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Organic hydroperoxide-dependent oxidation of ethanol by microsomes: lack of a role for free hydroxyl radicals.

Abstract：

:Organic hydroperoxides can replace NADPH in supporting the oxidation of ethanol by liver microsomes. Experiments were carried out to evaluate the role of hydroxyl radicals in the organic hydroperoxide-catalyzed reaction. Maximum rates of ethanol oxidation occurred in the presence of either 0.5 mM cumene hydroperoxide or 2.5 mM t-butyl hydroperoxide and were linear for 2 to 4 min. The Km for ethanol was about 12 mM and Vmax was about 8 nmol ethanol oxidized/min/mg microsomal protein. Besides ethanol, the organic hydroperoxides supported the oxidation of longer-chain alcohols (1-butanol), and secondary alcohols (isopropanol). The organic hydroperoxide-supported oxidation of alcohols was not affected by several hydroxyl-radical scavengers such as dimethylsulfoxide, mannitol, or 2-keto-4-thiomethylbutyrate which blocked NADPH-dependent oxidation of alcohols by 50% or more. Iron-EDTA, which increases the production of hydroxyl radicals, increased the NADPH-dependent oxidation of ethanol, whereas desferrioxamine, which blocks the production of hydroxyl radicals, inhibited the NADPH-dependent oxidation of ethanol. Neither iron-EDTA nor desferrioxamine had any effect on the organic hydroperoxide-supported oxidation of ethanol. Cumene-and t-butyl hydroperoxide did not support microsomal oxidation of hydroxyl-radical scavengers. These results suggest that, in contrast to the NADPH-dependent oxidation of ethanol, free-hydroxyl radicals do not play a role in the organic hydroperoxide-dependent oxidation of ethanol by microsomes. Ethanol appears to be oxidized by two pathways in microsomes, one which is dependent on hydroxyl radicals, and the other which appears to be independent of these oxygen radicals.

journal_name

Arch Biochem Biophys

journal_title

Archives of biochemistry and biophysics

authors

Cederbaum AI

doi

10.1016/0003-9861(83)90377-6

subject

Has Abstract

pub_date

1983-11-01 00:00:00

pages

329-38

issue

1

eissn

0003-9861

issn

1096-0384

pii

0003-9861(83)90377-6

journal_volume

227

pub_type

杂志文章

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