Vitamin E reduces lipid peroxidation in experimental hepatotoxicity in rats

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).

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 F2 alpha (8-iso-PGF2 alpha). Cyclooxygenase-catalyzed enzymatic lipid peroxidation was measured with a major PGF2 alpha metabolite, 15-keto-13,14-dihydro-prostaglandin F2 alpha (15-K-DH-PGF2 alpha). Malondialdehyde and antioxidants in plasma were also quantified.

CCl4 treatment alone resulted in significantly higher levels of plasma, urinary and liver 8-iso-PGF2 alpha, and of plasma and urinary 15-K-DH-PGF2 alpha compared to controls. Rats supplemented with vitamin E prior to CCl4 treatment had significantly lower levels of urinary and liver 8-iso-PGF2 alpha, urinary 15-K-DH-PGF2 alpha, and plasma malondialdehyde than rats treated with CCl4 alone. However, plasma 8-iso-PGF2 alpha and plasma 15-K-DH-PGF2 alpha were not affected by vitamin E supplementation.

Thus, both non-enzymatic and enzymatic lipid peroxidation during experimental hepatic oxidative injury were suppressed by dietary vitamin E supplementation in rats.