The hepatic concentrations of copper, zinc and manganese, the activity of the mitochondrial enzyme manganese-superoxide dismutase (MnSOD), and the activity of the cytosolic enzyme copper-zinc SOD (CuZnSOD) were measured in control and ethanol-fed monkeys. In the ethanol-fed group, liver Zn levels were decreased while the Mn concentration was increased. The activity of MnSOD was higher in the ethanol-fed group while the activity of CuZnSOD tended to be lower. The finding of increased activity of MnSOD is consistent with the finding of enlarged mitochondria and increased liver Mn in the ethanol-fed group. Increased MnSOD may reflect substrate induction, since superoxide anions are generated by ethanol metabolism. On the other hand, insufficient CuZnSOD activity may contribute to increased ethanol-induced lipid peroxidation with resultant mitochondrial damage. Thus, the chronic consumption of ethanol results in altered levels of trace minerals and SOD activities in the liver which in turn may contribute to hepatic injury.