Oxidation of isopropanol by rat liver microsomes. Possible role of hydroxyl radicals

Arthur I. Cederbaum, Aziz Qureshi, Philip Messenger

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Isopropanol, a branched chain alcohol, served as a substrate for the microsomal alcohol oxidizing system. Isopropanol oxidation required NADPH; H2O2 or an H2O2-generating system did not effectively support isopropanol oxidation, indicating that isopropanol was not a substrate for the peroxidatic activity of catalase. The addition of azide by itself or H2O2 (in the presence of azide and NADPH) stimulated isopropanol oxidation, suggesting a pivotal, indirect role for H2O2 in the system. H2O2 may serve as a precursor of hydroxyl radicals. Accordingly, the oxidation of isopropanol was inhibited by hydroxyl radical scavenging agents, namely dimethylsulfoxide, mannitol, benzoate and 2-keto-4-thiomethylbutyric acid. Fe-EDTA, which is known to increase hydroxyl radical generation, stimulated the oxidation of isopropanol. The stimulation by Fe-EDTA was blocked by competing hydroxyl radical scavengers. Model hydroxyl radical generating systems such as the coupled oxidation of xanthine by xanthine oxidase, especially in the presence of Fe-EDTA, or the autoxidation of ascorbate in the presence of Fe-EDTA could also oxidize isopropanol. These results indicate that (a) rat liver microsomes are capable of oxidizing branched chain alcohols, and (b) hydroxyl radicals or a species with the oxidizing power of the hydroxyl radical, generated from microsomal electron transfer, may play a role in isopropanol oxidation.

Original languageEnglish
Pages (from-to)825-831
Number of pages7
JournalBiochemical Pharmacology
Issue number8
StatePublished - 15 Apr 1981
Externally publishedYes


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