Lipid peroxidation, iron mobilization and radical generation induced by alcohol.

Increasing evidence points to a major role for free radicals in the pathogenesis of alcohol-induced liver injury. In vitro, free radicals may be generated during ethanol metabolism by the further metabolism of acetaldehyde by molybdenum-dependent oxidases such as xanthine oxidase. Ferritin iron mobilized by such free radicals may serve as catalytic iron. Increased stores of ferritin iron and induction of microsomal P-450 reductase activity are mechanisms by which chronic alcohol feeding may potentiate the acute effects of alcohol.