Abstract
1. Chronic ethanol administration to rats for 21-27 days increases the rate of O(2) consumption as measured in liver slices. The extra respiration can be abolished by inhibition of the active transport of Na(+) and K(+). Dinitrophenol activates the respiratory rate in the liver of the treated animals only in the presence of ouabain. 2. Active (ouabain-sensitive) transport of (86)Rb and (Na(+)+K(+))-stimulated adenosine triphosphatase activity were increased in the livers of the ethanol-treated animals. 3. Chronic ethanol administration also led to a decrease in the phosphorylation potential ([ATP]/[ADP][P(i)]) in the liver cell owing to a decrease in [ATP] and an increase in [P(i)]. 4. It is suggested that an increased sodium pump activity is responsible for the increased oxidative capacity and for the insensitivity to dinitrophenol observed in the livers of ethanol-treated animals.