Teschke R, Hasumura Y, Lieber C S
J Biol Chem. 1975 Sep 25;250(18):7397-404.
Oxidation of methanol, ethanol, propanol, and butanol by the microsomal fraction of rat liver homogenate is described. This microsomal alcohol-oxidizing system is dependent on NADPH and molecular oxygen and is partially inhibited by CO, features which are common for microsomal drug-metabolizing enzymes. The activity of the microsomal alcohol-oxidizing system could be dissociated from the alcohol peroxidation via catalase-H2O2 by differences in substrate specificity, since higher aliphatic alcohols react only with the microsomal system, but not with catalase-H2O2. Following solubilization of microsomes by ultrasonication and treatment with deoxycholate, the activity of the microsomal alcohol-oxidizing system was separated from contaminating catalase by DEAE-cellulose column chromatography, ruling out an obligatory involvement of catalase-H2O2 in the activity of the NADPH-dependent microsomal alcohol-oxidizing system. In intact hepatic microsomes, the catalase inhibitor sodium azide slightly decreased the oxidation of methanol and ethanol, but not that of propanol and butanol, indicating a facultative role of contaminating catalase in the microsomal oxidation of lower aliphatic alcohols only. It is suggested that the microsomal alcohol-oxidizing system accounts, at least in part, for that fraction of hepatic alcohol metabolism which is independent of the pathway involving alcohol dehydrogenase activity.
本文描述了大鼠肝脏匀浆微粒体部分对甲醇、乙醇、丙醇和丁醇的氧化作用。这种微粒体醇氧化系统依赖于NADPH和分子氧，并且部分受CO抑制，这些都是微粒体药物代谢酶的常见特征。由于高级脂肪醇仅与微粒体系统反应，而不与过氧化氢酶-H2O2反应，通过底物特异性的差异，微粒体醇氧化系统的活性可以与过氧化氢酶-H2O2介导的醇过氧化作用区分开来。通过超声处理使微粒体溶解并用脱氧胆酸盐处理后，通过DEAE-纤维素柱色谱将微粒体醇氧化系统的活性与污染的过氧化氢酶分离，排除了过氧化氢酶-H2O2在NADPH依赖性微粒体醇氧化系统活性中的必然参与。在完整的肝微粒体中，过氧化氢酶抑制剂叠氮化钠略微降低了甲醇和乙醇的氧化，但不影响丙醇和丁醇的氧化，表明污染的过氧化氢酶仅在低级脂肪醇的微粒体氧化中起辅助作用。有人提出，微粒体醇氧化系统至少部分地解释了肝脏醇代谢中与涉及醇脱氢酶活性的途径无关的那一部分。
