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One of the molecular mechanisms of alcohol-induced toxicity is mediated by oxidative stress. We investigated the protective effects of orally administered vitamin C (VC) in different doses on oxidative damage in rat eyes induced by chronic ethanol intake.
Eight groups of rats were treated for 30 days: control (C), VC (50, 100 and 200 mg/kg), ethanol (4 g/kg) and, ethanol + VC (50, 100 and 200 mg/kg).Eyes were then removed for analysis of oxidant/antioxidant markers including superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdeyde (MDA).
Ethanol decreased the activities of SOD, CAT and GPx in the eye. These changes were accompanied by enhanced lipid peroxidation measured as increased MDA levels. Although VC (50 and 100 mg/kg) restored antioxidant enzymes activity and lipid peroxidation, there were still significant differences compared to control animals. However, 200 mg/kg VC clearly prevented the pro-oxidant and antioxidant imbalance. Interestingly, the highest dose of VC produced a potent inhibition of lipid peroxidation and improvement in antioxidant defense enzymes compared to other doses in non-alcoholic rats.
Oral administration of VC 200 mg/kg for 30 days prevented redox imbalance induced by chronic ethanol exposure in rat eyes by enhancing the activities of antioxidant enzymes and inhibiting lipid peroxidation. Relative to other chemical medications, vitamin treatments may be free of major side effects; therefore this antioxidant vitamin may provide a potential alternative for prevention of ethanol toxicity which deserves consideration and further examination.