Numerous studies dealing with prolonged feeding of rats with ethanol l
iquid regimens high in fat and low in carbohydrate showed that the res
ulting hepatic pathologic changes, including increased lipid peroxidat
ion, are due to dietary aberrations rather than to ethanol toxicity. T
he amount and particularly the type of dietary fat significantly modul
ate the hepatic oxidative stress and morphofunctional reactivities. Al
though dietary vitamin E modulated oxidative stress or lipid peroxidat
ion, it did not influence the development of hepatic pathologic change
s in different animal models of chronic alcoholism. The old observatio
n that lipotropes modulate the hepatic alterations associated with pro
longed 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 amoun
ts 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, ubiquinol
s and glutathione peroxidase). Ethanol regimens relatively low in vita
min E increased the hepatic thiobarbituric acid-reactive substances an
d chemiluminescence and reduced some of the antioxidant factors. Howev
er, the hepatic prooxidant factors were unaffected, and no liver damag
e was detected. These and other findings indicated that the eventual d
etection of oxidative stress in experimental alcoholic liver disease p
rimarily depends on the type of diet and that oxidative stress may not
play a significant pathogenic role in this condition.