Chronic ethanol consumption results in a generalized depression in hepatic mitochondrial energy metabolism. Both the rate and efficiency of ATP synthesis via the oxidative phosphorylation system are decreased. Alterations in the activities of several components of the oxidative phosphorylation system contribute to the overall decrease in the capacity for ATP synthesis. There appears to be no alteration in any particular component which is rate-limiting. Although changes in membrane lipids may play a minor role, it appears that the decreased levels of mitochondria-derived polypeptide components of the oxidative phosphorylation system are primarily responsible for the depression in both the rate and efficiency of ATP synthesis. The concentrations of these mitochondrial gene products are lowered due to effects of chronic ethanol consumption on the mitochondrial translational process.