Abstract
Summary
Pyrazole, an inhibitor of liver alcohol dehydrogenase and ethanol metabolism, was used to distinguish between acute biochemical responses produced directly by alcohol and secondarily by its metabolic effects. Over the 40 hr period studied, accumulation of hepatic triglvcerides was dependent upon an initial uptake of fattv acids from adipose stores and continued oxidation of ethanol by the liver. The increased efficiency of mitochondrial function, as monitored by the magnitude of respiratory control ratios, followed a time course isochronous with the blood alcohol curve and was dependent upon in situ exposure of the organelle to the alcohol molecule, not its metabolic seauelae. These relatively short-term responses are not sustained in well nourished animals receiving ethanol chronically.
The technical assistance of Mrs. Regina Foster is gratefully acknowledged.
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