Abstract
Castration atrophy of the prostates and seminal vesicles of male rats was not accompanied by a decrease in beta-glucuronidase concn. although the admn. of estradiol benzoate to castrated males effected a marked rise in the enzyme activity of these organs. The proliferation of deciduomata in the rat and endometria of rabbits under the influence of progesterone was not paralleled by an increase in beta-glucuronidase activity. Ovariectomy in the rabbit and pseudopregnancy in the rat resulted in a decrease in uterine enzyme concn. Progesterone, when admd. to ovariectomized female rats, while effective in antagonizing the growth effects of estradiol benzoate on the rat uterus, failed to inhibit the estrogen-induced increase in uterine enzyme activity. Testosterone propionate increased the uterine beta-glucuronidase concn. of ovariectomized rats to a value which was half that found in uteri stimulated to the same wt. with estrogen. Ovariectomy of immature rats resulted in a decrease in uterine wt. which was not accompanied by a decrease in enzyme activity. The admn. of estrogen to these animals while effecting a 156% increase in uterine wt., was without effect on the uterine enzyme concn. The proliferative changes observed in mammary glands of estrogen treated female rats were accompanied by a rise in beta-glucuronidase activity, but this hormone was without effect in hypophysectomized females in terms of mammary growth and mammary enzyme concn. The uteri of the latter animals, however, did respond to hormone treatment by an increase in enzyme activity. Thus, changes in beta-glucuronidase activity are not a generalized phenomenon associated with growth per se and the evidence presented lends support to the view that these changes may be specifically related to the action of estrogenic hormones.