Vitamin E reduces lipid peroxidation in experimental hepatotoxicity in rats

Background and aims Lipid peroxidation is believed to be involved in the pathophysiology of a number of diseases and in the process of aging. This study investigates the effects of dietary supplementation with vitamin E (20 g/kg diet of all-rac-alpha -tocopheryl succinate for 3 weeks) on both non-enzymatic and enzymatic lipid peroxidation in experimental rats with carbon tetrachloride (CCl4)-induced hepatotoxicity (2.5 mL/kg body). Methods Plasma, urine and liver samples from control rats (n = 6), CCl4-treated rats (n = 6), and rats supplemented with vitamin E prior to CCl4 treatment (n = 8) were collected. Non-enzymatic lipid peroxidation induced by free radicals was investigated by measurement of a major F-2-isoprostane, 8-iso-prostaglandin F-2 alpha (8-iso-PGF(2 alpha)). Cyclooxygenase-catalyzed enzymatic lipid peroxidation was measured with a major PGF(2 alpha), metabolite, 15-keto-13,14-dihydro-prostaglandin F-2 alpha (15-K-DH-PGF(2 alpha)). Malondialdehyde and antioxidants in plasma were also quantified. Results CCl4 treatment alone resulted in significantly higher levels of plasma, urinary and liver 8-iso-PGF(2 alpha), and of plasma and urinary 15-K-DHPGF(2 alpha) compared to controls. Rats supplemented with vitamin E prior to CCl4 treatment had significantly lower levels of urinary and liver 8-iso-PGF(2 alpha), urinary 15-K-DH-PGF(2 alpha) and plasma malondialdehyde than rats treated with CCl4 alone. However, plasma 8-isoPGF(2 alpha) and plasma 15-K-DH-PGF(2 alpha) were not affected by vitamin E supplementation. Conclusion Thus, both non-enzymatic and enzymatic lipid peroxidation during experimental hepatic oxidative injury were suppressed by dietary vitamin E supplementation in rats.