1. Chronic ethanol administration to rats for 21–27 days increases the rate of O2 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 86Rb 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][Pi]) in the liver cell owing to a decrease in [ATP] and an increase in [Pi]. 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.

This content is only available as a PDF.
You do not currently have access to this content.