacteria Fermentation, heat treatments Chicken intestinal microbes
Kiermeier and Mashaley (1977), Yousef and Marth (1985); Lee and others (2007) Niderkorn and others (2007), Young and others (1987) Duvick (2001), Hendrich and others (1993), Jackson and others (1996) Paster and others (1985) Boudra and others (1995), Scudamore (2005), La Pera and others (2008) Osborne and others (1996) Kurtbay and others (2008) Del Prete and others (2007) Kadakal and Nas (2003), Ough and Corison (1980) Young and others (2007)
OTA OTA OTA OTA OTA Patulin Trichothecene mycotoxins
also been reported (Nony and others 1999). A delayed dystonia syndrome in children subsequent to initial gastrointestinal symptoms and acute noninammatory encephalopathy on ingestion of mildewed sugarcane containing 3-nitropropionic acid (3-NPA) has been reported by He and others (1995). Onyalai disease. Onyalai, an endemic disease of Africa (southern Sahara region) is caused by the mycotoxin produced by isolates of Phoma sorghina, which often contaminates millet. Onyalai has also been reported in a few black populations of central southern Africa (Kavango, Namibia) with a recorded incidence of 1 in 660 inhabitants/year (Hesseling 1992). The disease is known to be produced in rats fed with intentionally contaminated maize and wheat. This disease is characterized by hemorrhaging lesions in the mouth (Rabie and others 1975). Information on the possible pathways of the toxin is scarce.
Pre- and postharvest methods adapted to control mycotoxins
Increasing knowledge and awareness on the consumption of food and feeds contaminated with mycotoxins has turned the focus towards development of inactivation procedures. Reports are available wherein inactivation or removal of some of the common mycotoxins (like aatoxins, OTA, fumonisins) have been explored, and in certain cases have been successful. However, a wide gap still persists with regard to exploring the possibilities of removal or inactivation of other commonly occurring mycotoxins (both in food and feed), which have been described previously. Even though good agricultural practice and good manufacturing practice (GAP and GMP, respectively) are the best available option to minimize mycotoxins at the eld level, certain reports are available wherein various processing methodologies have been
adapted to eliminate these toxins. Table 2 highlights some of the recent postharvest methods adapted for removal of mycotoxins in human food, while Table 3 details on the maximum tolerable limits set for certain mycotoxins in food and feed. In the following text, a few are being discussed with regard to aatoxins, OTA, and Fusarium toxins. Removal or inactivation of aatoxins. Cotty and Bhatnagar (1994) proposed a new method that involves isolation of A. avus and A. parasiticus (nonvirulent strains that do not produce aatoxins), to compete with the natural toxin-producing strains. These strains occupied the same ecological niche as toxin-producing strains and they decreased the level of contamination with toxinproducing molds. Fungal co-occurrence in any product indicates the possible competition and succession or antagonism among the colonizing fungi. Co-occurrence of fungal species has been shown to inhibit or reduce the toxin concentration in a substrate (Mann and Rehm 1976). Co-inoculation of A. niger and Trichoderma viride onto maize or peanuts contaminated with A. avus has been shown to reduce aatoxin production (Wicklow and others 1980; Aziz and Shahin 1997). Reports are available (El-Nemazi and others 1998; Yoon and Baeck 1999) wherein specic strains of lactic acid bacteria (such as propionibacteria and bidobacteria) possessing typical cell wall structures can bind aatoxins and limit their bioavailability. These toxins could then be eliminated in the feces/excreta without any negative impact on the animals or any risk for toxic residues to be found in edible animal products. Also, some of the microbes (for example, Corynebacterium rubrum) have been shown to metabolize mycotoxins (aatoxins) in contaminated feed or to bio-transform them (Nakazato and others 1990).
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Table 3 --- Maximum tolerable limits set for certain mycotoxins in food and feed. Products 2ppb for AFB1 and 4 ppb for AF B1+B2+G1+G2 50 ng/kg 5 ng/kg body weight/d 10 g/kg 120 ng/kg body weight Limits set Reference
Mycotoxin
Aatoxins
in cereals, peanuts, and dried fruits
AFM1 OTA OTA OTA
Moss (2002), Stroka and Anklam (2002) EC (European Commission) (2006) Anonymous (2001) Skaug (1999) CEC (2002) EU Commission Regulation (2006a) WHO (2002) EU Commission Regulation (2006a) WHO (2002) Miller and others (1996) Creppy (2002), JECFA (2000) JECFA (2001) JECFA (2001) EU Commission Regulation (2006b) www.mycotoxin-certication.eu (accessed on 24 July 2009) Anonymous (1996)
Fumonisins
in milk in milk in dried wine fruits cereals, cereal products, raisins, roasted coffee, wine, grape juice, and food for children from all food source 2 g/kg body weight (bw)/d for fumonisins 200 g/kg (infants and young children) 80 ng/kg/d 5 to 50 g/g for horses 0.5 g/kg of body weight 1250 g/kg 1 g/kg body weight 0.061 g/kg body weight 0.4 g/kg body weight. 10 g/kg body weight 50 g/kg and 25 g/kg, respectively 5 ng/g
Fumonisins Fumonisin B1 Fumonisins
ZEN DON Trichothecenes (T-2 toxin ) Trichothecenes (HT-2 toxin) Patulin Patulin
maize-based formulae maize and other cereals animal feed for horses and other equine species, and for cattle in food and feed in raw cereals in food & feed
in food and feed in adult foods in baby food
Patulin Phomopsins
apple juice and in solid apple products lupin-based food

Presently, natural organic mycotoxin binders (such as glucomannans extracted from the external part of the cell wall of the yeast Saccharomyces cerevisiae) are also being used to bind certain mycotoxins. Devegowda (2000) has shown that 500 g of glucomannans from yeast cell-wall have the same adsorption capacity as 8 kg of clay. These types of binders have been shown to reduce the AFM1 content of milk by 58% in cows supplemented with diets contaminated with aatoxin B1 at a concentration of 0.05% of dry matter (Withlow and Hagler 1999). Degradation of mycotoxins, particularly aatoxins in contaminated feeds through the application of various chemical agents such as acids, bases (ammonia, caustic soda), oxidants (hydrogen peroxide, ozone), reducing agents (bisultes), chlorinated agents, and formaldehyde have been reported by Scott (1998). However, no detailed reports are available on the side effects of using these agents. Previously, Masimango and others (1978) reported that adsorbents like bentonite clay can bind and remove aatoxin B1 from solutions. Also, bentonite was able to remove AFM1 from milk up to 79% (Doyle and others 1982). Addition of hydrogen peroxide (1%) to UV-irradiated milk (10 min) completely (100%) eliminated the AFM1 (Yousef and Marth 1985). The impact of radiation processing (a physical, nonthermal method of preservation) on the sensitivity of fungi and mycotoxins has been well established for various foodstuffs (Mitchell 1988; Refai and others 1996). Inhibition of AFB1 production in A. avus-contaminated soybeans and groundnuts (peanuts) by radiation has been reported by Ogbadu (1980). Radiation processing by gamma rays reduced AFB1 by 75% and 100% in peanut meal at doses of 1 and 10 kGy (Temcharoen and Thilly 1982). Significant reduction of AFB1 at 10 kGy irradiation dose in Mucuna pruriens seeds, an underutilized nutraceutically valued legume, has been reported recently (Bhat and others 2007). The reduction/destruction was attributed mainly to the radiolysis of water that leads to formation of highly reactive free radicals, which readily attack the AFB1 at the terminal furan ring, producing products of low biological activities. The decomposition temperature of aatoxin is very high (237 to 306 C). Betina (1989) reported that AFB1 can be degraded at high temperature of 267 C. Roasting of articially contaminated peanut meal (in a microwave oven) for 4 min has been shown to destroy aatoxin by about 95% (Staron and others 1980). Treatments with ozone have also been reported to eliminate AFB1 and G1 in aqueous model systems (McKenzie and others 1997). According to Purchase and others (1972), pasteurization of milk at 62 C for 30 min was found to reduce AFM1 by 32%. Also, storage of milk at 5 C for 1 and 3 d reduced AFM1 in milk by 18.8% and 24.2%, respectively (Kiermeier and Mashaley 1977). The ability of Lactobacillus and Bidobacterium species to remove AFM1 in reconstituted milk has recently been reported by Kabak and Var (2008). However, contradictory to their results, reports are also available wherein AFM1 could not be destroyed during pasteurization or during yogurt and cheese preparation (Galvano and others 1996; Creppy 2002). Certain plant-derived natural products like spices, herbs, and essential oils are known to contain compounds that can inhibit fungal growth and mycotoxin production (Bullerman and others 1984). Decreases in the medicinal potency of herbal drugs due to fungal contamination that affect the chemical composition of the raw materials have been reported (Roy 2003). Inhibition of mold growth by mustard, green garlic, and cinnamon bark along with the reduction of toxin production by peppers, cloves, thyme, and green tea has been reported (Hitokoto and others 1978). Bullerman and others (1977) reported strong antimycotic properties and inhibition of aatoxin production by cinnamon, clove, and their oils. Antimycotic properties (like cinnamon, cloves, and mustard) and antiaatoxigenic properties (as with thyme and oregano spices) have been reported by Llewellyn and others (1981). Alderman and Marth (1976) showed the efcacy of employing essential oils extracted from citrus fruits (lemon and orange) in inhibiting the growth of A. avus and A. niger, thus suppressing aatoxin formation. Singh and others (2008) in 1 of their studies explored the fungal infection and AFB1 contamination of 6 medicinal plant samples. They were able to recover a total of 858 fungal isolates from the raw materials. High levels of AFB1 (394.95 ppb) were produced by the isolates of A. avus in Glycyrrhiza glabra Linn. Further, they were able to show the efcacy of employing the essential oil (obtained from leaves) of Cinnamomum camphora (L.) Presl. The oil completely inhibited AFB1 production at low levels (750 ppm), and thus the oil of C. camphora has been recommended as an herbal fungistat/fungicide against mold contamination of raw materials. Natural honey has been shown to possess a rich antifungal, antiaatoxigenic effect (against A. avus and A. parasiticus) (Wellford and others 1978). Kensler and others (2004) reported the possible protective role of chlorophyllin (a water-soluble, semisynthetic sodium or copper derivative of chlorophyll, which is commonly used as a food additive as well as in alternative medicine) against AFB1 toxicity in humans. Peterson and others (2006) have shown that a regular diet which includes apiaceous vegetables (carrots, celery, and parsley), reduces the carcinogenic effects of aatoxin. Recently, Reddy and others (2009) reported a reduction in AFB1 by a few plant extracts and bio-control agents in stored rice. From their results, an extract of Syzigium aromaticum (5 g/kg) showed complete inhibition on the growth of A. avus and AFB1 production, while Curcuma longa, Allium sativum, and Ocimum sanctum effectively inhibited A. avus growth (65% to 78%) and AFB1 production (72.2% to 85.7%, 5 g/kg concentration). With regard to the biocontrol agents used, culture ltrate of Rhodococcus erythropolis completely inhibited AFB1 production at 25 mL/kg concentration, while Pseudomonas uorescens, Trichoderma virens, and Bacillus subtilis showed 93%, 80%, and 68% reduction of A. avus growth and 83.7%, 72.2%, and 58% reduction of AFB1 at 200 mL/kg, respectively. The inhibitory activity has been attributed to the antifungal components in plant extracts and extracellular metabolites produced by these biocontrol agents in the growth medium. Diaz and others (2004) used 6 sequestering agents that can bind dietary AFB1 in animal models. Usually, the sequestering agents bind dietary AFB1 and reduce absorption from an animals gastrointestinal tract. As a result, they protect an animal from the toxic effects of AFB1 and reduce transfer of the metabolite, aatoxin M1, into milk. A total of 6 agents used by Diaz and others (2004) (SA-20 R , an activated carbon [AC-A]; Astra-Ben-20 R , a sodium bentonite [AB-20]; MTB-100 R , an esteried glucomannan [MTB-100]; Red Crown R , a calcium bentonite [RC]; Flow Guard R , a sodium bentonite [FG]; and Mycrosorb R , a sodium bentonite [MS]) were previously tested for AFB1 binding in vitro. The results revealed that 5 of the 6 sequestering agents signicantly reduced AFM1 contamination of milk (AB-20, 61%; FG, 65%; MS, 50%; MTB-100, 59%; and RC, 31%); whereas ACA and activated carbon had no effect on AFM1 transmission at 0.25% of feed. Removal/inactivation of OTA. Apart from good agricultural and manufacturing practices, designing proper storage conditions is the only available alternative for minimizing OTA contaminants. Paster and others (1985) have indicated the application of radiation-processing for the removal of OTA. However, concerns are being raised on the application of ionizing radiation at doses that can damage spores but do not kill them, which might possibly enhance OTA production when these spores germinate
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on the return of favorable conditions. Also, once OTA has been formed in food it would be very difcult to remove it by the usual food processing. Boudra and others (1995) have reported that temperature as high as 250 C cannot completely destroy OTA. Wheat our production that involves polishing and milling has been reported to reduce ochratoxin levels (Osborne and others 1996). Similarly, a decrease in OTA has been reported after wet milling of corn wherein reduction in its germ and grits fractions was 96% and 49%, respectively (Wood 1982). Appropriate and safe thermal, chemical, and physical treatments can effectively reduce OTA levels in food products. For example, methods like decaffeination, roasting, brewing, and other similar thermal processing methods have been shown to reduce the level of OTA in coffee (Heilmann and others 1999; Van der Stegen and others 2001; Scudamore 2005; La Pera and others 2008). Reduction in OTA levels in cocoa beans by use of essential oil of Aframomum danielli (at concentrations of 500, 1000, 1500, and 2000 ppm) has been reported by Aroyeun and others (2009). The presence of active components of A. danielli such as monoterpenes, alkaloids, and phenolic acids are opined to be responsible for the reduction of OTA. Reduction of OTA in cocoa shells by chemical methods (using aqueous solutions of 2% sodium bicarbonate and potassium carbonate) has also been successful (Am ezqueta and others 2008b). Removal/detoxication of fusario-toxins. Reduction in fumonisin (FB1) levels and activity has been shown by alkaline treatments, wherein ester bonds of fumonisin are hydrolyzed to release its tricarballylic groups to yield aminopentol (Hendrich and others 1993). The ability to remove Fusarium toxins by fermentative bacteria was evaluated in vitro by Niderkorn and others (2006). Nearly 29 strains of lactic (LAB) and propionic acid bacteria (PAB) were tested for their capacity to remove DON and FB1 and FB2 from an acidic medium (pH 4). LAB proved to be useful and more efcient than PAB for the toxin removal. However, differences among strains of LAB were observed. Elimination was up to 55% for DON, 82% for FB1, and 100% for FB2. Selected strains were also capable of removing up to 88% ZEN. From their observations the researchers concluded that selected fermentative bacteria were able to bind major Fusarium mycotoxins and the binding ability by selected strains could be used to decrease the bioavailability of toxins in contaminated silages. Niderkorn and others (2007) studied the potentiality of employing various fermentative bacteria to detoxify corn silage contaminated by Fusarium toxins (DON, ZEN, and FB1 and FB2). They reported that nearly 8 lactobacilli and 3 leuconostoc bacteria biotransformed ZEN into alpha-zearalenol, without any apparent biotransformation of DON and fumonisins. Bacteria capable of binding the toxins belonged to Streptococcus and Enterococcus species that could bind up to 33%, 49%, 24%, and 62% of DON, ZEN, FB1, and FB2, respectively. Accordingly, the researchers concluded that fermentative bacteria have the capacity to bind Fusarium toxins and thereby could decrease their toxicity in animals. Sydenham and others (1994) reported on the effects of physical treatments for the partial decontamination of fumonisincontaminated maize in bulk shipments. They randomly selected 10 maize samples from a bulk shipment imported into South Africa and further characterized them by dividing them based on particle size. Fractionation by sieving through a 3-mm screen was done, wherein the kernels (fractions > or = 3 mm), between 80% and 95.3% of the samples by mass, revealed contamination by fumonisin levels that ranged between 530 and 1890 ng/g. The fractions that were termed as nes (< 3 mm) had signicantly higher total fumonisin concentrations of between 12340 and 27460 ng/g and accounted for 4.7% and 20% of the samples by mass. They concluded that removal of the nes can result in
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overall reductions in total fumonisin levels (between 26.2% and 69.4%) and recommended that initial removal of nes from bulk shipments of maize, prior to further processing, can serve as an initial step for fumonisin decontamination. Signicant reduction in fumonisin concentrations on heating aqueous solutions (150 C and above) have been reported by Jackson and others (1996). Heating moist maize kernels were also successful in reducing this toxin (Murphy and others 1996). Other thermal treatments usually employed during conventional food processing like baking and frying has been shown to reduce fumonisin levels in corn. Mufns prepared by baking corn batter at around 175 to 200 C (for 20 min) reduced fumonisin levels up to 30%. Further decrease was observed with an increase in temperature. Reductions in fumonisin levels were higher on the surface of mufns, which has been attributed to better heat penetration corresponding to enhanced baking temperatures (Jackson and others 1997). Heating results in the hydrolysis of the primary amine of the fumonisins. Also, autoclaving at 121 C (1 h) in the presence of 8.33% aqueous sodium bisulte has been shown to reduce DON levels in corn by 95% (Young and others 1987). Transformation of DON to a lesser toxic metabolite (de-epoxyDON) by microbes in the large intestine of chickens has been reported by He and others (1992). Hendrich and others (1993) have reported reduction in fumonisin levels by alkaline processing, wherein the ester bonds of the toxin were hydrolyzed to release its tricarballylic groups and yield aminopentol (Hendrich and others 1993). The application of chemical methods has been unsuccessful for the elimination of fumonisins. Wang and others (1991) used the commercially available enzymes and tested their ability for detoxifying fumonisins; however, the reduction in the fumonisins was not signicant. However, to date no reliable and effective methods have been developed for the removal of fusario-toxins in food, a gap that needs to be lled at the earliest to reduce further economic losses, as well as for safety purpose. Inactivation/removal of Patulin. Even though removal of the rotten and injured portion of the fruits has been recommended for minimizing patulin concentrations, this does not completely ensure the elimination of the toxin (Beretta and others 2000). Ough and Corison (1980) have reported that fermentation can destroy patulin during cider production. Filtration employed to clarify apple juice and concentrates has been reported to decrease patulin levels up to 40% (Bissessur and others 2001). Also, a pasteurization or evaporation condition, wherein the temperature is between 70 and 100 C, has been shown to reduce patulin (by 25%) in naturally contaminated apple juice (Kadakal and Nas 2003). The adoption of various control methods for patulin in food products has been well reviewed by Moake and others 2005.
Mycotoxinsmode of action
Generally, understanding the chemical structure and basic mechanism of action of an individual mycotoxin can provide sufcient base to develop protocols or methods to efciently manage the mycotoxins associated problems, as well as to understand their biological effects. Even though several mycotoxins have been identied to date, the basic mechanism of action has been workedout for only a few of them (aatoxins, OTA, fumonisins) indicating a wide gap to persist. Of late, several excellent studies are available wherein the basic mechanisms of action of certain mycotoxins have been discussed in detail (like aatoxins, DON, fumonisin, OTA) (Kiessling 1986; Ueno 1991; Riley and Norred 1996; Riley 1998; Tashiro 2000).
Methods of mycotoxin detection
For qualitative, quantitative, and accurate determinations of mycotoxins in foods and feeds, several analytical methods have

been developed and rened since the 1960s. Accurate detection of mycotoxins depends on various factors, as their distribution is not uniform in a substrate. According to Whittaker and others (1991), a statistically valid sample must be drawn from a single lot; if not, a sampling error of up to 90% may occur. Also, mycotoxin analysis should always be performed in replicates (n = 3 to 5) for conformation of the actual concentration in the samples. However, if the method is validated in a proper way, and the validation results are satisfactory, there is no need to run every sample for 3 to 5 times. Care should be taken to nely grind a sample and further divide it into subsamples for analysis. Traditionally employed analytical methods to detect mycotoxins involve lengthy extraction procedures, expensive chemical clean-up, and use of hazardous materials (Donnelly and others 2003). Such concerns and the necessity for the rapid analysis of mycotoxins have led to the development of many test kits that can qualitatively or quantitatively provide results within a few minutes. Also, improved protocols to minimize sampling errors have been established (Campbell and others 1986; Park and Pohland 1989). According to Magan (2004), availability of rapid diagnostics instruments is an area that has been developed in the recent past, principally as a response to fulll governmental legislative regulatory requirements put forth and recommendations such as by the FAO (1995). Limits and regulations for mycotoxins and their validation have been reported by many researchers (van Egmond 1989; Stoloff and others 1991; Boutrif and Canet 1998; Rosner 1998; van Egmond and others 2007). Table 1 details some of the recently employed methods for the detection of several mycotoxins. In the subsequent section, a few of the most important techniques available today have been discussed to provide some basic information. Several analytical methods have been developed and standardized to detect mycotoxins: thin-layer chromatography (TLC), liquid chromatography, high-performance liquid chromatography (HPLC) with uorescence or diode array detector, gas chromatography coupled to mass spectrometry (GCMS) or electron capture detection (GCECD), enzyme-linked immunosorbent assays (ELISAs), and a combination of immuno-afnity column techniques (WHO 2002). In recent years, liquid chromatographymass spectrometry and liquid chromatography-tandem mass spectrometry (LC-MS/MS) technique has also been often applied for multiple-mycotoxin detection, and this approach looks to be the most promising one at the moment. These analytical methods are exclusively employed for the detection of various types of mycotoxins and have been proven successful, especially with aatoxins, ochratoxin A, fumonisin, and deoxynivalenol (DON) in different commodities, like cereals and legumes (Scudamore and others 2003; Yumbe-Guevara and others 2003), coffee (Pittet and Royer 2002; Santos and Vargas 2002; Sibanda and others 2002; Vatinno and others 2008), black pepper (Gatt and others 2003), paprika seed (Hernandez-Hierro and others 2008), wine and beer (Leitner and others 2002; Stefanaki and others 2003), and cheese (Zambonin and others 2002; Manetta and others 2009). Some of the analytical methods developed are considerably more suitable for certain types of mycotoxins than others. For example, mini-columns and scanning of crushed-sample for bluegreenyellow uorescence (BGYF) with a black light (UV lamp) have been used extensively as an initial screening test for aatoxins (Chu 1991). Use of mini-column methods is limited to those emitting uorescence, including aatoxins, OTA, ZEN (Shotwell 1983), and sterigmatocystin (Ramakrishna and Bhat 1990). The use of different types of analytical techniques in combination with others or singly to detect a single mycotoxin has often been successful. For example, according to the WHO (2002), both thin-layer chromatography and liquid chromatography with uorescent detection along with ELISA can be used to identify ochratoxin A. Thin-layer chromatography (TLC) is one of the most popular and easy methods to detect mycotoxins in a sample; and more than one toxin can be detected simultaneously. This technique is based on the separation of compounds by how far they migrate on a specic matrix (TLC coated plates) in the presence of specic solvents. The distance traveled by a compound is specic for that compound, and based on the retention factor (Rf) a mycotoxins identity can be determined. As with any other detection method, a control containing puried mycotoxins must be run in parallel to ensure accuracy. However, today, with the availability of many other options and modern instruments, in the majority of labs this technique is being used for preliminary screening only. Immunological assays. Mycotoxins are not immunogenic and are recognized as haptens or small molecules that do not stimulate antibody production by themselves. However, in some instances, antibodies can be produced for a specic mycotoxin by conjugating it to a protein carrier, which might cause the mycotoxin to become immunogenic. Animals that recognize various regions of foreign particles produce several types of antibodies, including antigens (a substance capable of stimulating an immune response) and haptens, when present on a carrier macromolecule. The various forms of antibodies include polyclonal and monoclonal types. Polyclonal antibodies react with multiple antigens or haptens on a foreign compound, whereas monoclonal antibodies react only with specic antigens or haptens (Fremy and Usleber 2003). An immunoafnity method is highly advantageous, as it is rapid and inexpensive. The extracted sample is placed on a mini-column lled with antibodies specic to the toxin and is eluted off the column using methanol. Then a bromine reagent is added and the sample is placed in a direct-reading uorometer. The mycotoxin is extracted, cleaned up on a silica column, developed on a high-performance plate, and is measured using a scanning uorometer. This method is used as a visual conrmatory test. Fumonisins are usually detected by purication with immunoafnity columns followed by TLC or liquid chromatography, however, more rapid screening tests based on TLC and ELISA have been developed (WHO 2002). New immunochemical methods have recently been developed. For example, a hit and run assay for T-2 toxin has been mentioned by Warden and others (1987, 1990). The T-2 toxin column is equilibrated with uoresceinisothiocyanate (FITCI-labeled Fab fragment of IgG -anti-T-2 toxins) and the sample containing T-2 toxin is injected into the column. The FITC-Fab that is eluted together with the sample containing T-2 toxin is then determined in a standard ow-through uorometer. Similarly, Warden and others (1990) have reported a method wherein ribonucleaselabeled-Fab is used as the indicator. A homogeneous immunoassay for T-2 toxin that involves the use of liposomes, which can virtually lead to the development of a biosensor, has been reported by Ligler and others (1987) and Williamson and others (1989). Determination of multiple mycotoxins (about 4 types) in a sample at nanogram per gram detection limits by immunochemical biosensor has been described by van der Gaag and others (2003). Nearly 4 mycotoxins (DON, FB1, ZEN, AFB1) could be detected within 25 min, which includes extraction and clean-up of the sample (approximately 15 min) and measurement (10 min, including regeneration of the sensor chip surface). This assay was designed as an inhibition assay, in which the principle of detection is based on surface plasmon resonance (SPR).
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For the determination of aatoxins (Sarwar and Jolley 2002) and DON (Maragos and Plattner 2002) in grains, PFS-uorescence polarization immunoassays (FP) have been developed. The assays are based on the competition between free aatoxin and an aatoxinuorescein tracer for an aatoxin-specic monoclonal antibody in solution. Degan and others (1989) have developed a time-resolved uoro-immunoassay aatoxin analysis, wherein the method involves the use of europium ion (Ed-labeled) antibodies. Takino and others (2004) reported on a highly reliable and sensitive method for the detection of aatoxins by employing an atmospheric pressure photo-ionization technique (APPI) wherein the level of detection was in the range of 0.11 to 0.5 ng/g. Nawaz and others (1992) have developed a rapid, simple, and reproducible method for the simultaneous determination of aatoxins (AFB1, AFB2, AFG1, and AFG2) in palm kernel samples by optimizing sample preparation, solvent extraction, clean-up, and quantication procedures. Aatoxins in the samples are extracted from palm kernel slurries with a mixture of acetonewater (80 + 20, v/v) and the crude extract is cleaned by solid-phase extraction using a phenyl-bonded phase cartridge. The extract is then passed through the cartridge with a watermethanol (93 + 7) mixture, and subsequent elution of aatoxins retained on the cartridge is achieved with a 3-mL aliquot of chloroform. The aatoxin content of eluates was further quantied by employing a bi-directional high-performance thin-layer chromatography (HPTLC) procedure. From this method, a consistent recovery of over 90% could be achieved from spiked palm kernel extracts and detection limits were 3.7, 2.5, 3, and 1.3 g/kg for AFB1, AFB2, AFG1, and AFG2, respectively. A novel method for the simultaneous determination of trichothecene mycotoxins (deoxynivalenol, nivalenol, 3acetyl-deoxynivalenol, and 15-acetyl-deoxynivalenol) has been developed by Shaban and others (2007) (for barley and malt extracts) using matrix-assisted laser desorption ionization time-ofight mass spectrometry (MALDI-TOF-MS). The matrices used were diamond and sodium azide and were suitable for the determination of mycotoxins. This technique was found to be highly sensitive, rapid, and detection can be performed using very minute sample quantities. Pestka (1991) has reported on a new method called HPTLCELISA-gram. In that method, separation of mycotoxins is performed by HPTLC, followed by blotting the chromatogram to a nitrocellulose membrane coated with antibody, incubation with mycotoxin-enzyme conjugate, and nally incubation with substrate to develop the color. However, application of this method is limited as use of a large amount of antibody is required. Currently, the polymerase chain reaction (PCR) and enzymelinked immunosorbent assay (ELISA) test are emerging as the most reliable tools to detect molds rather than mycotoxins (Chung and others 1989; Zur and others 2002; Niessen 2008; Hooper and others 2009). These techniques are useful for detecting the responsible coding genes of mycotoxin-producing molds. However, the techniques are very expensive, require trained analysts, and cannot be employed routinely in eld assessments of contamination. Detection of mycotoxins using commercially available ELISAs is mainly dependent on the competition between the toxins from the sample and a labeled toxin (such as a toxinenzyme conjugate) for a limited number of antibody-binding sites. The higher the concentration of the toxin, the lower is the binding of the labeled toxin and the lower the signal generated by the assay (Anklam and others 2002; Seefelder and others 2002). Based on random amplied polymorphic DNA (RAPD) and amplied fragment length polymorphism (AFLP) markers, specic primers for PCR- detection of A. ochraceus and A. carbonarius in coffee beans have been developed recently (Schmidt and others 2003, 2004; Fungaro and others 2004).
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Of late, use of electronic nose and soft X-ray imaging for the detection of fungi in food commodities have received positive attention (Perkowski and others 2008; Concina and others 2009; Narvankar and others 2009). However, these techniques might be useful for the rapid detection of the fungal pathogens only rather than a mycotoxin itself. It is highly imperative to develop newer detection methods for the rapid analysis of mycotoxins in food, particularly considering the new open global market under the new World Trade Organization (WTO) regime. The new analytical tools developed would be more useful if several mycotoxins could be screened simultaneously within a fraction of minutes in a large number of samples. For example, Gachok and others (2008) have reported the development of a uorescence polarization immunoassay, which could detect mycotoxins like OTA, AFB1, and ZEN in the samples present in low amounts up to 1 ng/mL, much lower than maximum residue limits (MRL) set for mycotoxins in food (from 10 to 100 ppb for different mycotoxins and in different foods).
Prevention and future outlook
Prevention of fungal contamination and thereby toxin production can be achieved either during preharvest stages by good crop husbandry and appropriate cultural practices and the use of a HACCP plan, as well as during postharvest stages by the application of proper drying, storage, and transport procedures (FAO 2006a, 2006b). Application of fungicides at eld levels might reduce mold growth resulting in the reduction of production of mycotoxins. However, it has been opined that the stress generated by the fungicides on the molds can also result in increased mycotoxin production (Gareis and Ceynowa 1994). Hence, further studies have to be initiated to look for a better and environmentally friendly alternative at the eld level rather than relying on chemicals. Development of resistant plant varieties with the application of modern biotechnological methods would prove to be benecial up to certain extent. Some studies in this regard are already being reported. For example, biotechnologically developed corn (Bt corn) has been reported to possess lower levels of contamination with fumonisin and aatoxin. A total prot of 23 million dollars annually due to Bt corns reduction of fumonisin and aatoxin in the U.S. has been estimated (Wu 2006). Even though organic farming is well established and has been forecast to reduce mycotoxin contamination in the food chain, it has not yet been possible to establish major differences in this regard when comparing it to conventional farming. However implementation of GAP in organic elds might denitely have a good impact on the contamination and production levels of mycotoxins. Removal of crop residues and undertaking crop rotation is a better option considering the fact that some viable pathogenic fungal spores might be present in the old crops after harvest. As the detoxication of human food and animal feeds (during postharvest stages) is performed mostly by employing chemical methods, safety, and efcacy along with handling, costs should be taken into consideration. Care should be taken to see that the preservatives or the chemicals employed do not degrade the overall nutritional, sensory, and functional properties of the food product. Hence, development of newer physical methods of preservation is a necessity in the near future. Of late, nonionizing radiation, like ultraviolet rays (UV), has been shown to be successful in reducing the microbial load and thereby toxin production. However, the penetration of UV rays is not deep at all. Application of UV in combination with heat treatment has been reported to be successful in the inactivation of conidia of Botrytis cinerea and Monilinia fructigena, which are the 2 major postharvest spoilage fungi of strawberries and cherries (Marquenie and others 2002). Successful prevention of the germination

of contaminating fungi during storage or further dehydration by UV irradiation of harvested grapes has been reported by Valero and others (2007). Also, effective inactivation of food spoilage fungi like A. avus, P. corylophilum, E. rubrum, and A. niger by UV irradiation has been reported by Begum and others (2009). Further public legislation and regulations with regard to mycotoxins should be instituted to protect health and to facilitate trade among various importing countries. Strict enforcement of the already existing regulations for mycotoxins, especially for aatoxins, ochratoxins, ZEN, fumonisins, and patulin in the food chain might prove to be successful in minimizing mycotoxin contaminants overall. Nearly 60 countries have now enacted or proposed regulations for the control of mycotoxins in food and animal feeds (van Egmond 1995). Dietary manipulation has been reported to reduce the adverse effects of mycotoxins. According to Ratcliff (2002), increasing the levels of selenium, methionine, carotenoids, and vitamin supplementation in food can be benecial in reducing adverse effects of mycotoxins. Jones and others (1994) have reported that increasing protein, energy (fats and carbohydrates), and vitamins in the diet may be advisable towards this end. The addition of antioxidants to animal diets might assist in dealing with the toxic effects of mycotoxins. However, the available data pertaining to dietary habits and mycotoxin reduction are very scarce and, hence, future studies ought to be initiated.
Alderman GG, Marth EH. 1976. Inhibition of growth and aatoxin production of Aspergillus parasiticus by citrus oils. Z Lebensm Unters Forsch 160:3558. Ali N, Hashim NH, Saad B, Safan K, Nakajima M, Yoshizawa T. 2005. Evaluation of a method to determine the natural occurrence of aatoxins in commercial traditional herbal medicines from Malaysia and Indonesia. Food Chem Toxicol 43:176372. Alm K, Dahlbom M, Saynajarvi M, Andersson MA, Salkinoja-Salonen MS, Andersson MC. 2002. Impaired semen quality of AI bulls fed with moldy hay: a case report. Theriogenology 58:1497502. Aly SA, Anwer W. 2009. Effect of naturally contaminated feed with aatoxins on performance of laying hens and the carryover of aatoxin B1 residues in table eggs. Pakistan J Nutr 8:181 6. E, Dachoupakan C, Murillo-Arbizu M, Lopez Am ezqueta S, Gonz alez-Penas De Cerain A, Guiraud JP. 2008a. OTA-producing fungi isolated from stored cocoa beans. Lett Appl Microbiol 47:197201. E, Lizarraga T, Murillo-Arbizu M, Lopez Am ezqueta S, Gonz alez-Penas De Cerain A. 2008b. A simple chemical method reduces ochratoxin A in contaminated cocoa shells. J Food Prot 71:14226. Anklam E, Stroka J, Boenke A. 2002. Acceptance of analytical methods for implementation of EU legislation with a focus on mycotoxins. Food Cont 13:17383. Annie P-L, Manderville RA. 2007. Ochratoxin A: an overview on toxicity and carcinogenicity in animals and humans. Mol Nutr Food Res 51:6199. Anonymous. 1983. Committee on protection against mycotoxins. National Research Council. Protection against trichothecene mycotoxins. Washington, D.C.: Natl. Academy Press. Anonymous. 1995. European Directive 95/2/CE of European Parliament and Council of European Community. Brussels, Belgium: European Parliament and Council of European Community. Anonymous. 1996. ACNFP report on seeds from the narrow-leafed lupin, Appendix IX. London: Ministry of Agriculture, Fisheries and Food (MAFF) Publications. 107 p. Anonymous. 2001. Comments submitted on the draft maximum level of aatoxin M1 in milk. Codex Committee on Food Additives and Contaminants, 33rd session. Hague, The Netherlands: Codex Committee on Food Additives and Contaminants. Anonymous. 2006. Health concerns associated with mold in water-damaged homes after hurricanes Katrina and RitaNew Orleans area, Louisiana October 2005. Morb Mortal Weekly Rep 55:414. Ansari AA, Shrivastava AK. 1990. Natural occurrence of Alternaria toxins in sorghum and ragi from North Bihar, India. Food Addit Contam 7:81520. Apeagyei F, Lamplugh SM, Hendrickse RG, Affram K, Lucas S. 1986. Aatoxins in the livers of children with kwashiorkor in Ghana. Trop Geo Med 38:2736. Applebaum RS, Brackett RE, Wiseman DW, Marth EH. 1982. Aatoxin: toxicity to dairy cattle and occurrence in milk and milk productsa review. J Food Prot 45:75277. Aroyeun SO, Adegoke GO, Varga J, Teren J. 2009. Reduction of aatoxin B1 and ochratoxin A in cocoa beans infected with Aspergillus via ergosterol value. World Rev Sci Technol Sust Dev 6:7589. Azcarate MP, Patriarca A, Terminiello L, Pinto FV. 2008. Research note. Alternaria toxins in wheat during the 2004 to 2005 Argentinean harvest. J Food Prot 71:12625. Aziz NH, Shahin AAM. 1997. Inuence of other fungi on aatoxin production by Aspergillus avus in maize kernels. J Food Saft 17:11123. Aziz NH, Attia ES, Farag SA. 1997. Effect of gamma-irradiation on the natural occurrence of Fusarium mycotoxins in wheat, our and bread. Nahrung 41:347. Aziz NH, Youssef YA, El-Fouly MZ, Moussa LA. 1998. Contamination of some common medicinal plant samples and spices by fungi and their mycotoxins. Bot Bull Acad Sin 39:27985. Baath H, Knabe O, Lepom P. 1990. Occurrence of Fusarium species and their mycotoxins in corn silage (Fusarium infestation in corn silage). Archiv fur Tierernahrung 40:397 405. Bailly JD, Querin A, Le Bars-Bailly S, Benard G, Guerre P. 2002. Citrinin production and stability in cheese. J Food Prot 65:131721. Balachandran C, Parthasarathy KR. 1996. Inuence of dietary rice culture material containing cyclopiazonic acid on certain biochemical parameters of broiler chickens. Mycopathologia 132:1616. Barhoumi R, Burghardt RC. 1996. Kinetic analysis of the chronology of patulin and gossypolinduced cytotoxicity in vitro. Fundam Appl Toxicol 30:2907. Barrios MJ, Medina LM, Cordoba MG, Jordano R. 1997. Aatoxin-producing strains of Aspergillus avus isolated from cheese. J Food Prot 60:1924. Battilani P, Magan N, Logrieco A. 2006. European research on ochratoxin A in grapes and wine. Int J Food Microbiol 111:S24 Batista LR, Chalfoun SM, Silva CF, Cirillo M, Varga EA, Schwan RF. 2009. Ochratoxin A in coffee beans (Coffea arabica L.) processed by dry and wet methods. Food Cont 20:78490. Beckett ST. 1994. Industrial chocolate manufacture and use. 2nd ed. London: Blackie Academic and Professional, Chapman and Hall. 488 p. Begum M, Hocking AD, Miskelly D. 2009. Inactivation of food spoilage fungi by ultraviolet (UVC) irradiation. Int J Food Microbiol 129:747. Benkhelil A, Grancher D, Giraud N, Bezille Et P, Bony S, Carcelen M, Camier Y. 2004. Outbreak of an endophyte toxicosis in a herd of bulls for service. Revue de Medecine Veterinaire 155:2437. Bennett JW, Klich M. 2003. Mycotoxins. Clin Microbiol Rev 16:497516. Berry CL. 1998. The pathology of mycotoxin. J Pathol 154:30111. Beretta B, Gaiaschi A, Galli CL, Restani P. 2000. Patulin in apple-based foods: occurrence and safety evaluation. Food Addit Contam 17:399406. Betina V. 1989. Mycotoxins-Chemical, biological and environmental aspects. In: Betina V, editor. Bioactive molecules. London: Elsevier Applied Science. p 11450. Bhat RV, Krishnamachari KAVR. 1977. Follow-up study of aatoxic hepatitis in parts of western India. Indian J Med Res 66:558. Bhat RV, Vasanthi S. 2003. Mycotoxin food safety risk in developing countries. In: Unnevehr LJ, editor. 2020 Focus 10: food safety in food security and food trade. Washington, D.C.: Intl. Food Policy Research Inst. Bhat R, Sridhar KR, Velmourougane K. 2007. Microbial quality evaluation of velvet bean seeds (Mucuna pruriens L. DC.) exposed to ionizing radiation. Trop Subtrop Agroecosyst 7:2940.
Conclusions
The occurrence of mycotoxins in the food chain is an unavoidable and serious problem the world is facing. Apart from practicing good sanitary measures, awareness has to be created to indicate the toxic effects associated with mycotoxin poisonings in humans and livestock. Wide gaps still exist on the toxicological effects of feeding animals mycotoxin-contaminated feeds. Research in this eld is a necessity as there is every possibility that the toxins will enter the human food chain. Further research also needs to be focused on the generation of data dealing with epidemiological and toxicity effects, especially in humans. Implementation of strict quarantine rules with regard to mycotoxin contamination has to be made mandatory worldwide. Emphasis should be laid towards development of newer low-cost mycotoxin detection instruments, which are portable, reliable, and easy to handle at eld levels. Development of new genetically modied plants by the application of genetic engineering that might be resistant to fungal invasion might also prove to be a good option. Developing new protocols and strategies to compare the costs and benets of various controlling agents against fungal pathogens and mycotoxin production might be benecial for economic stability of a commodity or an agricultural area.
Acknowledgments
The authors gratefully acknowledge the scientic editor, Prof. Dr. Manfred Kroger, and the anonymous referees for comments and constructive suggestions provided for improving the manuscript.
References
Abdulrazzaq YM, Osman N, Yousif ZM, Al-Falahi S. 2003. Aatoxin M1 in breast-milk of UAE women. Ann Trop Paediatr 23:1739. Abnet CC, Borkowf CB, Qiao Y-L, Albert PS, Wang E, Merrill AH Jr, Mark SD, Dong Z-W, Taylor PR, Dawsey SM. 2001. Sphingolipids as biomarkers of fumonisin exposure and risk of esophageal squamous cell carcinoma in China. Cancer Causes Cont 12:8218. Abramson D, Lombaert G, Clear RM, Sholberg P, Trelka R, Rosin E. 2009. Production of patulin and citrinin by Penicillium expansum from British Columbia (Canada) apples. Mycotoxin Res 25:858. Adhikari M, Ramjee G, Berjak P. 1994. Aatoxin, kwarshiorkor and morbidity. J Nat Tox 2:13.
75

Bissessur J, Permaul K, Odhav B. 2001. Reduction of patulin during apple juice clarication. J Food Prot 64:12169. Blanco JL, Carrion BA, Liria N, Diaz S, Garcia ME, Dominguez L, Suarez G. 1993. Behavior of aatoxins during manufacture and storage of yoghurt. Milchwiss 48:3857. Bonomi A, Quarantelli A, Mazzali I, Cabassi E, Corradi A, Lecce R, Ubaldi A, Fusari A, Chizzolini A. 1994. Effects of aatoxin B1 contaminated rations on the productive efciency and on the meat yield and quality in fattening pigs (experimental contribution). Riv Sci Aliment 22:35177. Botha CJ, Naude TW, Moroe ML, Rottinghaus GE. 2004. Gangrenous ergotism in cattle grazing fescue (Festuca elatior L.) in South Africa. J South African Vet Assoc 75:458. Boudra H, Le Bars P, Le Bars J. 1995. Thermostability of ochratoxin A under two moisture conditions. Appl Environ Microbiol 61:11568. Boudra H, Barnouin J, Dragacci S, Morgavi DP. 2007 Aatoxin M1 and ochratoxin A in raw bulk milk from French dairy herds. J Dairy Sci 90:3197201. Boutrif E, Canet C. 1998. Mycotoxin prevention and control: FAO programmes. Revue de M edecine V et erinaire 149:68194. Brackett RE. 1989. Strategies for dealing with aatoxins in peanuts. In: Yam TC, Tan C, editors. Trends in food product development. Singapore: Singapore Inst. of Food Science and Technology. p 8391. Breitholtz-Emanuelsson A, Minervini F, Hult K, Visconti A. 1994. Ochratoxin A in human serum samples collected in Southern Italy from healthy individuals and individuals suffering from different kidney disorders. Nat Tox 2:36670. Britannia Foods. Available from: http://www.britanniafood.com. Accessed Jun 12, 2009. Bullerman LB, Lieu FY, Seier SA. 1977. Inhibition of growth and aatoxin production by cinnamon and clove oils, cinnamic aldehyde and eugenol. J Food Sci 42:11078. Bullerman LB, Schroeder LL, Park KY. 1984. Formation and control of mycotoxins in food. J Food Prot 47:63746. Burfening PJ. 1973. Ergotism. J Am Vet Med Assoc 163:128890. Burrows GE, Tyril RJ. 2001. Toxic plants in North America. Ames, Iowa: Iowa State Press. p 6256. Campbell AD, Whitaker TB, Pohland AE, Dickens JW, Park DL. 1986. Sampling, sample preparation, and sampling plans for foodstuffs for mycotoxin analysis. Pure Appl Chem 58:30514. Canady RA, Coker RD, Egan SK, Krska R, Kuiper-Goodman T, Olsen M, Pestka J, Resnik S, Schlatter J. 2001. Deoxynivalenol. In: Safety evaluation of certain mycotoxins in food. Geneva: World Health Organization. p 420529. [CAST] Council for Agricultural Science and Technology. 1989. Mycotoxins: economic and health risks. Task force report nr 116. Ames, Iowa: Council for Agricultural Science and Technology. [CAST] Council for Agricultural Science and Technology. 2003. Mycotoxins: risks in plant, animal and human systems. Task force report, ISSN 0194-4088, Ames, Iowa: Council for Agricultural Science and Technology. Castegnaro M, Mcgregor D. 1998. Carcinogenic risk assessment of mycotoxins. Revue de M edecine V eterinaire 149:6718. Castegnaro M, Chernozemsky IN, Hietanen E, Bartsch H. 1990. Are mycotoxins risk factors for endemic nephropathy and associated urothelial cancers? Arch Geschwulstforsch 60:295 303. Casteels-van Daele M, Eggermont E. 1994. Reyes syndrome. Br Med J 308:91920. Casteel SW, Turk JR, Rottinghaus GE. 1994. Chronic effects of dietary fumonisin on the heart and pulmonary vasculature of swine. Fund Appl Toxicol 23:51824. Castelo MM, Sumner SS, Bullerman LB. 1998. Occurrence of fumonisins in corn-based food products. J Food Prot 61:7047. [CEC] Commission of the European Communities. 2002. EC Regulation 2002/472. 12.02.2002. Ofcial Journal of the European communities L 75/18. Chan WH. 2007. Citrinin induces apoptosis via a mitochondria-dependent pathway and inhibition of survival signals in embryonic stem cells, and causes developmental injury in blastocysts. Biochem J 404:31726. Cheeke PR. 1995. Endogenous toxins and mycotoxins in forage grasses and their effects on livestock. J Ani Sci 73:90918. Chelule PK, Gqaleni N, Dutton MF, Chuturgoon AA. 2001. Exposure of rural and urban populations in KwaZulu Natal, South Africa, to fumonisin B1 in maize. Environ Health Perspt 109:2536. Chernozemsky IN. 1991. Balkan endemic nephropathy and the associated tumours of the urinary system: a summary of epidemiological features in Bulgaria. Mycotoxins, endemic nephropathy and urinary tract tumours. IARC Scientic Publications 115:3 4. Chiavaro E, DallAsta C, Galverna G, Biancardi A, Gambarelli E, Dossena A, Marchelli R. 2001. New reversed-phase liquid chromatographic method to detect aatoxins in food and feed with cyclodextrins as uorescence enhancers added to the eluent. J Chromat A 937:3140. Chiavaro E, Lepiani A, Colla F, Bettoni P, Pari E, Spotti E. 2002. Ochratoxin A determination in ham by immunoafnity clean-up and a quick uorometric method. Food Addit Cont 19:57581. Chourasia HK. 1990. Aatoxin contamination in drug-yielding plant. J Indian Bot Soc 69:281 3. Chu FS. 199l. Detection and determination of mycotoxin. In: Sharma RP, Salunkhe DK, editors. Mycotoxin and phytoalexins in human and animal health. Boca Raton, Fla.: CRC Press. p 3379. Chu FS, Li GY. 1994. Simultaneous occurrence of fumonisin B1 and other mycotoxins in moldy corn collected from Peoples Republic of China in regions with high incidences of esophageal cancer. Appl Environ Microbiol 60:84752. Chulze SN, Torres AM, Dalcero AM, Etcheverry MG, Ramirez ML, Farnochi MC. 1995. Alternaria mycotoxins in sunower seeds: incidence and distribution of the toxins in oil and meal. J Food Prot 58:11335. Chun HS, Choi EH, Chang H-J, Choi S-W, Eremin S A. 2009. A uorescence polarization immunoassay for the detection of zearalenone in corn. Anal Chim Acta 639:839. Chung D-H, Abouzied MM, Pestka JJ. 1989. Immunochemical assay applied to mycotoxin biosynthesis: ELISA comparison of sterigmatocystin production by Aspergillus versicolor and Aspergillus nidulans. Mycopathologia 107:93100. Combe RG, Jacobs JJ, Watson TR. 1970. Metabolite of some Alternaria species. The structure of altenuisin and dehydroaltenuisin. Aust J Chem 23:234351. Concina I, Falasconi M, Gobbi E, Bianchi F, Musci M, Mattarozzi M, Pardo M, Mangia A, Careri M, Sberveglieri G. 2009. Early detection of microbial contamination in processed tomatoes by electronic nose. Food Cont 20:87380. Coulumbe RA. 1993. Symposium: biological action of mycotoxins. J Dairy Sci 76:88091. Cotty PJ, Bhatnagar D. 1994. Variability among atoxigenic Aspergillus avus strains to prevent aatoxin contamination and production of aatoxin biosynthetic pathway enzymes. Appl Environ Microbiol 60:224851. Creppy EE. 2002. Update of survey, regulation and toxic effects of mycotoxins in Europe. Toxicol Lett 127:1928. Cullen JM, Wilson M, Halger Jr. WM, Ort JF, Cole RJ. 1988. Histologic lesions in broiler chicks given cyclopiazonic acid orally. Am J Vet Res 49:72831. Culvenor CC J, Beck AB, Clarke M, Cockrum PA, Edgar JA, Frahn JL, Jago MV, Lanigan GW, Payne AL, Peterson JE, Petterson DS, Smith LW, White RR. 1977. Isolation of toxic metabolites of Phomopsis leptostromiformis responsible for lupinosis. Aust J Biol Sci 30:26977. Cunha SC, Faria MA, Fernandes JO. 2009. Determination of patulin in apple and quince products by GCMS using 13C57 patulin as internal standard. Food Chem 115:3529. D anicke S, Brussow K, Valenta H, Uebersch ar KH, Tiemann U, Schollenberger M. 2005. On the effects of graded levels of fusarium toxin-contaminated wheat in diets for gilts on feed intake, growth performance and metabolism of deoxynivalenol and zearalenone. Mol Nutr Food Res 49:93243. Degan P, Montagnoli G, Wild CP. 1989. Time-resolved uoroimmunoassay of aatoxins. Clin Chem 35:230810. R.2007. Del Prete V, Rodriguez H, Carrascosa AV, de las Rivas B, Garcia-Moruno E, Munoz In vitro removal of ochratoxin A by wine lactic acid bacteria. J Food Prot 70:2155 60. ` viennent les glucomannanes Devegowda G. 2000. Mettre les mycotoxines sur la touche: dou esteries. Feed Times 4:124. Devegowda G, Radu MVL, Nazar A, Swamy HVLM. 1998. Mycotoxin picture worldwide: novel solutions for their counteraction. In: Proceedings of Alltechs 14th Annual Symposium, Biotechnology in Feed industry. Passport of the year 2000. Nottingham, U.K.: Nottingham Univ. Press. De Vries HR, Maxwell SM, Hendrickse RG. 1990. Aatoxin excretion in children with kwashiorkor or marasmic kwashiorkor: clinical investigation. Mycopathologia 110:19. Diaz DE, Hopkins BA, Leonard LM, Hagler Jr. WM, Whitlow LW. 2000. Effect of fumonisin on lactating dairy cattle. J Dairy Sci 83:1171. Diaz D, Hagler W, Blackwelder J, Eve J, Hopkins B, Anderson K, Jones F, Whitlow L. 2004. Aatoxin binders II: reduction of aatoxin M1 in milk by sequestering agents of cows consuming aatoxin in feed. Mycopathologia 157:23341. D az GA, Torres R, Vega M, Latorre BA. 2009. Ochratoxigenic Aspergillus species on grapes from Chilean vineyards and Aspergillus threshold levels on grapes. Int J Food Microbiol 133:1959. D az-Llano G, Smith TK. 2006. Effects of feeding grains naturally contaminated with Fusarium mycotoxins with and without a polymeric glucomannan mycotoxin adsorbent on reproductive performance and serum chemistry of pregnant gilts. J Anim Sci 84:236166. Diekman MA, Green ML. 1992. Mycotoxins and reproduction in domestic livestock. J Anim Sci 70:161527. Diener UL, Pettit RE, Cole RJ. 1982. Aatoxins and other mycotoxins in peanuts. In: Pattee HE, Young CT, editors. Peanut science and technology. Yoakum, Texas: American Peanut Research and Education Society. p 486519. Dmello JPE, Macdonald AMC. 1997. Mycotoxins. Anim Food Sci Technol 69:15566. Donnelly C, Marley E, Dunnigan P, Gallagher M. 2003. Diagnostic test systems for mycotoxins. In: Mycotoxins in food production systems aspects of applied biology. Nr. 68. Warwick, U.K.: Assoc. of Applied Biologists. dos Santos VM, Dorner JW, Carreira F. 2003. Isolation and toxigenicity of Aspergillus fumigatus from moldy silage. Mycopathologia 156:1338. Doyle MP, Applebaum RS, Brackett RE, Marth EH. 1982. Physical, chemical and biological degradation of mycotoxins in foods and agricultural commodities. J Food Prot 45:96471. Dragacci S, Grosso F, Bire F, Fremy JM, Coulon SA. 1999. French monitoring programme for determining ochratoxin A occurrence in pig kidneys. Nat Tox 7:16773. Driehuis F, Spanjer MC, Scholten JM, te Giffel MC. 2008. Occurrence of mycotoxins in feedstuffs of dairy cows and estimation of total dietary intakes. J Dairy Sci 91:426171. Drusch S, Ragab W. 2003. Mycotoxins in fruits, fruit juices, and dried fruits. J Food Prot 66:151427. Dutton MF, Westlake K, Anderson MS. 1984. The interaction between additives, yeasts and patulin production in grass silage. Mycopathologia 87:2933. Duvick J. 2001. Prospects for reducing fumonisin contamination of maize through genetic modication. Environ Health Perspect 109:33742. Dvorackova I, Kusak V, Vesely D, Vesela J, Nesnidal P. 1977. Aatoxin and encephalopathy with fatty degeneration of viscera (Reye). Ann Nutr Alim 31:97790. [EC] European Commission. 2006. Commission regulation (EC) no. 1881/2006 of 19 December 2006 setting maximum levels for certain contaminants in foodstuffs. Off J Eur Union L364:524. Edgar JA. 1991. Phomopsins: antimicrotubule mycotoxins. In: Keeler RF, Tu AT, editors. Toxicology of plant and fungal compounds. Handbook of natural toxins. 6. New York: Marcel Dekker. p 37195. Egal S, Hounsa A, Gong YY, Turner PC, Wild CP, Hall AJ, Hell K, Cardwell KF. 2005. Dietary exposure to aatoxin from maize and groundnut in young children from Benin and Togo, West Africa. Int J Food Microbiol 104:21524. Egmond HP, Paulsch WE. 1986. Mycotoxins in milk and milk products. Netherlands Milk Dairy J 40:17588. Ellis WO, Smith JP, Simpson JP, Oldham JH. 1991. Aatoxins in food: occurrence, biosynthesis, effects on organisms detection and methods of control. Crit Rev Food Sci Nutr 30:40339. El-Nezami HS, Nicoletti G, Neal GE, Donohue DC, Ahokas JT. 1995. Aatoxin M1 in human breast milk samples from Victoria, Australia and Thailand. Food Chem Toxicol 33:1739. P, Salminen S, Mykk El-Nemazi HS, Kankaanp aa anen H, Ahokas JT. 1998. Use of probiotic bacteria to reduce aatoxin uptake. Vety Med Rev 149:570.
76

El-Sayed Abd Alla AM, Neamat-Allah AA, Aly SE. 2000. Situation of mycotoxins in milk, dairy products and human milk in Egypt. Mycotoxin Res 16:91100. Escoula L, Thomsen M, Bourdiol D, Pipy B, Peuriere S, Roubinet F. 1988. Patulin immunotoxicology: effect on phagocyte activation and the cellular and humoral immune system of mice and rabbits. Int J Immunopharmacol 10:9839. EU Commission Regulation. 2006a. Commission regulation (EC) no 1881/2006 of 19 December 2006 setting maximum levels for certain contaminants in foodstuffs. Available from: http://europa.eu/legislation summaries/food_safety/contamination environmental factors/ l21290 en.htm. Accessed Jul 25, 2009. EU Commission Regulation. 2006b. Available from: http://www.mycotoxin-certication.eu. Accessed Jul 24, 2009. EUROPA. Available from: http:// europa.eu.int/eur-lex/en/archive/2004. Accessed Jul 15, 2009. [FAO] Food and Agriculture Organization. 1995. Worldwide regulations for mycotoxins, FAO food and nutrition paper nr 64. Rome, Italy: FAO. [FAO] Food and Agriculture Organization. 1997. Agriculture food and nutrition for Africa: a resource book for teachers of agriculture. [FAO] Food and Agriculture Organization. 2005. Methyl bromide: supporting documentation from the Republic of Korea. Rotterdam Convention on the Prior Informed Consent Procedure for Certain Hazardous Chemicals and Pesticides in International Trade Chemical Review Committee First meeting Geneva, 1118 February 2005. Available from: http://www.pic.int/INCs/CRC1/r18add1)/English/CRC%201-18-Add1%20methyl%20 bromide%20korea.pdf. Accessed Dec 2008. [FAO] Food and Agriculture Organization. 2006a. Safety evaluation of certain contaminants in food. Prepared by the sixty-fourth meeting of the Joint FAO/WHO Expert Committee on Food Additives (JECFA). FAO Nutr Paper 82:1778. [FAO] Food and Agriculture Organization. 2006b. FAO/WHO guidance to governments on the application of HACCP in small and/or less-developed food businesses. 86:174. [FAO/WHO] Food and Agriculture Organization/World Health Organization. 1990. FAO/WHO standards programme. Codex Alimentarius Commission. Alinron 91/29 and 93/12. [FDA] Food and Drug Administration. Available from: http://www.fda.gov/ora/compliance ref/cpg. Accessed Jun 12, 2008. V, Soldado A, Mart Fern andez-Ibanez nez-Fern andez A, de la Roza-Delgado B. 2009. Application of near-infrared spectroscopy for rapid detection of aatoxin B1 in maize and barley as analytical quality assessment. Food Chem 113:62934. Fink-Gremmels J. 2005. Mycotoxins in forages. In: Diaz DE, editor. The mycotoxin blue book. Nottingham, U.K.: Nottingham Univ. Press. p 24968. Flajs D, Domijan A-M, Ivi c D, Cvjetkovi c B, Peraica M. 2009. ELISA and HPLC analysis of ochratoxin A in red wines of Croatia. Food Contam 20:5902. Flannigan B. 1991. Mycotoxins. In: DMello FJP, Duffus CM, Duffus JH, editors. Toxic substances in crop plants. Cambridge, U.K.: Woodhead Publishing Ltd. p 22657. Flieger M, Wurst M, Shelby R. 1997. Ergot alkaloids: sources, structures and analytical methods. Food Microbiol 42:330. Food Safety Authority of Ireland. Available from: http://www.fsai.ie. Accessed Jun 15, 2009. Foroud NA, Eudes F. 2009. Trichothecenes in cereal grains. Int J Mol Sci 10:14773. Frank HK. 1991. Food contamination by ochratoxin A in Germany. [meta-analysis] Lyon, France: IARC Sci Publ 115:7781. Franceschi S, Bidoli E, Baron AE, La Vecchia C. 1990. Maize and risk of cancers of the oral cavity, pharynx and esophagus in Northeastern Italy. J Nat Can Inst 82:140711. Fremy JM, Usleber E. 2003. Policy on characterization of antibodies used in immunochemical methods of analysis for mycotoxins and phycotoxins. J AOAC Int 86:86871. Frisvad JC, Thrane U. 1996. Mycotoxin production by food-borne fungi. In: Samson RA, Hoekstra ES, Frisvad JC, Filtenborg O, editors. Introduction to food-borne fungi. 5th ed. Baarn, The Netherlands: Centraalbureau vorr Schimmelcultures. p 25160. Fuchs S, Sontag G, Stidl R, Ehrlich V, Kundi M, Knasmuller S. 2008. Detoxication of patulin and ochratoxin A, two abundant mycotoxins, by lactic acid bacteria. Food Chem Toxicol 46:1398407. Fungaro MJLP, Vissotto PC, Sartori D, Vilas-Boas LA, Furianeto MC, Taniwaki MH. 2004. A molecular method for detection of Aspergillus carbonarius in coffee beans. Curr Microbiol 49:1237. Gachok IV, Bondarenko AP, Saeger SD, Lobeau M, Peteghem CV, Shim WB, Chung D-H, Eremin SA. 2008. Multi-detection of mycotoxins by uorescence polarization immunoassay. Toxicol Lett 180:S28. Gajdusek DC. 1953. Acute infectious hemorrhagic fevers and mycotoxicoses in the Union of Soviet Socialistic Republics. Medical science publications no 2. Washington, D.C.: Walter Reed Army Medical Center. Galvano F, Galofaro V, Galvano G. 1996. Occurrence and stability of aatoxin M1 in milk and milk products. A worldwide review. J Food Prot 59:107990. Galvano F, Galofaro V, Bognanno M, De Angelis A, Galvano G. 2001. Survey of the occurrence of aatoxin M1 in dairy products marketed in Italy, Second year of observation. Food Addit Contam 18:6446. Galvano F, Ritieni A, Pietri A. 2005. Mycotoxins in the human food chain. In: Diaz D, editor. Mycotoxin blue book. Nottingham, U.K.: Nottingham Univ. Press. p 187224. Gareis M, Ceynowa J. 1994. Inuence of the fungicide Matador (tebuconazole/triadimenol) on mycotoxin production by Fusarium culmorum. Z Lebensm Unters Forsch 198:2448. Gareis M, M artlbauer E, Bauer J, Gedek B. 1988. Determination of ochratoxin A in human milk. Z Lebensm Unters Forsch 186:1147. Gatt MJ, Fraga ME, Magnoli C, Dalcero AM, da Rocha Rosa CA. 2003. Mycological survey for potential aatoxin and ochratoxin producers and their toxicological properties in harvested Brazilian black pepper. Food Addit Contam 20:11206. Gazzotti T, Lugoboni B, Zironi E, Barbarossa A, Serraino A, Pagliuca G. 2009. Determination of fumonisin B1 in bovine milk by LC-MS/MS. Food Cont 20:11714. Gelderblom WCA, Jaskiewicz K, Marasas WFO, Thiel PG, Horak RM, Vleggar R, Kriek NPJ. 1988. Fumonisins, novel mycotoxins with cancer promoting activity produced by Fusarium moniliforme. J Appl Environ Microbiol 54:180611. Gelderblom WCA, Marasas WFO, Vleggar R, Thiel PG, Cawood ME. 1992. Fumonisins: isolation, chemical characterization and biological effects. Mycopathologia 117: 116. Gentles A, Smith EE, Kubena LF, Duffus E, Johnson P, Thompson J, Harvey RB, Edrington TS. 1999. Toxicological evaluations of cyclopiazonic acid and ochratoxin A in broilers. Poult Sci 78:13804. George WL, Payne AL, Smith LW, Wood PM, Petterson DS. 1979. Phomopsin A production by Phomopsis leptostromiformis in liquid media. Appl Environ Microbiol 37:289 92. Ghali R, Hmaissia-khlifa K, Ghorbel H, Maarou K, Hedili A. 2009 HPLC determination of ochratoxin A in high-consumption Tunisian foods. Food Cont 20:71620. Ghazani MH. 2009. Aatoxin M1 contamination in pasteurized milk in Tabriz (northwestern Iran). Food Chem Toxicol 47:16245. Goehring LS, van Maanen C, Sloet van Oorgh-Oosterbaan, MM. 2005. Neurological syndromes among horses in The Netherlands. A 5-year retrospective survey (19992004). Vet Quart 27:1120. Goryacheva IY, Karagusheva MA, Peteghem CV, Sibanda L, Saeger SD. 2009. Immunoafnity pre-concentration combined with on-column visual detection as a tool for rapid aatoxin M1 screening in milk. Food Cont 20:8026. Groger D. 1972. Ergot. In: Solomon K, Ciegler A, Ajl S, editors. Microbial toxins. New York: Academic Press. p 32174. Groopman JD, Cain LG, Kensler TW. 1988. Aatoxin exposure in human populations: measurements and relationship to cancer. Crit Rev Toxicol 19:11346. Gruber-Schley S, Thalmann A. 1988. Vorkommen von Alternaria spp. und deren Toxine in Getreide und mogliche Zusammenh angen mit Leistungsminderungen landwirtschaftlicher Nutztiere. Landwirtsch Forschung 41:1129. Hajian R, Ensa AA. 2009. Determination of aatoxins B1 and B2 by adsorptive cathodic stripping voltammetry in groundnut. Food Chem 115:10347. Hald B. 1991. Porcine nephropathy in Europe. IARC Sci Publ 115:4956. Hall AJ, Wild CP. 2003. Liver cancer in low and middle income countries. Br Med J 326:994 5. Harris LJ, Desjardins AE, Plattner RD, Nicholson P, Butler G, Young YC, Weston G, Proctor RH, Hohn TM. 1999. Possible role of trichothecene mycotoxins in virulence of Fusarium graminearum on maize. Plant Dis 83:95460. Hawksworth DL. 1991. The fungal dimension of biodiversity: magnitude, signicance, and conservation. Mycol Res 95:64155. Hawksworth DL, Kirk PM, Sutton BC, Pegler DN. 1995. Ainsworth and Bisbys dictionary of the fungi. 8th ed. Wallingford, U.K.: CAB Intl. 616 p. He P, Young LG, Forsberg C. 1992. Microbial transformation of deoxynivalenol (vomitoxin). Appl Environ Microbiol 58:385763. He F, Zhang S, Qian F, Zhang C. 1995. Delayed dystonia with striatal CT lucencies induced by a mycotoxin (3- nitropropionic acid). Neurology 45:217883. Heenan CN, Shaw KJ, Pitt JI. 1998. Ochratoxin A production by Aspergillus carbonarius and A. niger isolates and detection using coconut cream agar. J Food Mycol 1:6782. Heilmann W, Rehfeldt AG, Rotzoll F. 1999. Behaviour and reduction of ochratoxin A in green coffee beans in response to various processing methods. European Food Res Technol 209:297300. Hendrich S, Miller KA, Wilson TM, Murphy PA. 1993. Toxicity of Fusarium proliferatum fermented nixtamalized corn-based diets fed to rats: effect of nutritional status. J Agric Food Chem 41:164954. Hendrickse RG, Maxwell SM. 1989. Aatoxins and child health in tropics. J Toxicol Tox Rev 8:3141. Hendry KM, Cole EC. 1993. A review of mycotoxins in indoor air. J Toxicol Environ Health 38:18398. Hern andez-Hierro JM, Garc a-Villanova RJ, Gonz alez-Mart n I. 2008. Potential of nearinfrared spectroscopy for the analysis of mycotoxins applied to naturally contaminated red paprika found in the Spanish market. Anal Chim Acta 622:18994. Herzallah SM. 2009. Determination of aatoxins in eggs, milk, meat and meat products using HPLC uorescent and UV detectors. Food Chem 114:11416. Hesseling PB. 1992. Onyalai. Baillieres Clin Haemat 5:45773. Hitokoto H, Morozumi S, Wauke T, Sakai S, Ueno I. 1978. Inhibitory effects of condiments and herbal drugs on the growth and toxin production of toxigenic fungi. Mycopathologia 66:1618. Hocking AD, Leong SL, Kazi BA, Emmett RW, Scott ES. 2007. Fungi and mycotoxins in vineyards and grape products. Int J Food Microbiol 119:848. Hogan GR, Ryan NJ, Hayes AW. 1978. Aatoxin B1 and Reyes syndrome. Lancet 8063:561. Hooper DG, Bolton VE, Guilford FT, Straus DC. 2009. Mycotoxin detection in human samples from patients exposed to environmental molds. Int J Mol Sci 10:146575. Huang B, Xiao H, Zhang J, Zhang L, Yang H, Zhang Y, Jin J. 2009. Dual-label time-resolved uoroimmunoassay for simultaneous detection of aatoxin B1 and ochratoxin A. Arch Toxicol 83:61924. Hult K, Fuchs R. 1986. Analysis and dynamics of ochratoxin A in biological systems. In: Steyn PS, Vleggaar R, editors. Mycotoxins and phycotoxins. Amsterdam, The Netherlands: Elsevier Science Publishers BV. p 36576. Hum S. 2005. Putative sporidesmin toxicity in an eastern grey kangaroo (Macropus giganteus). Aust Vet J 83:67879. IARC. 1986. Some naturally occurring and synthetic food components, Furo-coumarins ultraviolet radiation. In: Monographs of the evaluation of the carcinogenic risk of chemical to human. Vol. 40. Lyon, France: IARC Press. p 8398. IARC. 1987. Overall evaluations of carcinogenicity. An updating of IARC monographs volumes 1 to 42. IARC monographs on the evaluation of carcinogenic risks to humans supplement 7:1440. IARC. 1993a. Overall evaluations of carcinogenicity. 1993a. Some naturally occurring substances: food items and constituents, heterocyclic aromatic amines and mycotoxins. IARC monographs on evaluation of carcinogenic risk to humans. No. 56. Lyons, France: IARC Press. p 4456. IARC. 1993b. International Agency for Research on Cancer. Monographs on the evaluation of carcinogenic risks of chemicals to humans. Lyon, France: IARC 56:489521. IARC. 1993c. International agency for research on cancer toxins derived from Fusarium moniliforme: fumonisins B1 and B2 and fusarin C, monographs on the evaluation of carcinogenic risks of chemicals to humans. Lyon, France: Intl. Agency for Research on Cancer. p 44566.
77

Iha MH, de Souza SVC, Sabino M. 2009. Single-laboratory validation of a liquid chromatography method for the determination of patulin in apple juice. Food Cont 20:56974. [IPCS] International Programme on Chemical Safety. 1990. Selected mycotoxins: ochratoxins, trichothecenes, ergot. Environmental Health Criteria 105. Geneva: WHO. Jackson LS, Hlwyka JJ, Senthil KR, Bullerman LB. 1996. Effect of thermal processing on the stability of fumonisins. In: Jackson LS, Devries JW, Bullerman LB, editors. Fumonisins in food. NewYork: Plenum Press. p 34553. Jackson LS, Katta SK, Fingerhut DD, DeVries JW, Bullerman LB. 1997. Effects of baking and frying on the fumonisin B1 content of corn-based foods. J Agric Food Chem 45:48005. [JECFA] Joint Expert Committee on Food Additives. 2000. Joint FAO/WHO Expert Committee on Food Additives, 53rd report. Safety evaluation of certain food additives. WHO food additives series 44. [JECFA] Joint Expert Committee on Food Additives. 2001. Joint FAO/WHO expert committee on food additives. Safety evaluation of certain mycotoxins in food. Prepared by the fty-sixth meeting of JECFA, WHO food additives series 47/ FAO food and nutrition 74International Programme on Chemical Society (IPCS). Geneva: WHO. Jensen AMD. 2005. Endophyte persistence and toxin (lolitrem b) production in a Danish seed crop of perennial ryegrass. Eur J Agron 23:6878. Jestoi M. 2008. Emerging Fusarium mycotoxins: fusaproliferin, beauvericin, enniatins and moniliformin: a review. Crit Rev Food Sci Nutr 48:2149. E, Peltonen K. 2009. Determination of Fusarium mycotoxins Jestoi M, Rokka M, J arvenp aa beauvericin and enniatins (A, A1, B, B1) in eggs of laying hens using liquid chromatography tandem mass spectrometry (LCMS/MS). Food Chem 115:11207. Joffe AZ. 1978. Fusarium poae and F. sporotrichioides as principal causal agents of alimentary toxic aleukia. In: Wyllie TD, Moorhouse LG, editors. Mycotoxic fungi, mycotoxins, mycotoxicosis: an encyclopedia handbook, Vol. 3. New York: Marcel Dekker. p 2186. Joffe AZ. 1986. Fusarium species: their biology and toxicology. New York: John Wiley and Sons Inc. p 1588. Johnson BA. 1997. Market report. Herbal Gram 40:4950. Jones FT, Genter MB, Hagler WM, Hansen JA, Mowrey BA, Poore MH, Whitlow LW. 1994. Understanding and coping with effects of mycotoxins in livestock feed and forage. North Carolina Cooperative Extension Service. p 114. Jonsyn FE, Maxwell SM, Hendrickse RG. 1995. Ochratoxin A and aatoxins in breast milk samples from Sierra Leone. Mycopathologia 131:1216. Jrgensen K. 2005. Occurrence of ochratoxin A in commodities and processed food: a review of EU occurrence data. Food Addit Contam 1:2630. Jorgensen K, Petersen A. 2002. Content of ochratoxin A in paired kidney and meat samples from healthy Danish slaughter pigs. Food Addit Contam 19:5627. Kabak B, Var I. 2008. Factors affecting the removal of aatoxin M1 from a food model by Lactobacillus and Bidobacterium strains. J Environ Sci Health B 43:61724. Kabak B, Dobson AD, Var I. 2006. Strategies to prevent mycotoxin contamination of food and animal feed: a review. Crit Rev Food Sci Nutr 46:593619. Kadakal C, Nas S. 2003. Effect of heat treatment and evaporation on patulin and some other properties of apple juice. J Sci Food Agric 83:98790. Kao C, Robinson RJ. 1972. Aspergillus avus deterioration of grain: its effect on amino acids and vitamins of whole wheat. J Food Sci 37:2613. Karbancioglu-Guler F, Heperkan D. 2009. Natural occurrence of fumonisin B 1 in dried gs as an unexpected hazard. Food Chem Toxicol 47:28992. Kataoka H, Itano M, Ishizaki A, Saito K. 2009. Determination of patulin in fruit juice and dried fruit samples by in-tube solid-phase micro-extraction coupled with liquid chromatography mass spectrometry. J Chromat A 1216:374650. Kensler TW, Egner PA, Wang JB, Zhu YR, Zhang BC, Lu PX, Chen JG, Qian GS, Kuang SY, Jackson PE, Gange SJ, Jacobson LP, Munoz A, Groopman JD. 2004. Chemoprevention of hepatocellular carcinoma in aatoxins endemic areas. Gastroenterology 127:3108. Keskin Y, Bas kaya R, Karsli S, Yurdun T, Ozyaral O. 2009. Detection of aatoxin M1 in human breast milk and raw cows milk in Istanbul, Turkey. J Food Prot 7:8859. Kiermeier F, Mashaley R. 1977. Inuence of raw milk processing on the aatoxin M1 content of milk products. Z Lebensm Unters Forsch 164:1837. Kiessling K-H. 1986. Biochemical mechanism of action of mycotoxins. Pure Appl Chem 58:32738. Kim H-J, Ji GE, Lee I. 2007. Naturally occurring levels of citrinin and monacolin K in Korean Monascus fermentation products. Food Sci Biotechnol 16:1425. King B. 1979. Outbreak of ergotism in Wollo, Ethiopia. Lancet 8131:1411. Klang DT, Kennedy BJ, Pathre SV, Mirocha CJ. 1978. Binding characteristics of zearalenone analogs to estrogen receptors. Cancer Res 38:3611. Kogika MM, Hagiwara MK, Mirandola RM. 1993. Experimental citrinin nephrotoxicosis in dogs: renal function evaluation. Vet Hum Toxicol 35:13640. Krishnamachari KAVR, Bhat RV, Nagarajan V, Tilak TBG. 1975. Hepatitis due to aatoxicosis. Lancet 7915:10613. Krogh P. 1974. Mycotoxic porcine nephropathy: a possible model for Balkan endemic nephropathy. In: Puchlev E, editor. Proceedings of the 2nd International Symposium on Endemic Nephropathy, 911 November 1972; Soa, Bulgaria. Soa, Bulgaria: Publishing House of the Bulgarian Academy of Sciences. p 26670. Krogh P. 1987. Ochratoxin A in food. In: Krogh P, editor. Mycotoxins in food. London: Academic Press. p 97121. Kubena LF, Smith EE, Gentles A, Harvey RB, Edrington TS, Phillips TD, Rottinghaus GE. 1994. Individual and combined toxicity of T-2 toxin and cyclopiazonic acid in broiler chicks. Poult Sci 73:13907. Kuiper-Goodman T, Scott PM, Watanabe H. 1987. Risk assessment of the mycotoxin zearalenone. Regul Toxicol Pharmacol 7:253306. Kumar M, Dwivedi P, Sharma AK, Singh ND, Patil RD. 2007. Ochratoxin A and citrinin nephrotoxicity in New Zealand White rabbits: an ultra structural assessment. Mycopathologia 163:2130. Kurata H. 1990. Mycotoxins and mycotoxicoses. In: Pohland AE, Dowell VR, Richards JL, editors. Microbial toxins in foods and feeds. New York: Plenum Press. p 24959. Kurtbay HM, Bekc i Z, Merdivan M, Yurdakoc K. 2008. Reduction of ochratoxin a levels in red wine by bentonite, modied bentonites, and chitosan. J Agric Food Chem 56:25415. Laan T, Bull S, Pirie R, Fink-Gremmels J. 2006. The role of alveolar macrophages in the pathogenesis of recurrent airway obstruction in horses. J Vet Int Med 20:16774. Lacey J. 1991. Natural occurrence of mycotoxins in growing and conserved forage crops. In: Smith JE, Henderson RE, editors. Mycotoxins and animal foods. Boca Raton, Fla.: CRC Press. p 36397. Lafont P, Lafont J, Mousset S, Frayssinet C. 1980. Etude de la contamination du lait de vache lors de lingestion de faibles quantit es daatoxine. Annales de Nutr etdAlimentation 34:699708. Langevin F, Eudes F, Comeau A. 2004. Effect of trichothecenes produced by Fusarium graminearum during Fusarium head blight development in six cereal species. Eur J Plant Pathol 110:73546. La Pera L, Avellone G, Lo Turco V, Di Bella G, Agozzino P, Dugo G. 2008. Inuence of roasting and different brewing processes on the ochratoxin A content in coffee determined by high-performance liquid chromatography-uorescence detection (HPLC-FLD). Food Addit Contam 25:125763. Le Bars J. 1979. Cyclopiazonic acid production by Penicillium camemberti Thom and natural occurrence of this in cheese. Appl Environ Microbiol 38:10525. Le Bars J, Le Bars P. 1996. Recent acute and sub-acute mycotoxicoses recognized in France. Vet Res 27:38394. Lee YJ, Hagler WM. 1991. Aatoxin and cyclopiazonic acid production by Aspergillus avus isolated from contaminated maize. J Food Sci 56:8712. Lee CL, Chen WP, Wang JJ, Pan TM. 2007. A simple and rapid approach for removing citrinin while retaining monacolin K in red mold rice. J Agric Food Chem 55:11101 8. Leitner A, Zollner P, Paolillo A, Stroka J. 2002. Comparison of methods for the determination of ochratoxin A in wine. Anal Chim Acta 453:3341. Leong SL, Hocking AD, Pitt JI, Kazi BA, Emmett RW, Scott ES. 2006. Australian research on ochratoxigenic fungi and ochratoxin A. Int J Food Microbiol 111:S107. Li F, Xu G, Li Y, Chen Y. 2003. Study on the production of citrinin by Monascus strains used in the food industry. J Hyg Res 32:6025. Li P, Zhang Q, Zhang W, Zhang J, Chen X, Jiang J, Xie L, Zhang D. 2009. Development of a class-specic monoclonal antibody-based ELISA for aatoxins in peanut. Food Chem 115:3137. Ligler FS, Bredehorst R, Talebian A, Shriver LC, Hammer CF, Sheridan JP, Vogel C. Gaber BP. 1987. A homogeneous immunoassay for mycotoxin T-2 utilizing liposomes, monoclonal antibodies, and complement. Anal Biochem 183:36975. Liu X, Luo X, Hu W. 1988. Arthrinium sp. and the deteriorated sugarcane poisoning. In: Aibara K, Kumagai S, Ohtsubo K, Yoshizawa T, editors. Mycotoxins and phycotoxins. Abstracts of the 7th International IUPAC Symposium, 1619 Aug 1988. Tokyo, Japan: Japanese Assoc. of Mycotoxicology. 26 p. Liu X, Luo X, Hu W. 1992. Studies on the epidemiology and etiology of moldy sugarcane poisoning in China. Biomed Environ Sci 5:16177. Liu BH, Wu TS, Yu FY, Su CC. 2007. Induction of oxidative stress response by the mycotoxin patulin in mammalian cells. Toxicol Sci 95:3407. Llewellyn GC, Burkett ML, Eadie T. 1981. Potential mold growth, aatoxin production and antimycotic activity of selected natural species and herbs. J Assoc Off Anal Chem 64:955 60. Logrieco A, Bottalico A, Visconti A, Vurro M. 1988. Natural occurrence of Alternaria mycotoxins in some plant products. Microbiol Ali Nutr 6:137. Logrieco A, Rizzo A, Ferracane R, Ritieni A. 2002. Occurrence of beauvericin and enniatins in wheat affected by Fusarium avenaceum head blight. Appl Environ Microbiol 68: 825. Ludolph AC, He F, Spencer PS, Hammerstad J, Sabri M. 1991. 3-Nitropropionic acid: exogenous animal neurotoxin and possible human striatal toxin. Canadian J Neuro Sci 18:4928. Luo X. 1994. Food poisoning caused by Fusarium toxins. Proc. Second Asian Conf. Food Safety. 12936. [MAFRI] Manitoba Agriculture, Food and Rural Initiatives. 2006. Grain drying and storage of damp grain: crop production. Available from: http://www.gov.mb.ca/ agriculture/crops/cropproduction/faa05s00.html#table. Accessed May 2009. Magan N. 2004. Mycotoxin research: progress and future prospects. In: Barug D, van Egmond HP, Lopez-Garcia R, van Osenbruggen WA, Visconti A, editors. Meeting the mycotoxin menace. Wageningen, The Netherlands: Wageningen Academic Press. p 295303. Manabe M. 2001. Fermented foods and mycotoxins. Mycotoxins 51:258. Manetta AC, Giammarco M, Giuseppe LD, Fusaro I, Gramenzi A, Formigoni A, Vignola G, Lambertini L. 2009. Distribution of aatoxin M1 during Grana Padano cheese production from naturally contaminated milk. Food Chem 113:5959. Mann R, Rehm HJ. 1976. Degradation products from aatoxin by Corynebacterium rubrum, Aspergillus niger, Trichoderma viride and Mucor ambrigus. Eur J Appl Microbial 2: 297306. Manova R, Mladenova R. 2009. Incidence of zearalenone and fumonisins in Bulgarian cereal production. Food Cont 20:3625. Maarou K, Achour A, Hammami M, El May M, Betbeder AM, Ellouz F, Creppy EE, Bacha H. 1995. Ochratoxin A in human blood in relation to nephropathy in Tunisia. Hum Exp Toxicol 14:60915. Maragos CM, Plattner RD. 2002. Rapid uorescence polarization immunoassay for the mycotoxin deoxynivalenol in wheat. J Agric Food Chem 50:182732. Marasas WFO, Nelson PE, Toussoun TA. 1984. Toxigenic Fusarium species. Identity and mycotoxicology. University Park, Pa.: Pennsylvania State Univ. Press. 328 p. Marasas WFO, Riley RT, Hendricks KA, Stevens VL, Sadler TW, Gelineau-van Waes J, Missmer SA, Cabrera J, Torres O, Gelderblom WCA, Allegood J, Martinez C, Maddox J, Miller JD, Starr L, Sullards MC, Roman AV, Voss KA, Wang E, Merrill AH. 2004. Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo: a potential risk factor for human neural tube defects among populations consuming fumonisin-contaminated maize. J Nutr 134:7116. Markaki P, Melissari E. 1997. Occurrence of aatoxin M1 in commercial pasteurized milk determined with ELISA and HPLC. Food Addit Contam 14:4516. Marquenie D, Lammertyn J, Geeraerd AH, Soontjens C, van Impe JF, Nicola BM, Michiels CW. 2002. Inactivation of conidia of Botrytis cinerea and Monilinia fructigena using UVC and heat treatment. Int J Food Microbiol 74:2735. Martin ML, Martin HM. 2000. Aatoxin M1 in raw and ultra-high-temperature treated milk commercialized in Portugal. Food Addit Contam 17:8714.
78

Martins ML, Gimeno A, Martins HM, Bernardo F. 2002. Co-occurrence of patulin and citrinin in Portuguese apples with rotten spots. Food Addit Contam 19:56874. Masimango N, Ramaut JL, Remacle J. 1978. The role of adsorption in the elimination of aatoxin B1 from contaminated media. Eur J Appl Microbiol 6:1015. Massey TE, Stewart RK, Daniels JM, Liu L. 1995. Biochemical and molecular aspects of mammalian susceptibility to aatoxin B 1 carcinogenicity. Proc Soc Exp Biol Med 208:213 27. McKenzie KS, Sarr A, Mayura K, Bailey RH, Miller DR, Rogers, TD, Norred WP, Voss KA, Plattner RD, Phillips TD. 1997. Chemical degradation of diverse mycotoxins using a novel method of ozone production. Food Chem Toxicol 35:80720. McMullen M, Jones R, Gallenberg D. 1997. Scab of wheat and barley: a re-emerging disease of devasting impact. Plant Dis 81:13408. Meister U. 2004. New method of citrinin determination by HPLC after polyamide column clean-up. Eur Food Res Technol 218:3949. Meky FA, Hardie LJ, Evans SW, Wild CP. 2001. Deoxynivalenol-induced immunomodulation of human lymphocyte proliferation and cytokine production. Food Chem Toxicol 39:827 36. Micco C, Brera C, Miraglia M, Onori R. 1987. HPLC determination of the total content of aatoxins in naturally contaminated eggs in free and conjugated forms. Food Addit Contam 4:40714. Micco C, Miraglia M, Brera C, Corneli S, Ambruzzi A. 1995. Evaluation of ochratoxin A level in human milk in Italy. Food Addit Contam 12:3514. Miller MA, Hanstead JP, Lovell RA. 1996. Regulatory aspects of fumonisins with respect to animal feed. In: Jackson LS, Devries JW, Bullerman LB, editors. Fumonisins in food. New York: Plenum Press. p 3638. Ming L. 1995. Moldy sugarcane poisoning: a case report with a brief review. Clin Toxicol 33:3637. Miraglia MA, de Dominicis C, Corneli BS, Cava E, Menghetti E, Miraglia E. 1995. Ochratoxin A levels in human milk and related food samples: an exposure assessment. Nat Tox 3:436 44. Miraglia M, Brera C. 2002. Assessment of dietary intake of ochratoxin A by the population of EU member states. Reports on tasks for scientic cooperation. Reports of experts participating in Task 3.2.7. Directorate-General Health and Consumer Protection, Rome, Italy. Mislivic PB, Bruce VR, Stack ME, Bandler R. 1987. Molds and tenuazonic acid in fresh tomatoes used for catsup production. J Food Prot 50:3841. Mitchell GE. 1988. Inuence of irradiation of food on aatoxin production. Food Technol Australia 40:3246. Moake MM, Padilla-Zakour OI, Worobo RW. 2005. Comprehensive review of patulin control methods in foods. Compr Rev Food Sci Food Safety 1:821. Monbaliu S, Van Poucke C, Van Peteghem C, Van Poucke K, Heungens K, De Saeger S. 2009. Development of a multi-mycotoxin liquid chromatography/tandem mass spectrometry method for sweet pepper analysis. Rapid Commun Mass Spectrom 23: 311. Montagna MT, Napoli C, De Giglio O, Iatta R, Barbuti G. 2008. Occurrence of aatoxin m(1) in dairy products in southern Italy. Int J Mol Sci 9:261421. Montemurro N, Visconti A. 1992. Alternaria metabolites, chemical and biological data. In: Chelkowski J, Visconti A, editors. Alternaria: biology, plant diseases and metabolites. Amsterdam: Elsevier. p 449557. Moreau C. 1979. Molds, toxins and food. New York: Interscience Publications, John Wiley and Sons. 144 p. Morrissey RE, Cole RJ, Dorner JW. 1984. The effects of cyclopiazonic acid on pregnancy and fetal development of Fischer rats. J Toxicol Environ Health 14:58594. Moss MO. 1995. Mycotoxins in foods, feeds and pastures. Biodeter Abst 9:25964. Moss MO. 1996. Mode of formation of ochratoxin A. Food Addit Contam 13:59. Moss MO. 2002. Enzymes and aatoxin biosynthesis. Int Biodeter Biodegr 50:13742. Moss MO. 2008. Fungi, quality and safety issues in fresh fruits and vegetables. J Appl Microbiol 104:123943. Moss MO, Frank M. 1987. Prevention: effects of biocides and other agents on mycotoxin production. In: Watson DH, editor. Natural toxicants in food. Chichester, U.K.: Ellis Horwood. p 23151. Munkvold GP. 2003. Cultural and genetic approaches to managing mycotoxins in maize. Ann Rev Phytopath 41:99116. E, Lopez Murillo-Arbizu M, Am ezqueta S, Gonz alez-Penas de Cerain A. 2009. Occurrence of patulin and its dietary intake through apple juice consumption by the Spanish population. Food Chem 113:4203. Murphy PA, Hendrich S, Hopmans EC, Hauck CC, Lu Z, Buseman G, Munkvold G. 1996. Effect of processing on fumonisin content of corn. In: Jackson LS, Devries JW, Bullerman LB, editors. Fumonisins in food. NewYork: Plenum Press. p 32334. Mycotoxin Certication Standard 2008. Available from: http://www.mycotoxincertication.eu. Accessed Jul 22, 2009. Nakazato M, Morozumi S, Saito K, Fujinuma K, Nishima T, Kasai N. 1990. Interconversion of aatoxin B1 and aatoxicol by several fungi. Appl Environ Microbiol 56:146570. Narvankar DS, Singh CB, Jayas DS, White NDG. 2009. Assessment of soft X-ray imaging for detection of fungal infection in wheat. Biosyst Eng 103:4956. Nawaz S, Coker RD, Haswell SJ. 1992. Development and evaluation of analytical methodology for the determination of aatoxins in palm kernels. Analyst 117:6774. Nelson PE, Desjardins AE, Plattner RD. 1993. Fumonisins, mycotoxins produced by Fusarium species: biology, chemistry and signicance. Ann Rev Phytopath 31:23349. Nibbelink SK. 1986. Aatoxicosis in food animals: a clinical review. Iowa State UniVet 48:2831. Niderkorn V, Boudra H, Morgavi DP. 2006. Binding of Fusarium mycotoxins by fermentative bacteria in vitro. J Appl Microbiol 101:84956. Niderkorn V, Morgavi DP, Pujos E, Tissandier A, Boudra H. 2007. Screening of fermentative bacteria for their ability to bind and biotransform deoxynivalenol, zearalenone and fumonisins in an in vitro simulated corn silage model. Food Addit Contam 24:406 15. Niessen L. 2008. PCR-based diagnosis and quantication of mycotoxin-producing fungi. Adv Food Nutr Res 54:81138. Nonaka Y, Saito K, Hanioka N, Narimatsu S, Kataoka H. 2009. Determination of aatoxins in food samples by automated on-line in-tube solid-phase microextraction coupled with liquid chromatography-mass spectrometry. J Chrom A 1216:441622. Nony PA, Scallet AC, Rountree RL, Ye X, Binienda Z. 1999. 3-Nitropropionic acid (3-NPA) produces hypothermia and inhibits histochemical labeling of succinate dehydrogenase (SDH) in rat brain. Met Brain Dis 14:8394. Norred WP, Voss KA. 1994. Toxicity and role of fumonisins in animal diseases and human esophageal cancer. J Food Prot 57:5227. Norred WP, Voss KA, Riley RT, Meredith FI, Bacon CW, Merrill Jr. AH. 1998. Mycotoxins and health hazards: Toxicological aspects and mechanism of action of fumonisins. J Toxicol Sci 23:1604. Northolt MD, Frisvad JC, Samson RA. 1996. Occurrence of food-borne fungi and factors for growth. In: Samson RA, Hoekstra ES, Frisvad JC, Filtenborg O, editors. Introduction to foodborne fungi. 5th edition. Baarn, The Netherlands: Centraalbureau vorr Schimmelcultures. p 24350. Ogbadu G. 1980. Inuence of gamma-irradiation of aatoxin B 1 production by Aspergillus avus growing on some Nigerian foodstuffs. Microbios 27:1926. Omurtag GZ, Yazicio glu D.2004. Determination of fumonisins B1 and B2 in herbal tea and medicinal plants in Turkey by high-performance liquid chromatography. J Food Prot 67:17826. ORiordan MJ, Wilkinson MG. 2008. A survey of the incidence and level of aatoxin contamination in a range of imported spice preparations on the Irish retail market. Food Chem 107:142935. ORiordan MJ, Wilkinson MG. 2009. Comparison of analytical methods for aatoxin determination in commercial chilli spice preparations and subsequent development of an improved method. Food Cont 20:7005. Osborne BG, Ibe FI, Brown GL, Patagine F, Scudamore KA, Bancks JN, Hetmanski MT. 1996. The effects of milling and processing on wheat contaminated with ochratoxin A. Food Addit Contam 13:14153. Osweiler GD. 1996. Toxicology. Philadelphia, Pa.: Williams and Wilkins Publishers. p 4289. Osweiler GD. 2000. Mycotoxins. Contemporary issues of food animal health and productivity. Vet Clin North America Food Anim Pract 16:51130. Otteneder H, Majerus P. 2000. Occurrence of ochratoxin A (OTA) in wines: inuence of the type of wine and its geographical origin. Food Addit Contam 17:7938. Ough CS, Corison CA. 1980. Measurement of patulin in grapes and wines. J Food Sci 45:476 8. Pandey I, Chauhan SS. 2007. Studies on production performance and toxin residues in tissues and eggs of layer chickens fed on diets with various concentrations of aatoxin AFB1. Br Poult Sci 48:71323. Park DL, Pohland AE. 1989. Sampling and sample preparation for determination and quantitation of natural toxicants in food and feed. J Assoc Anal Chem 72:399 404. Park DL, Liang B. 1993. Perspectives on aatoxin control for human food and animal feed. Trends Food Sci Technol 4:33442. Paster N, Barkai-Golan R, Padova R. 1985. Effect of gamma radiation on ochratoxin. production by the fungus Aspergillus ochraceus. J Sci Food Agric 36:4459. Peraica M, Radic B, Lucic A, Pavlovic M. 1999.Toxic effects of mycotoxins in humans. Bull World Health Org 7:75466. Perkowski J, Bu sko M, Chmielewski J, Goral T, Tyrakowska B. 2008. Content of trichodiene and analysis of fungal volatiles (electronic nose) in wheat and triticale grain naturally infected and inoculated with Fusarium culmorum. Int J Food Microbiol 126:12734. Pero RW, Harvan D, Blois MC. 1973. Isolation of the toxin altenuisol from the fungus Alternaria tenuis Auct. Tetrahedron Lett 12:9458. Pestka JJ. 1991. High-performance thin-layer chromatography ELISAGRAM: application of a multi-hapten immunoassay to analysis of the zearalenone and aatoxin mycotoxin families. J Immun Meth 136:17783. Petersen A, Thorup I. 2001. Preliminary evaluation of fumonisins by the Nordic countries and occurrence of fumonisins (FB1 and FB 2) in corn-based foods on the Danish market. Food Addit Contam 18:2216. Peterson JE, Jago MV, Payne AL, Stewart PL. 1987. The toxicity of phomopsin for sheep. Aust Vet J 64:2938. Peterson S, Lampe JW, Bammler TK, Gross-Steinmeyer K, Eaton DL. 2006. Apiaceous vegetable constituents inhibit human cytochrome P-450 1A2 (hCYP1A2) activity and hCYP1A2-mediated mutagenicity of aatoxin B1. Food Chem Toxicol 44:147484. Petkova-Bocharova T, Castegnaro M. 1991. Ochratoxin A in human blood in relation to Balkan endemic nephropathy and urinary tract tumours in Bulgaria. Mycotoxins, endemic nephropathy and urinary tract tumours. IARC Sci Publ 115:1357. Petzinger E, Ziegler K. 2000. Ochratoxin A froma toxicological perspective. J Vet Pharmacol Ther 23 918. Pfohl-Leszkowicz A. 2000. Risques mycotoxicologiques pour la sant e des animaux et de lhomme. Cah Nutr Di etics 35:38997. Piermarini S, Volpe G, Micheli L, Moscone D, Palleschi G. 2009. An ELIME-array for detection of aatoxin B1 in corn samples. Food Cont 20:3715. Pietri A, Bertuzzi T, Gadolini F, Gualla A. 2001a. Aatoxin B1 residues in eggs of laying hens fed a naturally contaminated diet. Proc A.S.P.A. XIV Congress, Firenze, June 1215. p 44850. Pietri A, Bertuzzi T, Pallaroni L, Piva G. 2001b. Occurrence of ochratoxin A in Italian wines. Food Addit Contam 18:64754. Pietri A, Zanetti M, Bertuzzi T.2009. Distribution of aatoxins and fumonisins in dry-milled maize fractions. Food Addit Contam Part A 26:37280. Pinto C, Santos VM, Dinis J, Peleteiro MC, Fitzgerald JM, Hawkes AD, Smith BL. 2005. Pithomycotoxicosis (facial eczema) in ruminants in the Azores, Portugal. Vet Rec 157:805 10. Pittet A. 1998. Natural occurrence of mycotoxins in foods and feeds: an update review. Vet Med Rev 149:47992. Pittet A, Royer D. 2002. Rapid, low-cost thin-layer chromatographic screening method for the detection of ochratoxin A in green coffee at a control level of 10 g/kg. J Agric Food Chem 50:2437. Pitt JI. 2000. Toxigenic fungi: which are important? Med Mycol 38:1722.
79

Ple stina R. 1992. Some features of Balkan endemic nephropathy. Food Chem Toxicol 30:177 81. de gram Poo L, Araya O. 1989. Ergotismo convulsivo en novillos debido a ingestion neas infectadas por Claviceps purpurea. Archs Med Vet 21:668. Proctor RH, Hohn TM, McCormick S P. 1995. Reduced virulence of Gibberella zeae caused by disruption of a trichothecene toxin biosynthetic gene. Mol Plant Microbe Interact 8:593 601. Purchase IFH, Steyn M, Rinsma R, Tustin RC. 1972. Reduction of the aatoxin M1 content of milk by processing. Food Cosm Toxicol 10:3837. Qureshi MA, Brake J, Hamilton PB, Hagler Jr. WM, Neshheim S. 1998. Dietary exposure of broiler breeders to aatoxin results in immune disfunction in progeny chicks. Poult Sci 77:8129. Rabie CJ, van Rensbrug SJ, Van Der Watt JJ, Lubben A. 1975. Onyalai: the possible involvement of a mycotoxin produced by Phoma sorghina in the aetiology. South African Med J 57:164750. Ramakrishna Y, Bhat RV. 1990. Minicolumn chromatography for the detection of sterigmatocystin in agricultural commodities. Mycopathologia 110:1535. Ramakrishna Y, Bhat RV, Ravindranath V. 1989. Production of deoxynivalenol by Fusarium isolates from samples of wheat associated with a human mycotoxicosis outbreak and from sorghum cultivars. Appl Environ Microbiol 55:261920. Rao CY. 2001. Toxigenic fungi in the indoor environment. In: Spengler JD, Samset JM, McCarthy JS, editors. Indoor air quality handbook. Washington, D.C.: McGraw-Hill. p 117. Rastogi S, Dwivedi PD, Khanna SK, Das M. 2004. Detection of aatoxin M1 contamination in milk and infant milk products from Indian markets by ELISA. Food Cont 15:287 90. Ratcliff J. 2002. The role of mycotoxins in food and feed Safety. Presented at AFMA (Animal Feed Manufacturers Association) meeting on 16 August, 2002. Available from: http://www.facs.org.uk. Accessed Jun 2008. Rates SMK. 2001. Plants as source of drugs. Toxicon 39:60313. Ratola N, Martins L, Alves A. 2004. Ochratoxin A in wines: assessing global uncertainty associated with the results. Anal Chim Acta 513:31924. Reddy KRN, Reddy CS, Muralidharan K. 2009. Potential of botanicals and biocontrol agents on growth and aatoxin production by Aspergillus avus infecting rice grains. Food Cont 20:1738. Refai MK, Aziz NH, El-Far FM, Hassan AA. 1996. Detection of ochratoxin produced by A. ochraceus in feedstuffs and its control by gamma-irradiation. Appl Radiat Isot 7:61721. Revankar SG. 2003. Clinical implications of mycotoxins and stachybotrys. Am J Med Sci 325:26274. Rice LG, Ross FB. 1994. Methods for detection and quantitation of fumonisins in corn, cereal products and animal excreta. J Food Prot 57:53640. Riley RT, Norred W. 1996. Mechanisms of mycotoxicity. In: Howard DH, Miller JD, editors. The mycota. Vol VI. Berlin, Germany: Springer. p 1945. Riley RT. 1998. Mechanistic interactions of mycotoxins: theoretical consideration. In: Sinha KK, Bhatanagar D, editors. Mycotoxins in agriculture and food safety. New York: Marcel Dekker. p 22754. Rizzo I, Vedoya G, Maurutto S, Haidukowski M, Varsavsky E. 2004. Assessment of toxigenic fungi on Argentinean medicinal herbs. Microbiol Res 159:11320. Rodricks JV, Stoloff L. 1977. Aatoxin residues from contaminated feed in edible tissues of food-producing animals. In: Rodricks JVC, Hesseltine W, Mehlman MA, editors. Mycotoxins in human and animal health. Park Forest South, Ill.: Patholox Publishers. 3:679. Romagnoli B, Menna V, Gruppioni N, Bergamini C. 2007. Aatoxins in spices, aromatic herbs, herb-teas and medicinal plants marketed in Italy. Food Cont 18:697701. Rosner H. 1998. Mycotoxin regulations: an update. Revue de M ed V et 149:67980. Ross PF, Rice LG, Osweiler GD, Nelson PE, Richard JL, Wilson TM. 1992. A review and update of animal toxicoses associated with fumonisin-contaminated feeds and production of fumonisins by Fusarium isolates. Mycopathologia 17:10914. Ross PF, Ledet AE, Owens DL, Rice LG, Nelson HA, Osweiler GD, Wilson TM. 1993. Experimental equine leukoencephalomalacia, toxic hepatosis, and encephalopathy caused by corn naturally contaminated with fumonisins. J Vet Diag Inv 5:6974. Rotter BA, Prelusky DB, Pestka JJ. 1996. Toxicology of deoxynivalenol (vomitoxin). J Toxicol Environ Health 48:134. Roy AK, Chourasia HK, Kumari N. 1987. Association of mycoora with some crude herbal drugs of Bhutan. Indian Bot Rept 6:489. Roy AK, Sinha KK, Chourasia HK. 1988. Aatoxin contamination of some common drug plants. Appl Environ Microbiol 54:8423. Roy AK. 2003. Mycological problems of crude herbal drugs: overview and challenges. Indian Phytopathol 56:113. Santos EA, Vargas EA. 2002. Immunoafnity column clean-up and thin-layer chromatography for determination of ochratoxin A in green coffee. Food Addit Contam 19:44758. ul u O, C Sarimehmetoolu B, Kupl elik TH. 2003. Detection of aatoxin M1 in cheese samples by ELISA. Food Cont 15:459. Sarwar NM, Jolley ME. 2002. Development of a uorescence polarization assay for the determination of aatoxins in grains. J Agric Food Chem 50:311621. Schiefer HB. 1990. Mycotoxins in indoor air: a critical toxicological viewpoint. Indoor air 90: Proceedings of the 5th International conference on indoor air. p 16772. Schmidt H, Ehrmann M, Vogel RE, Taniwaki MH, Niessen L. 2003. Molecular typing of Aspergillus ochraceus and construction of species specic SCAR-primers based on AFLP. Syst Appl Microbiol 26:13846. Schmidt H, Taniwaki MH, Vogel RE, Niessen L. 2004. Utilization of AFLP markers for PCRbased identication of Aspergillus carbonarius and indication of its presence in green coffee samples. J Appl Microbiol 97:899909. Schneweis I, Meyer K, Hormansdorfer S, Bauer J. 2000. Mycophenolic acid in silage. Appl Environ Microbiol 66:363941. Schneweis I, Meyer K, Hormansdorfer S, Bauer J. 2001. Metabolites of Monascus ruber in silages. J Anim Physiol Anim Nutr 85:3844. Schoental R. 1984. Mycotoxins and the bible. Persp Biol Med 28:11720. Schoental R. 1991. Mycotoxins, porphyrias and the decline of the Etruscans. J Appl Toxicol 11:4534. Schumacher DM, Muller C, Metzler M, Lehmann L. 2006. DNA: DNA cross-links contribute to the mutagenic potential of the mycotoxin patulin. Toxicol Lett 166:26875. Scott PM. 1996. Mycotoxins transmitted into beer from contaminated grains during brewing. J AOAC Int 79:87582. Scott PM. 1998. Industrial and farm detoxication processes for mycotoxins. Vet Med Rev 149:5438. Scudamore KA. 2005. Prevention of ochratoxin A in commodities and likely effects of processing fractionation and animal feeds. Food Addit Contam 22:1725. Scudamore KA, Banks J, MacDonald SJ. 2003. Fate of ochratoxin A in the processing of whole wheat grains during milling and bread production. Food Addit Contam 20:115363. Seefelder W, Gossman M, Humpf HU. 2002. Analysis of fumonisin B1 in Fusarium proliferatum-infected asparagus spears and garlic bulbs from Germany by liquid chromatography: electrospray ionization mass spectrometry. J Agric Food Chem 50:277881. Seo E, Yoon Y, Kim K, Shim WB, Kuzmina N, Oh KS, Lee JO, Kim DS, Suh J, Lee SH, Chung KH, Chung DH. 2009. Fumonisins B1 and B2 in agricultural products consumed in South Korea: an exposure assessment. J Food Prot 72:43640. Sewram V, Nair JJ, Nieuwoudt TW, Leggott NL, Shephard GS. 2000. Determination of patulin in apple juice by high-performance liquid chromatography-atmospheric pressure chemical ionization mass spectrometry. J Chrom A 897:36574. Shaban E, Gajdo sov a D, H egrov a B, Havel J. 2007. MALDI TOF mass spectrometry of selected mycotoxins in barley. J Appl Biomed 5:3947. Sharma RP. 1993. Immunotoxicity of mycotoxins. J Dairy Sci 76:8927. Shim WB, Dzantiev BB, Eremin SA, Chung DH. 2009. One-step simultaneous immunochromatographic strip test for multianalysis of ochratoxin A and zearalenone. J Microbiol Biotechnol 19:8392. Shotwell OL. 1983. Successful interagency cooperation: the Diehlstadt story1983 AOAC Wiley Award Address. J Assoc Off Anal Chem 66:2247. Shundo L, Navas SA, Lamardo LCA, Ruvieri V, Sabino M. 2009. Estimate of aatoxin M1 exposure in milk and occurrence in Brazil. Food Cont 20:6557. Sibanda L, Desaeger S, Barna-Vetro I, Vanpeteghem C. 2002. Development of a solid-phase clean-up and portable rapid ow-through enzyme immunoassay for the detection of ochratoxin A in roasted coffee. J Agric Food Chem 50:69647. Singh ND, Sharma AK, Dwivedi P, Patil RD, Kumar M. 2007. Citrinin and endosulfan-induced teratogenic effects in Wistar rats. J Appl Toxicol 27:14351. Singh P, Srivastava B, Kumar A, Dubey NK. 2008. Fungal contamination of raw materials of some herbal drugs and recommendation of cinnamomum camphora oil as herbal fungitoxicant. Microb Ecol 56:55560. Skaug MA. 1999. Analysis of Norwegian milk and infant formulas for ochratoxin A. Food Addit Contam 16:758. Skaug MA, Stormer FC, Saugstad OD. 1998. Ochratoxin A: a naturally occurring mycotoxin found in human milk samples from Norway. Acta Paediatrica 87:12758. Skaug MA, Helland I, Solvoll K, Saugstad OD. 2001. Presence of ochratoxin A in human milk in relation to dietary intake. Food Addit Contam 18:3217. Smith JE, Moss MO. 1985. Mycotoxins formation, analysis and signicance. New York: John Wiley and Sons. 148 p. Smith JE, Henderson RS. 1991. Mycotoxins and animal foods. Boston, Mass.: CRC Press. p 683. Smith TK, Seddon IR. 1998. Toxicological synergism between Fusarium mycotoxins in feeds. In: Lyons TP, Jacques KA, editors. Biotechnology in the feed industry. Loughborough, U.K.: Nottingham Univ. Press. p 25769. Smith EE, Kubena LF, Braithwaite CE, Harvey RB, Phillips TD, Reine AH. 1992. Toxicological evaluation of aatoxin and cyclopiazonic acid in broiler chickens. Poult Sci 71:113644. Smith JE, Solomons G, Lewis C, Anderson JG. 1995. The role of mycotoxins in human and animal nutrition and health. Nat Tox 3:18792. Speijers GJ, Franken MA, van Leeuwen FX. 1988. Subacute toxicity study of patulin in the rat: effects on the kidney and the gastro-intestinal tract. Food Chem Toxicol 26:2330. Srinivasan U, Bala A, Jao S-C, Starke DW, Jordan TW, Mieyal JJ. 2006. Selective inactivation of glutaredoxin by sporidesmin and other epidithiopiperazinediones. Biochem 45:897887. Staron T, Thirouin D, Perrin L, Frere G. 1980. Microwave treatment of biological food production. Industrie Alimentari Agricole 12:130512. Stefanaki I, Foufa E, Tsatsou-Dritsa A, Dais P. 2003. Ochratoxin A concentrations in Greek domestic wines and dried vine fruits. Food Addit Contam 20:7483. Stoloff L, van Egmond HP, Park DL. 1991. Rationales for the establishment of limits and regulations for mycotoxins. Food Addit Contam 8:21322. Stoltz DR, Widiastuti R, Maryam R, Akoso BT, Amang UD. 1988. Suspected cyclopiazonic acid mycotoxicosis of quail in Indonesia. Toxicon 26:3940. Stroka J, Anklam E. 2000. Development of a simplied densitometer for the determination of aatoxins by thin-layer chromatography. J Chromatogr A 904:2638. Stroka J, Anklam E. 2002. New strategies for the screening and determination of aatoxins and the detection of aatoxin-producing molds in food and feed. Trends Anal Chem 21:905. Studer-Rohr I, Schlatter J, Dietrich DR. 2000. Kinetic parameters and intraindividual uctuations of ochratoxin A plasma levels in humans. Arch Toxicol 74:499510. Sugiyama K, Hiraoka H, Sugita-Konishi Y.2008. Aatoxin M1 contamination in raw bulk milk and the presence of aatoxin B1 in corn supplied to dairy cattle in Japan. Shokuhin Eiseigaku Zasshi 49:3525. Sun XM, Zhang XH, Wang HY, Cao WJ, Yan X, Zuo LF, Wang JL, Wang FR. 2002. Effects of sterigmatocystin, deoxynivalenol and aatoxin G1 on apoptosis of human peripheral blood lymphocytes in vitro. Biomed Environ Sci 15:14552. Sydenham EW, Shephard GS, Thiel PG, Marasas WFO, Stockenstrom S. 1991. Fumonisin contamination of commercial corn-based human foodstuffs. J Agric Food Chem 39:20148. S, Shephard GS, Thiel PG. 1994. Sydenham EW, Van Der Westhuizen L, Stockenstrom Fumonisin-contaminated maize: physical treatment for the partial decontamination of bulk shipments. Food Addit Contam 11:2532. Sypecka Z, Kelly M, Breteton P. 2004. Deoxynivalenol and zearalenone residues in eggs of laying hens fed with a naturally contaminated diet: effects on egg production and estimation of transmission rates from feed to eggs. J Agric Food Chem 52: 546371. Tabata S, Iida K, Kimura K, Iwasaki Y, Nakazato M, Kamata K, Hirokado M. 2008. Simultaneous determination of ochratoxin A, B and citrinin in foods by HPLC-FL and LC/MS/MS. J Food Hyg Soc Japan 49:1005.
80

Takino M, Tanaka, T, Yamaguchi K, Nakahara T. 2004. Atmospheric pressure photo-ionization liquid chromatography/mass spectrometric determination of aatoxins in food. Food Addit Contam 21:7684. Tanaka, T, Hasegawa, A, Yamamoto, S, Lee, US, Sugiura, Y, Ueno, Y. 1988. Worldwide contamination of cereals by the Fusarium mycotoxins, nivalenol, deoxynivalenol, and zearalenone, Survey of 19 countries. J Agric Food Chem 36:97983. Tan Y, Chu X, Shen G-L, Yu R-Q. 2009. A signal-amplied electrochemical immunosensor for aatoxin B1 determination in rice. Anal Biochem 387:826. Tangnia EK, Waegeneersa N, Overmeireb IV, Goeyensb L, Pussemier L. 2008. Mycotoxin analyses in some home-produced eggs in Belgium reveal small contribution to the total daily intake. Sci Total Environ 407:44118. Tashiro F. 2000. Mode of action of zearalenone, an estrogenic mycotoxin. J Japanese Assoc Mycotoxicol 50:10510. Temcharoen P, Thilly WG. 1982. Removal of aatoxin B1 toxicity but not mutagenicity by 1 megarad gamma irradiation of peanut meal. J Food Saft 4:199205. Thrane U, Adler A, Clasen P-E, Galvano F, Langseth W, Lew H, Logrieco A, Nielsen KF, Ritieni A. 2004. Diversity in metabolite production by Fusarium langsethiae, Fusarium poae and Fusarium sporotichioides. Int J Food Microbiol 95:25766. Trail F, Mahanti N, Linz J. 1995. Molecular biology of aatoxin biosynthesis. Microbiology 141:75565. Tripathi S, Mishra HN. 2009. A rapid FT-NIR method for estimation of aatoxin B 1 in red chili powder. Food Cont 20:8406. Ueno Y. 1971. Toxicological and biological properties of fusarenon-X, a cytotoxic mycotoxin of Fusarium nivelae Fn-2B. In: Purchase IFH, editor. Proc Symp Mycotoxins Hum Health 24 Sep 1970, Pretoria, South Africa. London: MacMillan. p 16378. Ueno Y. 1991. Biochemical mode of action of mycotoxins. In: Smith JE, Henderson RS, editors. Mycotoxins and animal foods. London: CRC Press Inc. p 43755. Uhlig S, Jestoi M, Parikka P. 2007. Fusarium avenaceum: the North European situation. Int J Food Microbiol 119:1724. Urano J, Trucksess M W, Beaver RW, Wilson DM, Dorner JW, Dowell F E. 1992. Cooccurrence of cyclopiazonic acid and aatoxin in corn and peanuts. J AOAC Int 75:838 41. Valenta H, Danicke S. 2005. Study on the transmission of deoxynivalenol and de-epoxydeoxynivalenol into eggs of laying hens using a hi-performance liquid chromatography ultraviolet method with clean-up by immunoafnity. Mol Nutr Food Res 49:77985. Valero A, Begum M, Leong SL, Hocking AD, Ramos AJ, Sanchis V, Mar n S. 2007. Effect of germicidal UVC light on fungi isolated from grapes and raisins. Lett Appl Microbiol 45:23843. Van Der Gaag B, Spath S, Dietrich H, Stigter E, Boonzaaijer G, van Osenbruggen T, Koopal K. 2003. Biosensors and multiple mycotoxin analysis. Food Cont 14:2514. Van Der Stegen GHD, Essens PJM, Van Der Lijn J. 2001. Effect of roasting conditions on reduction of ochratoxin A in coffee. J Agric Food Chem 49:47135. Van Der Westhuizen L, Shephard GS, Scussel VM, Costa LL, Vismer HF, Rheeder JP, Marasas WF. 2003. Fumonisin contamination and Fusarium incidence in corn from Santa Catarina, Brazil. J Agric Food Chem 51:55748. Van Dongen PWJ, De Groot ANJA. 1995. History of ergot alkaloids from ergotism to ergometrine. Eur J Obst Gyn Rep Biol 60:10916. van Egmond HP. 1989. Current situation on regulations for mycotoxins: overview of tolerances and status of standard methods of sampling and analysis. Food Addit Contam 6:13988. van Egmond HP. 1995. Mycotoxins: regulations, quality assurance and reference materials. Food Addit Contam 12:32130. van Egmond HP, Jonker MA. 2004. Worldwide regulations for mycotoxins in food and feed. Draft FAO Food and Nutrition Paper. Bilthoven, The Netherlands: National Institute for Public Health & the Environment. van Egmond HP, Schothorst RC, Jonker MA. 2007. Regulations relating to mycotoxins in food. Perspectives in a global and European context. Anal Bioanal Chem 389:14757. van Rensburg S, Altenkirk B. 1974. Claviceps purpurea. Ergotism. In: Purchase I, editor. Mycotoxins. Amsterdam, The Netherlands: Elsevier. p 6996. Varga E, Kevei E, Rinyu E, T eren J, Kozakiewicz Z. 1996. Ochratoxin production by Aspergillus species. Appl Environ Microbiol 62:44614. Varga J, Kozakiewicz Z. 2006. Ochratoxin A in grapes and grape-derived products. Trends Food Sci Technol 17:7281. Vatinno R, Aresta A, Zambonin CG, Palmisano F.2008. Determination of ochratoxin A in green coffee beans by solid-phase microextraction and liquid chromatography with uorescence detection. J Chrom A 1187:14550. Vecchio A, Finoli C. 2007. Ochratoxin A occurrence in cocoa products. Ind Aliment 46:1015 23. Viquez OM, Castell Perez ME, Shelby RA, Brown G. 1994. Aatoxin contamination in corn samples due to environmental conditions, aatoxin producing strains, and nutrients in grain grown in Costa Rica. J Agric Food Chem 42:25515. Vinas I, Dadon J, Sanchis V. 1993. Citrinin production capacity of Penicillium expansum strains from apple packaging houses of Lerida (Spain). Int J Food Microbiol 19:1536. o Vukeli c M, S stari c B, Belicza M. 1992. Pathomorphology of Balkan endemic nephropathy. Food Chem Toxicol 30:193200. Wang E, Norred WP, Bacon CW, Riley RT, Merill AH Jr. 1991. Inhibition of sphingolipid biosynthesis by fumonisins. J Biol Chem 266:1448690. Wang ZG, Feng JN, Tong Z. 1993. Human toxicosis caused by mouldy rice contaminated by Fusarium and T-2 toxin. Biomed Environ Sci 6:6570. Warden BA, Allam K, Sentissi A, Cecchini DJ, Giese RW. 1987. Repetitive hit-and-run uoroimmunoassay for T-2 toxin. Anal Biochem 162:3639. Warden BA, Sentissi A, Ehrat M, Cecchini DJ, Allam K, Giese RW. 1990. Chromatographic enzyme immunoassay for T-2 toxin. J Immunol Meth 131:7782. Weiss R, Freudenschuss M, Kriska R, Mizaikoff B. 2003. Improving methods of analysis for mycotoxins: molecularly imprinted polymers for deoxynivalenol and zearalenone. Food Addit Contam 20:38695. Wellford TE, Eadie TT, Llewellyn GC. 1978. Evaluating the inhibitory action of honey on fungal growth, sporulation and aatoxin production. Z Lebensm Unters Forsch 166:2803. Whittaker TB, Dickens JW, Giesbrecht FG. 1991. Testing animal feedstuffs for mycotoxins: sampling, subsampling, and analysis. In: Smith JE, Henderson RS, editors. Mycotoxins and animal foods. Boca Raton, Fla.: CRC Press. p 15364. [WHO] World Health Organization. 1978. Selected mycotoxins: ochratoxins, trichothecenes, ergot. Environmental health criteria 105. Geneva, Switzerland: WHO. p 136. [WHO] World Health Organization. 2001. Ochratoxin A. In: Safety evaluation of certain mycotoxins in food, international program on chemical safety, WHO food additives. Series 47. Geneva: World health Organization. p 281415. [WHO] World Health Organization. 2002. Evaluation of certain mycotoxins in food. WHO Technical Report Series 906:1,1144. Wichmann G, Herbarth O, Lehmann I. 2002. The mycotoxins citrinin, gliotoxin, and patulin affect interferon-gamma rather than interleukin-4 production in human blood cells. Environ Toxicol 17:2118. Wicklow DT, Hesseltine CW, Shotwell OL, Adams GL. 1980. Interference competition and aatoxin levels in corn. Phytopathology 70:7614. Wicklow DT, Dowd PF, Gloer JB. 1994. Antiinsectant effects of Aspergillus metabolites. In: Powell KA, Renwick A, Perberdy JF, editors. The genus Aspergillus. NewYork: Plenum Press. p 93114. Williams JH, Phillips TD, Jollym PE, Stiles JK, Jolly CM, Aggarwal D. 2004. Human aatoxicosis in developing countries: a review of toxicology, exposure, potential health consequences, and interventions. Am J Clinic Nutr 80:110622. Williamson ML, Atha DH, Reeder DL, Sundaram PV. 1989. Anti-T 2 monoclonal antibody immobilization on quartz bers: Kinetics of inactivation and recognition of T-2 mycotoxin. Anal Lett 22:80316. Willis RM, Mulvihill JJ, Hoofnagle JH. 1980. Attempted suicide with puried aatoxins. Lancet 11989. Wilson TM, Ross PF, Nelson PE. 1991. Fumonisin mycotoxins and equine leukoencephalomalacia. J Am Vet Med Assoc 198:11045. Withlow LM, Hagler WM Jr. 1999. Managing mycotoxin impact: An association of mycotoxins with production, health and reproduction in dairy cattle and guidelines for prevention and treatment. In: Lyons TP, Jacques KA. Proc Alltechs 15th Annual Symp. Nottingham, U.K.: Nottingham Univ. Press. p 38199. Wolzak A, Pearson AM, Coleman TH, Pestka JJ, Gray JI. 1985. Aatoxin deposition and clearance in the eggs of laying hens. Food Chem Toxicol 23:105761. Wood GM. 1982. Effects of processing on mycotoxin in maize. Chem Ind 24:9724. Wood GE. 1992. Mycotoxins in foods and feeds in the United States. J Anim Sci 70:39419. Wouters MFA, Speijers GJA. 1996. Toxicological evaluations of certain food additives and contaminants in food: Patulin. WHO Food Additive Series 35:377402. Wu F. 2006. Mycotoxin reduction in Bt corn: potential economic, health, and regulatory impacts. Transgenic Res 15:27789. Wu T-S, Liao Y-C, Yu F-Y, Chang C-H, Liu B-H. 2008. Mechanism of patulin-induced apoptosis in human leukemia cells (HL-60). Toxicol Lett 183:10511. Yang H-H, Aulerich RJ, Helferich W, Yamini B, Chou KC, Miller ER, Bursian SJ. 1995. Effects of zearalenone and/or tamoxifen on swine and mink reproduction. J Appl Toxicol 15:22332. Yiannikouris A, Jonany J. 2002. Mycotoxins in feeds and their fate in animals: a review. Anim Res 51:819. Yoon Y, Baeck YJ. 1999. Aatoxin binding and antimutagenic activities of Bidobacterium bidum HY strains and their genotypes. Korean J Dairy Sci 21:2918. Young JC, Trenholm HL, Friend DW, Prelusky DB. 1987. Detoxication of deoxynivalenol with sodium bisulte and evaluation of the effects when pure mycotoxin or contaminated corn was treated and given to pigs. J Agric Food Chem 35:25961. Young JC, Zhou T, Yu H, Zhu H, Gong J. 2007. Degradation of trichothecene mycotoxins by chicken intestinal microbes. Food Chem Toxicol 45:13643. Yousef AE, Marth EH. 1985. Degradation of aatoxin M1 in milk by ultraviolet energy. J Food Prot 48:6978. Yoshizawa T. 1983. Red-mold diseases and natural occurrence in Japan. In: Ueno Y, editor. Trichothecenes - Chemical, biological, and toxicological aspects. New York: Elsevier Publishers. p 195209. Yu FY, Liao YC, Chang CH, Liu BH. 2006. Citrinin induces apoptosis in HL-60 cells via activation of the mitochondrial pathway. Toxicol Lett 161:14351. Yumbe-Guevara BE, Imoto T, Yoshizawa T. 2003. Effects of heating procedures on deoxynivalenol, nivalenol and zearalenone levels in naturally contaminated barley and wheat. Food Addit Contam 20:113240. Zambonin CG, Monaci L, Aresta A. 2002. Solid-phase microextraction high-performance liquid chromatography and diode array detection for the determination of mycophenolic acid in cheese. Food Chem 78:24954. Zhang X, Boesch-Saadatmandi C, Lou Y, Wolffram S, Huebbe P, Rimbach G. 2009a. Ochratoxin A induces apoptosis in neuronal cells. Genes Nutr 4:418. Zhang X, Cudjoe E, Vuckovic D, Pawliszyn J. 2009b. Direct monitoring of ochratoxin A in cheese with solid-phase micro-extraction coupled to liquid chromatography-tandem mass spectrometry. J Chrom A 1216:75059. Zhou HR, Harkema JR, Hotchkiss JA, Yan D, Roth RA, Pestka JJ. 2000. Lipopolysaccharide and the trichothecene vomitoxin (deoxynivalenol) synergistically induce apoptosis in murine lymphoid organs. Toxicol Sci 53:25363. Zimmerli B, Dick R. 1995. Determination of ochratoxin A at the ppt level in human blood, serum, milk and some foodstuffs by high-performance liquid chromatography with enhanced uorescence detection and immunoafnity column cleanup: methodology and Swiss data. J Chrom B Biomed Sci Appl 666:8599. Zimmerli B, Dick R. 1996. Ochratoxin A in table wine and grape-juice occurrence and risk assessment. Food Addit Contam 13:65568. J. 2009. Pressurized liquid Zinedine A, Blesa J, Mahnine N, El Abidi A, Montesano D, Manes extraction coupled to liquid chromatography for the analysis of ochratoxin A in breakfast and infant cereals from Morocco. Food Cont 21:1325. Zollner P, Jodlbauer J, Kleinova M, Kahlbacher H, Kuhn T, Hochsteiner W, Lindner W. 2002. Concentration levels of zearalenone and its metabolites in urine, muscle tissue, and liver samples of pigs fed with mycotoxin-contaminated oats. J Agric Food Chem 50:2494 501. Zur G, Shimoni E, Hallerman E, Kashi Y. 2002. Detection of Alternaria fungal contamination in cereal grains by a polymerase chain reaction-based assay. J Food Prot 65:143340.
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Mycotoxins in Food and Feed: Present Status and Future Concerns

Rajeev Bhat, Ravishankar V. Rai, and A.A. Karim

2010 Institute of Food Technologists R

Vol. 9, 2010COMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETY

CRFSFS: Comprehensive Reviews in Food Science and Food Safety

Fungi, Conditions Promoting Their Growth, and Production of Mycotoxins

COMPREHENSIVE REVIEWS IN FOOD SCIENCE AND FOOD SAFETYVol. 9, 2010