Abstract
Chronic alcohol-feeding to mice results in an increased utilization of DPNH by hepatic mitochondria, in the presence and absence of “malate-aspartate shuttle” components. The utilization of alcohol and α-glycerophosphate by these mitochondria is also increased. Succinic dehydrogenase activity assayed with phenazine methosulphate as an index of mitochondrial permeability showed higher activity in mitochondria from chronic alcohol-treated mice compared to pair-fed controls. Alcohol-withdrawal from chronically-treated animals showed a lack of correlation between blood alcohol clearance, and hepatic microsomal alcohol-oxidizing activity on one hand, and between blood alcohol clearance and alcohol dehydrogenase activity on the other.
Published Version
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