Control of ethanol utilization by rat hepatocytes.
Ethanol oxidation by hepatocytes from fasted rats was determined in the presence and absence of 0.2 mM ethyl hydrazinoacetate, a transaminase inhibitor which blocks the malate-aspartate cycle. 20 muM phenazine methosulfate caused the largest increase (nearly 150%) in ethanol utilization. 5 muM norepinephrine caused a 50% increase in ethanol oxidation, and most of this increase was caused by stimulation of the alpha-glycerophosphate shuttle, since it remained in the presence of ethyl hydrazinoacetate. 1 muM 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 muM dinitrophenol increased ethanol use by 20% and this increase was nearly unaffected by ethyl hydrazinoacetate. The results indicate that ethanol utilization, under the conditions used, is primarily controlled by the capacity of the shuttle systems, and not by the capacity of the respiratory chain.
D000818:Animals; D004140:Dinitrophenols / Q000494:pharmacology; D000431:Ethanol / Q000378:metabolism*; D005215:Fasting; D005934:Glucagon / Q000494:pharmacology; D006834:Hydrazines / Q000494:pharmacology; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008773:Methylphenazonium Methosulfate / Q000494:pharmacology; D009638:Norepinephrine / Q000494:pharmacology; D010084:Oxidation-Reduction; D051381:Rats; D000637:Transaminases / Q000037:antagonists & inhibitors
D004140:Dinitrophenols; D006834:Hydrazines; D008773:Methylphenazonium Methosulfate; D000431:Ethanol; C023496:ethylhydrazinoacetate; D005934:Glucagon; D000637:Transaminases; D009638:Norepinephrine