In cholestatic rats, effects of phenobarbital or cholic acid on hepatic microsomal cytochrome p-450 and b₅ were investigated. The total contents of both cytochrome p-450 and cytochrome b₅ were decreased after bile duct ligation and the administration of estradiol. When cholic acid or phenobarbital was adminstrated in cholestatic rats, the decrease of cytochrome p-450 was prevented. The effects of cholic acid or phenobarbital on both ring-hydroxylation and N-hydroxylation of AAF in cholestatic rat hepatic microsomal fraction were studied. N-hydroxylation of AAF in bile duct ligated rat liver microsomes was reduced by 34%, but ring-hydroxylation was increased by 51%. In estradiol administrated rat, both ring-hydroxylation and N-hydroxylation of AAD was increased by 20 to 25%. In cholic acid administration, both ring-hydroxylation and N-hydroxylation was increased by about 10%. N-hydroxylation of AAF in phenobarbital treated rats was reduced more than ring-hydroxylation was reduced compared to the bile duct ligated group. Estradiol treated group which administrated with cholic acid or phenobarbital exhibited inhibited effects of N-hydroxylation.

Cytochrome P-450 is a terminal oxidase of the hepatic microsomal monooxygenase system associated with the oxidative biotransformation of a varity of lipophilic endogenous and exogenous compounds, and generally is assayed by CO-binding spectro-photometry of dithionite-reduced samples. In well fed normal male rats with or without stress condition, the dffect of antiulcer drug; cimetidine, sulpiride and diazepam on the level of microsomal cytochrome P-450 were determined. Only stress condition produced on significant effect in cytochrome P-450 contents. Administration of cimetidine, sulpiride and diazepam in this condition caused a 44.1%~87.5% increment in cytochrome P-450, diazepam produced the most increase. After diazepam treatment of rats, the peak position of cytochrome P-450 shifted to a longer wave length of 452 nm.