Effect of hypophysectomy and castration on hepatic, pulmonary and intestinal aryl hydrocarbon hydroxylase activities in the rat.

The importance of the pituitary gland in the regulation of hepatic drug and steroid metabolism has been previously demonstrated. The present studies involving castrated and hypophysectomized-castrated male rats confirm that the pituitary gland is essential for the expression of the effects of testosterone and dihydrotestosterone on hepatic aryl hydrocarbon hydroxylase (AHH) activity and cytochrome P-450 content. Furthermore, the pituitary gland is required for the inhibitor effects of estradiol on hepatic AHH activity in castrated male rats. Neither castration nor hypophysectomy-castration alters AHH activity in lungs or intestine. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) administration to control animals increased AHH activity by 2-, 15-, and 66.5-fold in liver, lungs and intestinal microsomes, respectively. Hypophysectomy did not prevent TCDD from acting as an inducer of AHH in any of the tissues, although the AHH activities in the three tissues were approximately 60% lower in TCDD-treated, hypophysectomized animals as compared to TCDD-treated, sham-operated control animals treated with TCDD. The results indicate that the pituitary gland plays an important role in regulating the extent of AHH induction in liver, lung and intestine.