SummaryAlthough alcoholic liver disease is often associated with some increase in hepatic iron stores, it is now established that when gross iron overload is present, this is due to genetic hemochromatosis. Furthermore, there appears to be a critical iron concentration necessary for the induction of hepatic fibrosis. Lipid peroxidation induced by ethanol and/or iron would appear to play a major role in hepatic damage in both humans and experimental animals. Although the exact mechanism(s) of induction of lipid peroxidation by ethanol and iron remains to be elucidated, both toxins can exert a synergistic effect upon hepatic lipid peroxidation. Iron overload has also been shown to stimulate directly hepatocyte and hepatic procollagen mRNA expression, which is further stimulated by ethanol. The observed synergism between iron and alcohol with respect to both hepatic lipid peroxidation and collagen biosynthesis offers a possible explanation of the apparent early onset of fibrosis and cirrhosis in patients with iron overload who have an excessive alcohol intake.