Dietary modulation of oxidative stress in alcoholic liver disease in rats

Numerous studies dealing with prolonged feeding of rats with ethanol liquid regimens high in fat and low in carbohydrate showed that the resulting hepatic pathologic changes, including increased lipid peroxidation, are due to dietary aberrations rather than to ethanol toxicity. The amount and particularly the type of dietary fat significantly modulate the hepatic oxidative stress and morphofunctional reactivities. Although dietary vitamin E modulated oxidative stress or lipid peroxidation, it did not influence the development of hepatic pathologic changes in different animal models of chronic alcoholism. The old observation that lipotropes modulate the hepatic alterations associated with prolonged excessive ingestion of ethanol has been amply confirmed by even those who for years did not accept the importance of lipotropes. Our recent studies in rats indicated that prolonged feeding of large amounts of ethanol and diets with variable amounts of lipotropes, vitamin E and minerals did not significantly modulate a large series of hepatic prooxidants, but decreased several antioxidants (vitamin E, ubiquinols and glutathione peroxidase). Ethanol regimens relatively low in vitamin E increased the hepatic thiobarbituric acid-reactive substances and chemiluminescence and reduced some of the antioxidant factors. However, the hepatic prooxidant factors were unaffected, and no liver damage was detected. These and other findings indicated that the eventual detection of oxidative stress in experimental alcoholic liver disease primarily depends on the type of diet and that oxidative stress may not play a significant pathogenic role in this condition.