Enzymatic sulfation of steroids: II. The control of the hepatic cortisol sulfotransferase activity and of the individual hepatic steroid sulfotransferases of rats by gonads and gonadal hormones

Abstract

Ovariectomy has relatively little effect on hepatic cortisol sulfotransferase activity (HCSA) in female rats, diminishing it only 30%. On the other hand, castration more than doubles HCSA in males. HCSA is due to 3 steroid sulfotransferases, STI, STII, and STIII. Its dimunition in ovariectomized rats is due to decreased STI and STII. Castration of males results in elevation of STII. Thus, ovaries appear to stimulate STI and STII production and testes appear to inhibit production of STII and perhaps STI. Studies with testosterone and estradiol-17beta support a role for sex hormones as mediators of gonadal effects on HCSA, by stimulating or inhibiting production of the individual enzymes. Estradiol-17beta administration reverses the effect of ovariectomy on HCSA. Testosterone administration to intact or castrated females decreases HCSA by 60-70%, due to disappearance of all STI and most STII activity. Thus, androgen administration appears to suppress both STI and STII production. In intact males testosterone administration elevates HCSA 70-80% due to increased STIII. Estradiol-17beta administration to intact or castrated males elevates HCSA 9-10-fold. In intact animals this is due to elevated STI and STII but not STIII. In castrates all three enzymes are elevated by the estrogen.