QSOX sulfhydryl oxidase in rat adenohypophysis: localization and regulation by estrogens

The expression of the rat quiescin sulfhydryl oxidase (rQSOX) and its putative regulation by estrogens were investigated in the adenohypophysis. Immunohistochemical observations revealed that rQSOX protein is abundantly expressed throughout the anterior lobe of the pituitary, and can be found in almost all the different cell populations. However, as shown by double immunohisto-chemistry, the cells displaying the strongest rQSOX labeling belong to a subset of gonadotrophs. Immunoelectron microscopy showed that, in adenohypophyseal cells, the protein is linked to the membranes of the rough endoplasmic reticulum, the Golgi apparatus and to dense-core secretory granules. These results are consistent with the secretion of the protein and its presumed role in the extracellular matrix. According to its sulfhydryl oxidase function, rQSOX could also participate in the intracellular folding of secreted proteins or hormones like LH and FSH and act as an endogenous redox modulator of hormonal secretion. A semiquantitative RT-PCR analysis of rQSOX level across the estrous cycle and the fact that chronic administration of 17 beta-estradiol to ovariectomized rats led to a sustained up-regulation of rQSOX in the pituitary suggest that rQSOX expression is controlled by sex hormone levels. Further investigations are needed in order to elucidate its precise roles in that gland and the mechanisms of its regulation.     

Action of 5 alpha-reduced diols on the uterus of sexually immature rats

The effect of testosterone (T), 5 alpha-androstane-3 alpha, 17 beta-diol (3 alpha-diol) and 5 alpha-and-rostane-3 beta, 17 beta-diol (3 beta-diol) on the uterus of immature rats was studied in combined with estradiol-17 beta (E2) and separate intraperitoneal administration. Repeated administration of T (100 micrograms per 100 g of body mass) caused no changes in the uterine mass whereas a similar dose of 3 alpha-diol resulted in a noticeable effect (0.05 greater than greater than p less than 0.1). 3 beta-diol administered repeatedly at a dose of 1.00 microgram per 100 g of body mass, produced the same uterotropic effect like E2. In combined administration of the above androgens (100 micrograms) and E2 (10 micrograms) 3 alpha-diol only inhibited the uterotropic effect of E2.     

The effect of conjugated estrogens on the renin-angiotensin system.

In a survey of 3 California communities by the Stanford Heart Disease Prevention Program, we obtained data on blood pressure, medications, age, height and weight, blood for measurement of plasma renin activity (PRA), plasma renin concentration (PRC), plasma renin reactivity (RR), and plasma renin substate concentration (PRS), and urine for measurement of urinary sodium and creatinine. No effect of conjugated estrogens (Premarin) on blood pressure could be discerned when the blood pressure, corrected for age and relative weight, of 575 women on no medication was compared to that of 82 women taking only Premarin. Premarin increased PRA, PRS, and RR, but had no effect on PRC. We also found in both Premarin-treated woman and controls 1) that RR was positively correlated with PRS, and 2) that PRA is dependent on PRC and PRS. These data indicate that the reninrenin substrate reaction of plasma, even at normal substrate concentration, is strongly deprendent on PRS.