Inhibition of the Chronic Ethanol-Induced Fatty Liver by Antioxidant Administration ∗

Abstract

Summary

Female rats were maintained for 21 days on nutritionally adequate liquid diets containing either “low” or “high” fat content and supplemented with ethanol or isocaloric sucrose as 35% of the calories. Liver triglyceride concentrations were significantly elevated in animals maintained on both diets supplemented with ethanol. However, a greater increment in triglyceride concentrations was manifested in the “high” fat ethanol group under conditions of similar caloric intake. The intraperitoneal administration of the lipid antioxidant, N,N′-diphenyl-p-phenylenediamine (DPPD), prior to, and during the dietary period significantly inhibited the ethanol-induced increment in hepatic triglyceride concentration. The inhibition of the chronic ethanol-induced steatosis, in conjuction with our previous studies of antioxidant modification of the acute ethanol-in-duced hepatic lesion, further accents the possible role of lipid peroxidation as a determinant in cell injury and the role of antioxidants as liver protective agents.