Effect of epinephrine on ethanol metabolism by isolated rat hepatocytes.

Effect of epinephrine on ethanol metabolism by isolated rat hepatocytes.
复制标题

肾上腺素对离体大鼠肝细胞乙醇代谢的影响。

DOI:
10.1016/0006-2952(90)90088-3
复制
发表时间:
1990
影响因子:
5.8
通讯作者:
Akinshola,BE
Akinshola,BE
中科院分区:
医学2区
文献类型:
--
作者:
Mezey,E;Potter,JJ;Sharma,S;Akinshola,BE

文献摘要

被引文献

相似文献

在离体大鼠肝细胞中测定肾上腺素对乙醇代谢的影响。肾上腺素(10 μM)在前5分钟内可增强乙醇的初始快速消除速率。此后,在5至90分钟之间,乙醇消除速率较慢,不受肾上腺素的影响。肾上腺素导致较高的乙醛浓度在2分钟,但不是此后。在肾上腺素存在和不存在的情况下,乙醛的产生受到4-甲基吡唑、低游离细胞外钙浓度和α1-肾上腺素能阻滞剂哌唑嗪的抑制。单独的乙醇和肾上腺素增加耗氧量,但效果不是累加的。乙醇诱导的细胞质NAD+/NADH和NADP+/NADPH比率以及线粒体NAD+/NADH比率的降低被肾上腺素延迟。通过将乙醇氧化与乳醛还原偶联,证明了足以解释肾上腺素所示的快速乙醇消除初始速率的加速的初始乙醇脱氢酶活性,该系统增加了NADH从酶解离并氧化回NAD+的速率。本研究的结果表明,乙醇脱氢酶在乙醇氧化过程中增加的NADH再氧化是肾上腺素产生的乙醇消除快速瞬时增加的基础。
The effect of epinephrine on ethanol metabolism was determined in isolated rat hepatocytes. Epinephrine (10 μM) enhanced an initial rapid rate of ethanol elimination observed in the first 5 min. Thereafter, between 5 and 90 min, the rate of ethanol elimination was slower and not affected by epinephrine. Epinephrine resulted in higher acetaldehyde concentrations at 2 min, but not thereafter. Acetaldehyde production in the presence and absence of epinephrine was inhibited by 4-methylpyrazole, by a low free extracellular calcium concentration, and by theα1-adrenergic blocker prazosin. Ethanol alone and epinephrine alone increased oxygen consumption, but the effects were not additive. The ethanol-induced decreases in the cytosolic NAD+/NADH and NADP+/NADPH ratios and in the mitochondrial NAD+/NADH ratio were delayed by the presence of epinephrine. An accelerated initial alcohol dehydrogenase activity sufficient to account for the rapid initial rate of ethanol elimination shown with epinephrine was demonstrated by coupling ethanol oxidation with lactaldehyde reduction, a system which increases the rate of dissociation of NADH from the enzyme and its oxidation back to NAD+. The findings in this study indicate that an increased reoxidation of NADH during ethanol oxidation by alcohol dehydrogenase is the basis for the rapid transient increase in ethanol elimination produced by epinephrine.