During the past year, abundant new information was gained on the metabolism and hepatotoxicity of ethanol. The molecular biology of hepatic alcohol dehydrogenase and the contribution of gastric alcohol dehydrogenase to the first-pass metabolism of ethanol and to alcohol-drug interactions were further described. The mechanism of the induction of the hepatic cytochrome P4502E1 (2E1) by chronic ethanol consumption was elucidated, and its contribution to hepatotoxicity via free radical formation and xenobiotic activation has been delineated. New roles for factors such as hepatitis C, cytokines, gender, genetics, and age have emerged. A better understanding of the pathology induced by ethanol (including enhanced fibrogenesis) has generated improved prospects for therapy.
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