肝脏乙醇代谢的重要途径。

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瑟曼RG,麦肯纳WR, Brentzel HJ Jr,黑森州

肝脏乙醇代谢的重要途径。

美联储Proc。1975年10月,34 (11):2075 - 81。

PubMed ID

240743年(在PubMed

]

文摘

大鼠肝微粒体氧化乙醇的两到三倍的速度比丙醇孵化时NADPH -或一个H2O2-generating系统。此外,可溶性,纯化微粒体小分支被发现含有蛋白质的电泳淌度相同的鼠肝过氧化氢酶在SDS聚丙烯酰胺凝胶,这表明过氧化氢酶的分离细胞色素p - 450和其他微粒体组件可能不是可行的。这些数据支持了假设过氧化氢酶负责NADPH-dependent微粒体乙醇氧化。直接读出技术吡啶核苷酸,catalase-H2O2复杂,和细胞色素p - 450是用来评估酒精脱氢酶的特异性抑制剂(4-methylpyrazole;4毫米)和过氧化氢酶(氨基三唑;1.0克/公斤)定性在灌注大鼠肝脏。4-Methylpyrazole和特定抑制剂氨基三唑醇脱氢酶和过氧化氢酶,分别在这些条件下。抑制剂和它们的组合改变了混合函数氧气p-nitroanisole p-nitrophenol所观察到的耗氧量和产品的形成。当乙醇利用测量浓度范围20 - 80 mM在肝脏灌注,观察到浓度依赖性。在低浓度的乙醇,乙醇氧化被4-methylpyrazole几乎完全废除; however, the contribution of 4-methylpyrazole-insensitive ethanol uptake increased as a function of ethanol concentration. At 80 mM ethanol, ethanol utilization was nearly 50% methylpyrazole-insensitive. This portion of ethanol oxidation, however, was abolished by aminotriazole. The data indicate that alcohol dehydrogenase and catalase-H2O2 are responsible for hepatic ethanol oxidation. At low ethanol concentrations (less than 20 mM), alcohol dehydrogenase is predominant; however, at higher ethanol concentrations (up to 80 mM), the contribution of catalase-H2O2 to overall ethanol utilization is significant. No evidence that the endoplasmic reticulum is involved in ethanol metabolism in the perfused liver emerged from these studies.

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药物靶点

药物	目标	类	生物	药理作用	行动
Fomepizole	过氧化氢酶	蛋白质	人类	是的	抑制剂	细节