Abstract
The effect of administration of two exogenous quinones on in vivo ethanol metabolism and ethanol-induced toxicity has been investigated. Menadione (vitamin K3; 50 mg/kg) or vitamin K1 (250 mg/kg) were given subcutaneously (sc) to male Sprague Dawley rats 1 hour before oral administration of ethanol (4 gm/kg). Menadione, a good quinone reductase substrate, increased the elimination rate of orally administered ethanol thereby decreasing its bioavailability (as measured by the area under the curve (AUC) relating blood level to time) and its induced hepatic triglyceride accumulation. On the other hand, closely related structural analog, vitamin K1, which was proven to be a poor substrate for quinone reductase, failed to show any significant effect. Thus, these results suggest that quinone reductase appear to play a role in in vivo ethanol metabolism and toxicity.
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