Human gastric alcohol dehydrogenase: its inhibition by H2-receptor antagonists, and its effect on the bioavailability of ethanol.
Human gastric alcohol dehydrogenase: its inhibition by H2-receptor antagonists, and its effect on the bioavailability of ethanol.
复制标题
人胃乙醇脱氢酶：H2 受体拮抗剂的抑制作用及其对乙醇生物利用度的影响。
DOI：
10.1111/j.1530-0277.1990.tb01843.x
复制
发表时间：
1990
期刊：
影响因子：
--
通讯作者：
Lieber,CS
中科院分区：
文献类型：
--
作者：
Hernández-Muñoz,R;Caballeria,J;Baraona,E;Uppal,R;Greenstein,R;Lieber,CS
已在人胃中鉴定出两种类型的乙醇脱氢酶同工酶（对乙醇的亲和力、对4-甲基吡唑的敏感性和电泳迁移不同）。在高浓度的乙醇在胃腔酒精消费期间，他们的活动的总和可以解释显着的乙醇氧化。在体外，这些活动被西咪替丁和雷尼替丁抑制，但不被法莫替丁。在体内，治疗剂量的西咪替丁（而不是法莫替丁）增加血液乙醇水平时，乙醇是口服给药，但不是当它是静脉注射，表明胃ADH的生物利用度的显着贡献，从而乙醇的潜在毒性。
Two types of alcohol dehydrogenase isoenzymes (differing in their affinity for ethanol, sensitivity to 4‐methylpyrazole, and electrophoretic migration) have been identified in the human stomach. At the high ethanol concentrations prevailing in the gastric lumen during alcohol consumption, the sum of their activities could account for significant oxidation of ethanol. In vitro, these activities were inhibited by cimetidine and ranitidine, but not by famotidine. In vivo, therapeutic doses of cimetidine (but not of famotidine) increased blood ethanol levels when ethanol was given orally, but not when it was given intravenously, indicating a significant contribution of the gastric ADH to the bioavailability and thereby the potential toxicity of ethanol.