Loss of hepatic monoamine oxidase activity resulting from replacement of its coenzyme flavin.

Abstract

SummaryWhen 7-methyl-8-ethyl-10-(1′-D-ribityl)isoalloxazine (7-methyl-8-ethylflavin or 8-Et) is utilized in place of riboflavin in rat tissues, its coenzyme function for hepatic MAO is so low that enzyme activity is virtually eliminated. The present evidence suggests that 8-Et cannot be covalently bound to the enzyme. The absence of hepatic MAO activity when 8-Et is utilized is confirmed by the inability of rats using this flavin to survive the stress of administered L-DOPA. The use of 7-ethyl-8-methyl-10-(1′-D-ribityl)isoalloxazine (7-ethyl-8-methylflavin or 7-Et) causes a severe decrease in hepatic MAO, however, the activity of the enzyme is great enough to provide evidence that 7-Et is covalently bound to the enzyme. Rats utilizing 7-Et as well as riboflavin-deficient rats are able to survive the stress of administered L-DOPA. Hepatic MAO may not be an essential enzyme for survival of the laboratory rat.