Vitamin E reduces lipid peroxidation in experimental hepatotoxicity in rats

Abstract

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-α-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 F₂-iso-prostane, 8-iso-prostaglandin F_2α (8-iso-PGF_2α). Cyclooxygenase-catalyzed enzymatic lipid peroxidation was measured with a major PGF_2α metabolite, 15-kto-13,14-dihydro-prostaglandin F_2α (15-K-DH-PGF_2α). 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_2α, and of plasma and urinary 15-K-DH-PGF_2α compared to controls. Rats supplemented with vitamin E prior to CCl₄ treatment had significantly lower levels of urinary and liver 8-iso-PGF_2α, urinary 15-K-DH-PGF_2α, and plasma malondialdehyde than rats treated with CCl₄ alone. However, plasma 8-iso-PGF_2α and plasma 15-K-DH-PGF_2α 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.