Pituitary-dependent masculinization of hepatic hexobarbital hydroxylase in Crl:CD-1(ICR)BR mice.
The sexual dimorphism in hepatic drug metabolism found in Crl:CD-1 mice is due to the normally repressive effects of testicular androgens on the activities of hepatic monooxygenases. The ability of testosterone to elevate the Michaelis constant (Km) and reduce the maximum velocity (Vmax) of hepatic hexobarbital hydroxylase is dependent upon the pituitary, so that in the hypophysectomized mouse androgens have no repressive effects on the activities of hepatic monooxygenases.
D000818:Animals; D002369:Castration; D005260:Female; D007016:Hypophysectomy; D007700:Kinetics; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D008862:Microsomes, Liver / Q000201:enzymology*; D006899:Mixed Function Oxygenases / Q000378:metabolism*; D010902:Pituitary Gland / Q000201:enzymology*; D012737:Sex Factors; D013739:Testosterone / Q000494:pharmacology
D013739:Testosterone; D006899:Mixed Function Oxygenases; C021352:hexobarbital hydroxylase