Effect of an acute dose of ethanol on lipid peroxidation in rats: action of vitamin E

Free radical generation is an important step in the pathogenesis of ethanol-associated liver injury. Administration of ethanol induces an increase in lipid peroxidation both by enhancing the production of oxygen reactive species and by decreasing the levels of endogenous antioxidants. This work focuses on the generation of free radicals provoked by an acute ethanol dose in rats, and the role of different dietary levels of vitamin E. The objective of this investigation was to study the effect of three different dietary levels of vitamin E (deficient, control and supplemented with 20 times higher levels) on plasma and liver lipid peroxidation (assayed by TBARS), vitamin E in plasma and liver, and hepatic glutathione concentration, in rats receiving the different diets. The animals were submitted to an acute dose of ethanol (5 g/kg body weight) administered by gavage at the end of an experimental 4 week period and were sacrificed at 0, 2, 4, 8 and 24 h after ethanol administration. Dietary vitamin E caused a dose-dependent increase in liver and plasma concentration of the vitamin, but ethanol administration decreased hepatic vitamin E in all groups. TBARS concentrations were higher in liver of rats that received the deficient diet, independent of ethanol, however, liver TBARS concentrations were low in control and supplemented groups, but increased with ethanol ingestion. Glutathione levels were lowered by ethanol administration in all groups, in different times, but recovered to this original level in 24 h time. In conclusion, vitamin E deficiency alone induces liver lipid peroxidation in rats, acute administration of ethanol affect vitamin E and GSH level and maintenance of adequate or higher vitamin E levels acts as a protective factor against free radical generation.