The alterations of the microsomal aryl hydrocarbon hydroxylase system in mice during riboflavin depletion and repletion have been examined. During the development of riboflavin deficiency, there was a decrease in the activity of the flavoprotein NADPH-cytochrome c reductase accompanied by an increase in cytochrome P-450 concentration. The aryl hydroxylase activities of the deficient animals were only slightly lower than the controls when isolated microsomes were used for the assay and the extent of decrease was more pronounced when liver homogenates were used for the assay. Upon repletion of flavin to the deficient mice, there were sharp rises in both the NADPH-cytochrome c reductase and aryl hydroxylase activities and a moderate decrease in cytochrome P-450 concentration in the first 2 days. The aryl hydroxylase activity of the microsomes of deficient mice can be elevated by preincubating with FAD or FMN, suggesting that the flavin coenzyme and hence the holo-reductase is rate limiting for the overall hydroxylation. During the recovery from riboflavin deficiency, the aryl hydroxylase can be induced by 3-methylcholanthrene to a greater extent than with the controls. The implications of these observations are discussed.
All Science Journal Classification (ASJC) codes
- Molecular Biology