Cederbaum A I, Dicker E, Cohen G
Adv Exp Med Biol. 1980;132:1-10. doi: 10.1007/978-1-4757-1419-7_1.
A series of hydroxyl radical (.OH) scavenging agents competitively inhibited microsomal oxidation of ethanol and 1-butanol. The inhibition by the scavengers was specific since these agents had no effect on catalase-dependent oxidation of ethanol, microsomal drug metabolism or microsomal electron transfer. Chemical evidence for production of .OH during microsomal electron transfer was provided by the generation of appropriate products from .OH scavenging agents. H2O2 was shown to play a role as a precursor of .OH. Fe-EDTA increased microsomal oxidation of ethanol without affecting drug metabolism. A role for cytochrome P-450 in catalyzing . OH generation remains to be evaluated. These results suggest that the molecular mechanism underlying the oxidation of ethanol by liver microsomes reflects the ability of ethanol to interact with .OH generated from microsomal electron transfer.
一系列羟基自由基（·OH）清除剂竞争性抑制了乙醇和1-丁醇的微粒体氧化。这些清除剂的抑制作用具有特异性，因为它们对过氧化氢酶依赖性乙醇氧化、微粒体药物代谢或微粒体电子传递均无影响。羟基自由基清除剂生成适当产物，为微粒体电子传递过程中产生·OH提供了化学证据。过氧化氢被证明是·OH的前体。Fe-EDTA增加了乙醇的微粒体氧化，而不影响药物代谢。细胞色素P-450在催化·OH生成中的作用仍有待评估。这些结果表明，肝微粒体氧化乙醇的分子机制反映了乙醇与微粒体电子传递产生的·OH相互作用的能力。
