Abstract
Ethanol oxidation by hepatocytes from fasted rats was determined in the presence and absence of 0.2 mM ethyl hyrazinoacetate, a transaminase inhibitor which blockes the malate-aspartate cycle. 20 μM phenazine methosulfate caused the larges increase (nearly 150%) in ethanol utilization. 5 μM norepinephrine caused a 50% increase in ethanol oxidation, and most fo this increase was caused by stimulation of the α-glycerophosphate shuttle, since it remained in the presence of ethyl hydrazinoacetate. 1 μM glucagon caused a 25% increase in ethanol uptake, and most of this increase was abolished by ethyl hydrazinoacetate, indicating that the malate-aspartate cycle was involved. 25 μM dinitrophenol increased ethanol use by 20% and this increase was nearly unaffected by ethyl hydrazinoacetate. The results indicate that ethanol utilization, under the conditionsused, is primarily controlled by the capacity of the shuttle systems, and not by the capacity of teh respiratory chain.
Published Version
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