Chung J H, Rubin R J, Cha Y N
Division of Toxicological Sciences, School of Hygiene and Public Health, Johns Hopkins University, Baltimore, MD 21205.
Drug Chem Toxicol. 1993;16(4):383-94. doi: 10.3109/01480549308998228.
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.
已研究了两种外源性醌类物质对体内乙醇代谢及乙醇诱导毒性的影响。在给雄性斯普拉格-道利大鼠口服乙醇（4克/千克）前1小时，皮下注射甲萘醌（维生素K3；50毫克/千克）或维生素K1（250毫克/千克）。甲萘醌是一种良好的醌还原酶底物，它提高了口服乙醇的消除率，从而降低了其生物利用度（通过血药浓度-时间曲线下面积（AUC）来衡量）及其诱导的肝脏甘油三酯积累。另一方面，结构紧密相关的类似物维生素K1，已被证明是醌还原酶的不良底物，未显示出任何显著影响。因此，这些结果表明醌还原酶似乎在体内乙醇代谢和毒性中发挥作用。
