Abstract
Treatment of rats for 21-28 days with a semiliquid diet containing ethanol resulted in a near doubling of liver microsomal cytochrome P-450 content. Concomitantly, statistically significant increases in the rate of NADPH oxidation, "endogenous" respiration, and acetaldehyde formation from ethanol in microsomes were observed. An average increase in NADPH-dependent hydrogen peroxide formation of 45 ± 7% (SE) was observed as a result of chronic ethanol treatment, employing the decrease in scopoletin fluorescence or the formation of cytochrome peroxidase complex II as hydrogen peroxide-detecting systems. Since it has been reported that the rate-limiting step for ethanol oxidation in microsomes is the rate of generation of hydrogen peroxide for the peroxidatic reaction of catalase [R. G. Thurman, H. G. Ley, and R. Scholz, Eur. J. Biochem. 25, 420-430 (1972)], this adaptive increase in hydrogen peroxide production due to chronic ethanol treatment most likely accounts for the enhanced ethanol oxidation via catalase-H2O2. The data are consistent with the hypothesis that microsomal ethanol oxidation is due to peroxidation via catalase utilizing microsomal hydrogen peroxide.
- Copyright ©, 1973, by Academic Press, Inc.
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Induction of Hepatic Microsomal Reduced Nicotinamide Adenine Dinucleotide Phosphate-Dependent Production of Hydrogen Peroxide by Chronic Prior Treatment with Ethanol
