A 10-fold difference in activity of the liver enzyme, N1-methylnicotinamide oxidase, was found between mice of strains C57BL/6 and DBA/2. The Km value for the enzyme from DBA/2 mice with low activity was twice that of the enzyme from C57BL/6 mice. The activity difference segregated in F1, F2, and backcross generations as though it were genetically controlled by a single autosomal locus with alleles acting in an additive manner. The 2- to 4-fold higher activity in the adult male as compared to the adult female within each strain indicated that hormonal control of N1-methylnicotinamide oxidation was operating in addition to direct genetic control. Evidence from immature mice and from castrated and testosterone-treated animals supports the role of testosterone in increasing N1-methylnicotinamide oxidation.
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Huff et al. (1967) studied this question.
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