Effect of various xenobiotics and steroids on aryl hydrocarbon hydroxylase activity of intestinal and hepatic microsomes from male rats.
The effects of four solvents and 37 xenobiotics and endogenous steroids on intestinal and hepatic microsomal aryl hydrocarbon hydroxylase (AHH) activity were determined. In general, hepatic AHH was more sensitive than intestinal AHH to inhibition by a wide variety of xenobiotics. Acetone, ethanol, dimethyl formamide, triamcinolone acetonide, 17 alpha-propyltestosterone, metronidazole, cimetidine and butylated hydroxyanisole (BHA) activated or stimulated intestinal AHH activity while inhibiting hepatic AHH activity at the same concentrations. Ethoxyquin, progesterone, pregnenolone acetate, deoxycorticosterone acetate, tamoxifen and SKF 525-A exerted markedly different concentration-dependent inhibitions of intestinal and liver AHH activities. The most potent inhibitors of AHH activity were captan, BHA, chlorpromazine, thioridazine, disulfiram and menadione. The ability of steroids to inhibit AHH activity correlated well with lipophilicity.
D000818:Animals; D001189:Aryl Hydrocarbon Hydroxylases / Q000378:metabolism*; D007422:Intestines / Q000187:drug effects / Q000201:enzymology*; D007700:Kinetics; D008297:Male; D008862:Microsomes, Liver / Q000187:drug effects / Q000201:enzymology*; D051381:Rats; D011919:Rats, Inbred Strains; D012995:Solubility; D012997:Solvents / Q000494:pharmacology; D013256:Steroids / Q000494:pharmacology*
D012997:Solvents; D013256:Steroids; D001189:Aryl Hydrocarbon Hydroxylases