Coq10

Vitamin C, also known as ascorbic acid, is a water-soluble antioxidant. Today we meet our requirements of vitamin C through consumption of fruits and vegetables or by supplementation. Homo sapiens cannot produce vitamin C like many other species that can convert glucose to vitamin C. The gene for enzyme production is dormant in humans. The gene, GULO, that we all carry converts glucose to Vitamin C. in other species but not in humans and primates. The open-label study showed Metadichol ® raised levels of vitamin C by 3 fold, endogenously without supplementation of Vitamin C. Possible mechanisms for the increased Vitamin C levels through antioxidant pathways are presented. Metadichol ® [1] is a nano-formulation of long chain alcohols derived from sugar cane. In addition to increased Vitamin C levels reduction in Potassium and uric acid, and decreased blood pressure and improvement in quality of life issues were also observed.

In this study, we aimed to investigate the effects of hesperidin and coenzyme Q10 on muscle ischemia/reperfusion injury in a rat model. A total of 28 Sprague-Dawley male rats were divided into four groups: Control, Sham, I/R+CoQ10 and I/R+Hesperidin groups. All rats were anesthetized with xylazine and ketamine. Except for the control group, the left lower limbs of the other 3 groups were applied to 2 hours of ischemia and 2 hours of reperfusion with tourniquet. TNF-α, IL-6, GSH, MDA levels, CAT, GPx, SOD activities were measured in the plasma. The levels of MDA with XO, CAT, SOD activities were determined in tissues. Increases in TNF-α, IL-6 and MDA levels, decreases in the CAT, GPx and SOD activities were significant in the sham group according to the control group but the differences in GSH were insignificant in plasma samples. The decreases in plasma TNF-α, IL-6 and MDA levels, the increases in CAT, GPx and SOD activities were statistically significant in the experimental groups compared to the sham group, but the GSH differences were insignificant. MDA and XO levels were higher in the
experimental groups than in the sham and control groups, CAT and SOD levels decreased, these differences were statistically significant. The results of this study support the possibility that hesperidin and CoQ10 may play a protective role against skeletal muscle injury caused by I/R in rats by reducing oxidative stress. Hence, hesperidin and coenzyme Q10 may be useful adjunctive therapeutic agents in some operations suspected of organ I/R damage.

Electromagnetic fields (EMFs) are reported to interfere with chemical reactions involving free radical production. Coenzyme Q 10 (CoQ10) is a strong antioxidant with some neuroprotective activities. The purpose of this study was to examine and compare the neuroprotective effects of EMF and CoQ10 in a mouse model of hippocampal injury. Hippocampal injury was induced in mature female mice (25-30 g), using an intraperitoneal injection of trimethyltin hydroxide (TMT; 2.5 mg/kg). The experimental groups were exposed to EMF at a frequency of 50 Hz and intensity of 5.9 mT for 7 hr daily over 1 week or treated with CoQ10 (10 mg/kg) for 2 weeks following TMT injection. A Morris water maze apparatus was used to assess learning and spatial memory. Nissl staining and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) tests were also performed for the histopathological analysis of the hippocampus. Antiapoptotic genes were studied, using the Western blot technique. The water maze test showed memory improvement following treatment with CoQ10 and coadministration of CoQ10 + EMF. The Nissl staining and TUNEL tests indicated a decline in necrotic and apoptotic cell count following treatment with CoQ10 and coadministration of CoQ10 + EMF. The Western blot study indicated the upregulation of antiapoptotic genes in treatment with CoQ10, as well as coadministration. Also, treatment with EMF had no significant effects on reducing damage induced by TMT in the hippocampus. According to the results, EMF had no significant neuroprotective effects in comparison with CoQ10 on hippocampal injury in mice. Nevertheless, coadministration of EMF and CoQ10 could improve the neuroprotective effects of CoQ10. K E Y W O R D S CoQ10, electromagnetic fields (EMFs), neuroprotective effect, trimethyltin hydroxide (TMT)

Oxidative stress (OS) is a key contributing factor in 30–80%ofmale infertility cases. To date, several antioxidant treatments have
been put forth to manage OS-induced male infertility. This study intended to elucidate the impact of coenzyme Q10 (CoQ10) and
selenium on seminal fluid parameters and antioxidant status in infertile men with idiopathic oligoasthenoteratospermia (OAT). In
this prospective study, 70 patients with idiopathic OAT were randomly allocated to receive CoQ10 (200 mg/day) or selenium
(200 μg/day) for 3 months. Semen quality parameters (followingWHO guidelines, 5th edition), total antioxidant capacity (TAC),
catalase (CAT), and superoxide dismutase (SOD) activitieswere compared before and after the treatment. The results of the study
showed an increase in sperm concentration with CoQ10 treatment (p < 0.01) as well as increased progressive sperm motility
(p < 0.01 and p < 0.05) and total sperm motility (p < 0.01 and p < 0.05) with CoQ10 and selenium treatment respectively. There
was also a significant improvement in TAC (p < 0.01 and p < 0.05) and SOD (p < 0.01 and p < 0.05) following treatment with
CoQ10 and selenium respectively while CAT improved only with CoQ10 therapy (p < 0.05). Sperm concentration, motility, and
morphology also correlated significantly with TAC, SOD, and CAT (r = 0.37–0.76). In conclusion, treatment with CoQ10
(200 mg) or selenium (200 μg) could improve sperm concentration, motility, and antioxidant status in infertile men with
idiopathic OAT with CoQ10 providing the higher improvement.