BIOCHEMISTRY ANS KEY

1.Ans. (d) All

[Ref: Lehninger 5th /e p591]
 In Diabetes Mellitus, the activity of catabolic enzymes is increased.
Carnitine Palmitoyl Transferase-I (CPT-I) is an enzyme of β-Oxidation which is a catabolic pathway. Therefore, is increased in
diabetes
 Phosphoenol Pyruvate Carboxykinase and Glucose -6-Phosphatase are enzymes of gluconeogenesis, which is a
catabolic pathway and hence also increased in Diabetes.
 Only one arabolic mechanism increased in diabetes is TG and VLDL synthesis, which is due to excess Acetyl CoA from
b-oxidation.

2.Ans .(a) 2 kilocalories

Explanation :Soluble fibers are fermented by bacteria producing short chain fatty acids which are actively absorbed
from the large intestine & provides 2-3 kcal energy per gram. Insoluble fibers do not provide energy.

Energy obtained per gram of macromolecules is as

follows:
 Dietary fibers: 2 kcal/gm
 Carbohydrates: 4 kcal/gm
 Proteins: 4.2 kcal/gm
 Fats: 9 kcal/g
 Alcohol: 7 kcal/gm (empty calories)

3.Ans. (b) ATP Citrate Lyase

[Ref: Harper 30th/e pg. 197]
• NADPH is synthesized by HMP (G-6PD), Malic enzyme & cytoplasmic Isocitrate Dehydrogenase.
• NADPH is used in reductive biosynthesis (anabolic pathways) .

4Ans. (a) Glucose

[Ref: Lippincott’s Illustrated Reviews 4th/e pg. 366]

 Glycemic Index (GI)- This is the increase in blood glucose after the test dose of a carbohydrate compared with that of
an equivalent amount of glucose. GI is a value assigned to foods based on how slowly or how quickly those foods cause an
increase in blood glucose levels.
 The highest glycemic index is for glucose and galactose (also lactose, maltose, trehalose and isomaltose get converted to
glucose, so they also have high GI).
 GI of fructose is less than that of glucose.
 Fructose and sugar alcohols have less glycemic index because they are not absorbed completely.
 Sucrose also has low glycemic index than glucose as it gets split to glucose and fructose.

5Ans. (d) Glycogen Storage

[Ref: Harper 30th/e pg. 176]

Low insulin means catabolic situation in body. So, question is that which of the following is not seen in catabolic state.
So, answer is Glycogen Storage, which is anabolic. Rest three pathways given are catabolic – Gluconeogenesis, Glycogen
Breakdown and Ketogenesis.

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6Ans. (a) Glycolysis

[Ref: Harper 30th/e pg. 168]

Glycolysis occurs in cytoplasm
The biochemical processes taking place in mitochondria are all catabolic pathways, Vital pathways i.e. TCA and ETC, Replication, Transcription
and Translation for mitochondrial DNA and apoptosis

7Ans. (a) Ketone bodies

[Ref: Lippincott 4th/e pg.327]

Glucose is the main/preferred fuel for the brain in fed as well as fasting state whereas during starvation, brain depends upon
Ketone Bodies as the fuel.

8Ans. (b) Glucokinase

[Ref: Harper 30th/e pg. 192]

Post prandial utilization of glucose i.e. in fed state. It is done by Glucokinase enzyme, which is active in fed state. Glucokinase
has high km for glucose i.e. more amount of glucose is required for this enzyme to work and more glucose is present during fed
state. Glucokinase is activated by insulin. Hexokinase has low Km and feedback inhibition from substrate glucose -6-
phosphate.

9.Ans. (b) 2 ATP

[Ref: Harper 30th/e pg. 169, figure 17-1]

In the end of anaerobic glycolysis, 2 ATP and 2 NAD are obtained. Gain is only of 2 ATP as 2 NAD is used also
(Glyceraldehyde-3-phosphate Dehydrogenase step) and 2 NAD produced also (LDH step). So, net gain of NAD is zero

10. Ans. c. Ito cells [Ref: Harper 30th/e pg. 545]

HSCs (Hepatic Stellate Cells) (also called vitamin A-storing cells, lipocytes, interstitial cells, fat-storing
cells or Ito cells, perisinusoidal cells) are pericytes which exist in the space between parenchymal cells
and liver sinusoidal endothelial cells of the hepatic lobule and store 50-80% of vitamin A in the whole
body as retinyl palmitate.

11.Ans. (c) Thiamine

[Ref: Harper 30th/e pg. 174]

Congenital lactic acidosis may occur due to defect in thiamine which is required for pyruvate dehydrogenase which converts
pyruvate to acetyl CoA. If this reaction is defective then pyruvate accumulates and leads to the formation of lactate. This leads
to lactic acidosis. Also this enzyme requires vitamins B1 , B2 , B3 , B5 and Lipoic acid. Option (a) is vitamin B7- Biotin.
Option (b) is PLP- vitamin B6. Option (d) is Pyruvate which is coming from food (carbohydrates).

12.Ans. (a) ATP

• Thiokinase of TCA produces ATP most of the times. But in liver and kidney, during starvation it produces GTP, for PEPCK
enzyme of gluconeogenesis. So, best answer here is ATP.

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13.Ans. (c) Mitochondria

[Ref: Harper 30th/e pg. 119]

• Complete oxidation of glucose to CO2 and H2O occurs in mitochondria, when TCA and ETC takes place.

14.Ans. (d) NAD+/NADH

Ref: Harper 30th/e pg. 120, table 12-1]

• NADH has minimum redox potential

• Oxygen has maximum R.P

15.Ans. (c) After going in brain in ETC, it gives high energy

[Ref: Harper 30th/e pg. 134]

• There are two shuttles for transport of NADH from cytoplasm to mitochondria. In brain, Glycerol-P shuttle is present which
gives 1.5 ATPs. This shuttle is a shorter shuttle, so, it is a quick source of ATP.

16.Ans. (b) Inhibitor of oxidative phosphorylation

[Ref: Harper 30th/e pg. 132]

• Atractyloside is inhibitor of ADP-ATP translocase, which transfers ADP and ATP across the inner mitochondrial membrane.
So, it is inhibitor of oxidative phosphorylation i.e. ETC.

17.Ans. C

18.Ans. (a) Mitochondria → Cytoplasm → ER

[Ref: Harper 30th/e pg. 171]

First step of gluconeogenesis (Pyruvate to oxaloacetate) occurs in mitochondria, then next many steps occur in cytoplasm and
the last step (glucose-6-Phosphatase) occurs in endoplasmic reticulum (ER).

19Ans. (c) Acetoacetate

Ref: Harper 30th/e pg. 171]

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 BIOCHEMISTRY ANS KEY

• Glucose can be synthesized from amino acids. Most glucogenic amino acid is Alanine.

• From Glycerol, glucose can be formed. • Lactic acid can form pyruvate by LDH, which further forms glucose.

• Ketone bodies, fats, or acetyl CoA can never be converted into carbohydrates. Acetoacetate is a ketone body.

20.Ans. (b) PLP (Pyridoxal phosphate)

[Ref: Harper 30th/e pg. 178]

• Rate limiting enzyme of glycogenolysis is glycogen Phosphorylase which requires PLP i.e. vitamin B6. This vitamin is
required as donor of phosphate as Glycogen phosphorylase transfers phosphate to glucose, releasing glucose-1-phosphate.

21.Ans. (a) Increased alanine levels in liver

[Ref: Harper 30th/e pg. 171]
• During fasting/ starvation, pyruvate in muscles gets converted to alanine, which enters liver and forms glucose via
gluconeogenesis

22.Ans. (a) Glucose-6-Phosphatase

[Ref: Lehninger 7th/e pg. 604]
This is because muscles lack the enzyme Glucose-6-Phosphatase. Liver cells have this enzyme and therefore liver can only
maintain blood glucose.

23.Ans. (b) 18

[Ref: Harper 30th/e pg. 149]

• Glycogen reserves can be used for 12-18 hours.

24.Ans. (d) Phosphorylase enzyme

• This is McArdle’s disease and the enzyme deficient is muscle phosphorylase. If GSD affects muscles, then patient presents
with muscle cramps and exercise intolerance because function of muscle glycogen is muscle contraction.

25.Ans. (c) Xylulose Reductase

[Ref: Harper 30th/e pg. 202]

Essential pentosuria occurs due to deficiency of enzyme Xylulose Reductase.

26. Ans. (a) Aldose Reductase

[Ref: Harper 30th/e pg. 202]

Glucose is reduced by Aldose Reductase enzyme to produce sorbitol/ polyol, which is responsible for snow flake cataract in a
diabetic patient.

27.Ans. (a) DHA

[Ref : Harper 30th /e pg. 214]

• Not all, but many studies have found that patients with Retinitis Pigmentosa tend to have lower blood levels of DHA (Docosa
Hexaenoic Acid), an omega -3 fatty acid found in the photoreceptor cells.

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28.Ans. (b) Linoleic acid

[Ref: Harper 30th/e pg. 214]
• Omega-6 fatty acids are gamma linolenic acid, linoleic acid and arachidonic acid.

29.Ans. (b) Triglycerides

[Ref: Harper 30th/e pg. 628]
• Triglycerides >> cholesterol
• Wolman's disease, also known as lysosomal Acid Lipase deficiency, is a rare autosomal recessive disease.
Triglycerides and cholesterol esters gets accumulated. They are accumulated in organs like liver, spleen, gut and
blood vessels.

30.Ans. (b) Oleic acid

[Ref: Harper 30th/e pg. 214]

• Oleic acid is a mono-unsaturated or monoenoic fatty acid i.e. 18 Carbons with one double bond at ω-9 position (ω-numbering
starts from methyl end of fatty acid)

31.Ans. (a) Phospholipids and sphingolipids

[Ref: Harper 30th/e pg. 250]

• Multiple sclerosis is a demyelinating disease in which there is loss of phospholipids and sphingolipids from white matter. So
lipid composition of white matter resembles that of gray matter. CSF shows raised phospholipid levels.

32.Ans. (a) Krabbe's – Galactosyl Ceramidase

[Ref: Harper 30th /e pg. 179]
• Krabbe’s Disease is caused due to defect in Galactosyl Ceramidase/ β- Galactosidase
• Gaucher’s Disease is caused due to defect in β-Glucosidase or β-Glucocerebrosidase.
• Farber’s Disease is caused due to defect in Ceraminidase.
• Sandhoff’s Disease is caused due to defect in Hexosaminidase A and B

33.Ans. (c) Chylomicrons

[Ref: Harper 30th/e pg. 263]

• Chylomicrons transport dietary or exogenous lipids or TGs from intestine to peripheral tissue.

34.Ans. (A) HDL

HDL has maximum density, that’s why the name, High Density Lipoproteins.
Chylomicrons have least density.

35.Ans.(A) 220
[Ref: Harper 30th/e pg. 249]
Friedwald’s equation:
Total cholesterol = HDL+LDL+VLDL
= HDL+ LDL+ TG/5
(we do not measure VLDL, we measure TG)
LDL= Total cholesterol –HDL-TG/5 (mg/dl)

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LDL= Total cholesterol – HDL – TG/2.2 (mmol/L)

LDL chol = total chol – HDL chol – TG/5
= 300 – 40 – 200/5
= 300 – 40 – 40
= 220
36.Ans.(a) Phytanic acid oxidase
[Ref: Harper 30th/e pg. 231]
 Refsum disease is a rare, autosomal recessive, neuro-logical disorder. It is a phytanic acid storage disease due to
deficiency of enzyme phytanic acid oxidase.
 Phytanic acid is found in meat, beef, ruminant fat and dairy products. Phytanic acid is thought to have effects on
membrane function, protein prenylation and gene expression.
 Clinical features include night blindness, retinitis pigmentosa, deafness, dry scaly skin, shortened fingers or toes,
anosmia and ataxia.

37.Ans. (d) Peroxisomes

[Ref: Harper 30th /e p 237]

Zellweger syndrome was earlier named Cerebro- Hepato- Renal syndrome.
It is a Peroxisome Biogenesis Disorder (PBD), which is very rare
Most severe PBD is Zellweger syndrome in which there is absence of peroxisomes in all tissues. So there is defect in
oxidation of very long chain fatty acids & also defect in alpha oxidation as both these pathways occur in peroxisomes.

38.Ans. (d) Karyotyping

[Ref: Ghai 8th/e/ ch 22, Nelson 20th/e/p 622]
In Klinefelter’s syndrome, there are two or more X-chromosome in a male. It is a trisomy (aneuploidy), which is best
detected by karyotyping.

39.Ans. (a) Agarose gel [Ref: Wilson & Walker 7th/e pg 419-421]
 Separation of RNA is done by Agarose gel electro-phoresis, which is used in Northern blotting, checking RNA integrity
and size selection of RNA cloning experiments.
 Agarose gel is usually used for Nucleic Acid separation and it separate large molecules.
 Whereas Polyacrylamide gel is used for DNA or Protein separation and it seperates small molecules.
40.ans. (d) All
This is reciprocal regulation of β-oxidation of Fatty acid and Fatty acid synthesis. Activated Fatty acid needs to be transported from
Cytoplasm to Mitochondria for β- oxidation by CPT-I: In fed state, Malonate (3 C) from Fatty acid synthesis inhibits CPT-I.

41.Ans. (b) HMG CoA Synthase

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[Ref: Lippincott 4th/e pg. 197]

Enzyme common to cholesterol synthesis and ketone body synthesis is HMG CoA Synthase and Thiolase. Best option here to
be marked is HMG CoA Synthase.

42.Ans. a. Acetyl CoA

[Ref: Harper 30th/e pg. 225]
Fatty acid is entirely synthesized from the carbons of Acetyl CoA. Malonyl CoA is used during fatty acid synthesis but all the carbons are
derived from Acetyl CoA. The extra carbon of malonyl is lost during condensation step of fatty acid synthase complex.

43.Ans. b. Allantion
[Ref: Harper 30th/e pg. 353]
End product of purine catabolism in non-primates mammals is Allantoin. But in primates it is uric acid.

44.Ans. d. PRPP Glutamyl Amido-Transferase

[Ref: Harper 30th/e pg. 348]
Rate limiting enzyme of purine nucleotide synthesis is PRPP GlutamylAmido-Transferase I. It catalyzes the conversion of PRPP to
PhosphoRibosyl Amine (PRA).Rate limiting enzyme of purine nucleotide catabolism is xanthine oxidase.

45.Ans. a. Allopurinol
[Ref: Harper 30th /e pg 355]
Allopurinol, a structural analogue of hypoxanthine, competitively inhibits Xanthine Oxidase activity. Xanthine Oxidase converts
Allopurinol to Oxypurinol, which inhibits Xanthine Oxidase. So this is suicidal inhibition. Allopurinol is used for the treatment of gout and
hyperuricemia.

46.Ans. (a) 1
[Ref: Robbins 9th/e pg. 165]
Number of barr bodies is always one less the total number of X-chromosomes. Barr body is the inactive X-
chromosome in a female somatic cell. If two X-chromosomes present, then number of Barr bodies present is 1.
47.Ans. a. 50% affected
[Ref: Robbin’s 8th/e pg. 141]
Mostly AD diseases have heterozygous trait.

48.Ans. c. Circular, double stranded

[Ref: Harper 30th/e pg. 378]
Eukaryotic DNA is linear, double stranded. Prokaryotic DNA is circular, double stranded.
Mitochondrial DNA is present in eukaryotes, but it resembles prokaryotic DNA i.e. it is circular, double stranded.

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49.Ans. c. Insertion
[Ref: Robbins 9th/pg 160; 8th/pg 160]
Frameshift mutation can occur due to insertion or deletion of nucleotides in numbers which are not in multiple of 3, so these mutations
alter genetic reading frame.
50.Ans. d. Huntington’s disease
[Ref: Internet]
Gain of function mutation means there is overactivity of gene. E.g. Huntington’s disease leads to formation of excessive Huntington
protein, which is toxic for neurons.
Loss of function mutation leads to underactivity of genes.

51.Ans. a. 18%
[Ref: Lehniniger 7th/e p286]
According to chargaff’s rule in a ds DNA, the total purine content is equal to the pyrimidine content.

Since [A] =[T], so [T] = 32%

[A]+[T] = 32 = 32 = 64%

[C]+[G] = 100–([A]+[T])= 100–64% =36%

As [C] = [G], so [G] = 36/2 = 18%

52.Ans. d. Frameshift> Nonsense > Missense

[Ref: Harper 30th/e pg. 417]
Frameshift mutation is deletion or insertion of a number of nucleotides not divisible by 3, resulting in misleading of all nucleotides
downstream.
Nonsense mutation means change of a codon with a stop codon (UAA, UAG, UGA). This leads to premature termination of Protein
synthesis.
Missense mutation means a codon is replaced by another codon, coding for a different amino acid.
53.Ans. a. Praderwilli syndrome
[Ref: Robbin’s 8th/e pg. 172-173]
Disease caused due to Genomic Imprinting arePrader Willi Syndrome and Angelman Syndrome.

54.Ans. c. 5’ → 3’ exonuclease
[Ref: Lehninger principles of biochemistry, 7th ed., Pg 994 and Lippincott’s illustrated reviews 6th ed., Pg 74-75]
Klenow fragment is a large fragment produced by Subtilisin mediated proteolytic cleavage of E.Coli DNA polymerase I. Proteolysis
removes the 5’ → 3’ exonuclease activity from N-terminal.

55.Ans. c. CCA at 3’end

[Ref: Harper 30th/e pg. 409, 416]
The specific CCA sequence is present at the 3’ end of tRNA which is also known as the Acceptor Arm. This CCA sequence acts as an
acceptor of the amino acids on the tRNA molecule.(Option c)
Poly A tail at the 3’end (Option a) and 7-methyl Guanosine cap at the 5’ end (Option b) are the characteristics of post transcriptional
modifications of mRNA
Option d has been added to confuse as CCA sequence is always present at the 3’end of t RNA.
56.Ans. b. DNA from RNA template
[Ref: Harper 30th/e pg. 364]
Reverse transcriptase is synthesis of DNA using RNA as template.

57.Ans. d. Hydroxyproline

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[Ref: Harper 30th/e pg. 60]

Aminoacyl tRNA is required for all twenty amino acids but Hydroxyproline is a derived amino acid. Aminoacyl tRNA is not required for any
derived amino aci

58.Ans. (d) Degenerate

[Ref: Harper 30th/e pg. 416]
Silent mutations occurs because codon is degenerate. Degeneracy or Redundancy is a property of codons that each
amino acid is having more than one codons.
Silent mutations means a codon is replaced by another codon, which is coding for same amino acid.

59.Ans. (a) Study of multiple genes

[Ref: Robbins 9th/e pg. 174, 175]
Microarray or chip can detect multiple mutations and multiple gene expression analysis simultaneously. Thousands of
oligonucleotide probes, corresponding to human genes are taken on a solid surface (gene chip), allowing detection of multiple
mutations at a single go or multiple patient samples to be assessed for a single molecular marker in one experiment.

60.Ans. b. RT PCR
[Ref: Harper 30th/e pg. 29, 457]
RT PCR is Reverse Transcriptase PCR, where starting material is RNA. It is used to make cDNA, which is amplified. Thus RNA can be
amplified by this method and quantification of mRNA can also be done.
Western blot is to detect protein.
Next generation sequencing & Sanger’s technique are for DNA sequencing.
61.Ans. c. Denature DNA, Anneal Primers, Extend DNA
[Ref: Harper 30th/e pg. 454]
Three steps involved in PCR are Denaturation at 94°C (separation of DNA strands), then Annealing at 60°C (primer added and they get
attached to template sequence) and then Extension at 72°C (polymerization or synthesis) occurs finally. These three steps are repeated again and
again to synthesize large amount of DNA.

62.Ans. b. FRAP
[Ref: Harper 30th/e pg. 456]
FRAP is Fluorescent Recovery After Photo bleaching. This technique is used to detect movement of proteins from one compartment of cell
to another and lateral diffusion of lipids and proteins in the membrane.

63.Ans. d) Method of choice for screening is urinary phenyl alanine by Guthrie’s test
[Ref: Harper 30th/e pg. 304]
Guthrie’s test (was the first method used to detect PKU) is replaced by tandem mass spectrometry
Guthrie test detects serum phenyl alanine levels (not urinary)
FeCl3 detects phenyl alanine levels in urine.
64.Ans. c. Leucine
[Ref: Harper 30th/e pg. 269]
In Cystinuria, there is a mutation in gene which is responsible for the reabsorption of basic amino acids & cysteine from kidneys. So amino
acids found in high concentration in urine are cystine, ornithine, arginine and lysine. High cysteine in blood will lead to the formation of cystine in
urine (made up of two cysteines).

65.Ans. a. Valine
[Ref: Harper’s 30thed pg. 289, 291]
After a protein rich meal, splanchnic tissues release branched chain amino acids (Valine, Leucine and Isoleucine) and they are mainly
extracted by peripheral tissues like skeletal muscles.
These branched chain amino acids provide energy to brain during fasting state.

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Therefore, branched chain amino acids have a special role in nitrogen metabolism.

66.Ans. a. Tryptophan
[Ref: Harper 30th/e pg 308]
Tryptophan is responsible for the formation of melatonin, which regulates the sleep-wake cycle.
Chemically melatonin is acetyl methyl serotonin.
67.Ans. b. SLC6A 19 [Ref: Harper 30th/e pg. 308, 557]
Hartnup’s disease is due to defect in transport of nuetral amino acid transporter. This transporter is a protein
encoded by gene SLC6A19 (located on chromosome 5). There is mutation in this gene in Hartnup's disease.

68. Ans. c. Serine

[Ref: Harper’s 30thed pg. 286]
Selenocysteine is the 21st amino acid, synthesized co-translationally by modification of a stop codon – UGA. The precursor amino acid of
selenocysteine is Serine, not cysteine.
Biosynthesis of selenocysteine requires ATP & the carbon skeleton is provided by Serine.

69.Ans. a. Arginine
[Ref: Harper 30th/e pg. 289]
NO is also called as Endothelium Derived Relaxing Factor (EDRF).
NO (nitric oxide) is synthesized from arginine by enzyme NOS (Nitric oxide synthase) in the endothelial cells.
The vasodilator – nitroglycerin also enters smooth muscle cells, where its metabolism also leads to the formation of NO.
70.Ans. b. Alpha-ketoglutarate [Ref: Lehninger 7th/e pg. 686, 687]
In hyperammonemia (i.e. excess amino groups in cells), alpha keto glutarate (intermediate of TCA) tries to use excess amino group in cells
to form glutamate. This leads to depletion of Alpha-KG.

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71.Ans. (b) Defect in ornithine transporter

[Ref: Harper 30th/e pg. 291]

Defect in ornithine transporter leads to HHH syndrome (Hyperornithinemia-Hyperammonemia-

Homocitrullinuria).
This prevents ornithine transport into mitochondria and hence if in the cytoplasm (Hyperornithinemia)
and its reduced ability to clear Carbamoyl phosphate and Ammonia (Hyperammonemia).
Mitochondrial Carbamoyl Phosphate carbamoylates Lysine to Homocitrulline leading to Homocitrulli-
nuria.

72.Ans. (c) X-ray crystallography

[Ref: Lehninger 7th/e pg. 134b-135b]

In the question, they have not mentioned that it is primary, secondary, tertiary or quaternary
structure. In this case, consider tertiary structure (the 3D structure present in vivo). So, mark X-ray
crystallography (which is best for tertiary).

73.Ans. a. Alzheimer disease

Alzheimer’s disease is a disease characterized by the aggregation of amyloid β proteins to form flexible soluble oligomers. These
oligomers are toxic to nerve cells.
Amyloid β are composed of peptides of 30-40 amino acids and formed from the proteolytic cleavage of precursor, APP (Amyloid
Precursor Protein). Amyloid plaques get deposited in this disease

74.Ans. b. Immunoglobulins
[Ref: Harper 30th/e pg 570]
All these are plasma proteins. All plasma proteins are synthesized by liver except Immunoglobulins, which are produced & released from
plasma cells (in RER).

75.Ans. (b) CO2

[Ref: Harper 30th/e pg. 330]
Heme Oxygenase uses Oxygen & it produces CO, Fe3+ and water. But it does not produces CO2.

76.Ans. d. ALA Dehydratase

[Ref: Harper 30th/e pg. 325]
The enzyme which is affected or decreased in lead poisoning is ALA dehydratase or PBG synthase. The
enzyme which is increased in lead poisoning is ALA Synthase.
77.Ans. a. Type I
Type I is present in skin and it is the most abundant collagen in body.
78.Ans. (a) SDS- PAGE

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[Ref: Harper 30th/e pg. 42]

SDS –PAGE is a special kind of electrophoresis which separates molecules on the basis of size.
But a normal electrophoresis depends on many factors like charge, size and shape. In affinity
chromatography, interaction (or affinity) between two compounds is used for separation. HPLC is high
performance liquid chromatography in which high pressure is applied to column chromatography in
order to increase the speed of chromatography and decrease the time required.

79.Ans. a. Transthyretin
[Ref: Harper 30th/e pg 672]
Iron storage: Ferritin and Haemosiderin
Haemosiderinhas higher iron content than Ferritin
Iron transport: Transferrin
Hepcidin: regulate iron transport in circulation
Ceruloplasmin: a Cu containing enzyme in ferro-xidase activity
Transthyretin: transports Thyroxine and Retinol binding protein

80.Ans. (b) Immunoglobulins

[Ref: Harper 30th/e pg 570]

All these are plasma proteins. All plasma proteins are synthesized by liver except Immunoglobulins,
which are produced & released from plasma cells (in RER).

81.Ans. b. RNA molecule that acts catalytically to change itself or another RNA molecule
[Ref: Harper 30th/e pg. 62]
Ribozyme is when RNA is acting as enzyme. Mostly they cleave phosphodiester bonds and they catalyze
themselves or other RNA molecules.

82.Ans. d. LDH-2
[Ref: Harper 30th/e pg. 66]
LDH-2 is raised in haemolytic anemia. LDH-1 is raised in Myocardial Infarction.

83.Ans. d. Ubiquitin
[Ref: Harper 30th/e pg. 289]
The Ubiquitin Proteosome Pathway (UPP) is the main and highly regulated mechanism for intracellular
protein catabolism. It occurs in cytoplasm and nucleus. Proteins which are bound to ubiquitin are degraded in
proteosomes.

84.Ans. b. Decreased Vmax [Ref: Harper 30th/e pg. 92]

In Competitive inhibition, Km increases and Vmax remains same. But in Non competitive inhibition, Km is
same and Vmax decreases.

85.Ans. c. The substrate concentration at half maximum velocity

[Ref: Harper 30th/e pg. 79]

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Km is Michaelis Menton constant. Km is that substrate concentration at which velocity of reaction is half of
Vmax. Km is inversely proportional to affinity. Km is signature of enzyme. It is not association or dissociation
constant.

86.Ans. (b) Arginine

[Ref: Lehninger 7th/e pg. 215]
Trypsin cleaves at the carboxy terminal of basic amino acid (Arginine, Lysine).

87.Ans. c. Succinate Dehydrogenase

[Ref: Harper 30th/e pg. 62]
Succinate Dehydrogenase is FAD linked and it is an enzyme involved in both TCA and ETC.
88.Ans. d. Mg+2
[Ref: Harper 30th/e pg. 62]
All Kinases require Mg, but Pyruvate Kinase requires K+>> Mg2+.

89.Ans. a. Lyase
[Ref: Harper 30th/e pg. 61]
Lyase breaks C-C bond. E.g. Aldolase, Synthase. (In this case, ATP is not used).

90.Ans. c. Prothrombin

[Ref: Medical biochemistry by Sheriff p. 94]

Prothrombin >> LDH
Functional plasma enzymes are those enzymes which are present in plasma as they have function in plasma e.g.
Lipoprotein Lipase, clotting factors e.g. Prothrombin.
Non–functional plasma enzymes do not have function in plasma, they are present inside cells. E.g. SGOT is present in
liver and heart.
Only LDG-2 is a functional plasma enzyme.

91.Ans. a. Catalyse the same reaction

[Ref: Harper 30/e p63]
Isoenzymes catalyse the same reaction. For example, LDH-1 to LDH-5 all convert Pyruvate to Lactate.
144
They have different quaternary structure. For example, the subunits in LDH-1 is different from LDH- 2. Tissue
distribution of each isoform is different. Enzyme name and number can be different.

92.Ans. c. It uses the same enzyme for activation and inactivation

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[Ref: Harper 30th/e pg. 90-91]

Covalent modification is a long term regulation (by hormones). It is slower than allosteric regulation. It is
reversible.
Most common covalent modification is phosphorylation and dephosphorylation. It uses different enzymes for
activation and inactivation. The enzyme which adds phosphate is Protein Kinase and the enzyme which removes
phosphate is Protein Phosphatase.

93.Ans. c. Lysine
[Ref: Harper 30th/e pg. 562]
Vitamin C is required for hydroxylation reactions. Proline to hydroxyl proline conversion
occurs by enzyme prolyl hydroxylase. Lysine to hydroxyl lysine conversion occurs by lysyl
hydroxylase. These reactions are required in collagen post translational modification.

94.Ans. d. Kidney
[Ref: Harper 30th/e pg. 551]
25-hydroxy cholecalciferol is formed in liver
1, 25 (OH)2cholecalciferol is formed in kidneys and it is the most potent form of Vitamin D.

95.Ans. b. Vitamin E
[Ref: Harper 30th/e pg. 553]
Vitamin E is a fat soluble and anti-oxidant vitamin.
96.Ans. b. Folic acid
[Ref: Harper 30th/e pg. 500]
Methionine (S-containing) metabolism requires three vitamins: folate, cobalamin and pyridoxine.
97. Ans. (c) 1
[Ref: Harper 30th/e pg. 119; Harper 30th /e p541
If exclusive carbohydrates given in Q, then RQ is 1. If excess carbohydrates given in Q, then RQ is
more than 1. Because if excess carbohydrates taken, then carbohydrates get converted to fats in body.
98.ANS. b. Vitamin C
[Ref: Harper 30th/e pg. 553]
When vitamin E or Tocopherol scavenges lipid peroxide radicals, then it is converted to Tocopheroxyl
radical. This is reduced back to Tocopherol with the help of vitamin C. Glutathione helps in
regenerating ascorbate.

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 BIOCHEMISTRY ANS KEY

99. Ans. d. All

[Ref: Harper 30th/e pg.596]

Applications of RIA (Radio Immuno Assay): In drug assays e.g. Barbiturates, Morphine, Digitoxin, Amphetamine etc.
Vitamin analysis e.g. Folic acid, Riboflavin
Hormone analysis e.g. Aldosterone, Insulin, Growth Hormone, Thyroxine
Analysis of anti-DNA antibodies like in SLE (Systemic Lupus Erythematosus)

100Ans. a. Vitamin B2 [Ref: Harper 30th/e pg. 556]

The marker enzyme of B2 deficiency is Glutathione Reductase and the marker for B1
deficiency is Transketolase. Clinical features of B2 deficiency i.e. Riboflavinosis are corneal
vascularization, cheilosis, glossitis, angular stomatitis.

102.

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