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Vitamins C and E alone and in combination partly protect against chronic ethanol-induced toxicity in rat erythrocytes
Parisa Hasanein1, Peyman Mohammadi-Raighan2, Alireza Komaki3
1Department of Biology, School of Basic Sciences, University of Zabol, Zabol, Iran.
Abstract:
Oxidative stress is part of the mechanisms involved in ethanol toxicity. We investigated effects of vitamins C (VC), E (VE) and the combination of VC+VE on chronic ethanol-induced toxicity in rat erythrocytes. The following groups were treated for 30 days: control (C), VC (200 mg/kg), VE (200 mg/kg), VC (200 mg/kg) + VE (200 mg/kg), ethanol 4 g/kg, ethanol + VC, ethanol + VE and ethanol + VC + VE. The doses of vitamins and ethanol were selected for per kilogram of animal's body weight. Blood samples collected at the end of treatments were analyzed for erythrocyte osmotic fragility and plasma scavenging activity. The washed erythrocytes were used to determine superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and malondialdeyde (MDA). Ethanol induced erythrocyte fragility (p < 0.001) and increased lipid peroxidation (p < 0.001) in rat erythrocytes. Furthermore, there were significant decreases in plasma scavenging (p < 0.001), SOD (p < 0.001), CAT (p < 0.01) and GPx (p < 0.001) activities in erythrocytes of ethanol-treated animals. Although VC or VE alone restored all of ethanol-induced disturbances to near normal (p > 0.05) but there were still significant differences compared to control animals. Combination therapy completely corrected ethanol-induced erythrocyte fragility, lipid peroxidation and prooxidant/antioxidant imbalance. We showed the beneficial effects of VC and VE combination in decreasing erythrocyte fragility and lipid peroxidation in both ethanol and control groups. Therefore this combination treatment may provide a new potential alternative for prevention of ethanol toxicity which deserves consideration and further examination.
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