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- W2079083023 abstract "Preliminary studies indicated that low doses of cyproterone acetate (Cyp Ac) potentiated the action of testosterone on mouse kidney. This unexpected observation prompted a more extensive evaluation of several progestins (progesterone, progesterone caproate, Cyp Ac, medroxyprogesterone acetate and megestrol acetate) as well as nonprogestational antiandrogens (flutamide, BOMT, cyproterone). The effects of these agents, both alone and in combination with testosterone, on the kidney arid male reproductive tract of the mouse were determined. Testosterone (0.1 mg/day) resulted in a 2- to 5-fold increase in kidney β3-glucuronidase activity after 6 days of treatment. Of the progestins tested, only medroxyprogesterone acetate (MPA) and megestrol acetate stimulated β-glucuronidase in the kidney. Androgen-insensitive (tfm/y) mice with defective androgen receptors did not respond to high doses of MPA, suggesting that androgens and progestins share a common mechanism of action on kidney. With the exception of progesterone, all the progestins studied potentiated testosterone action on kidney but not on prostate or preputial glands. The dose required to elicit this synergism varied with the progestin. Cyp Ac was the most potent in this regard with 0.1–0.5 mg/day potentiating and 1.0–10 mg/day inhibiting testosterone (0.1 mg/day) action. Megestrol acetate, like Cyp Ac, had both a syn- and antiandrogenic effect. That the synandrogenic action of these compounds was. related to their progestational ratjier than their antiandrogenic activities was suggested by the observations that none of the 3 nonprogestational antiandrogens tested potentiated androgen action. The evidence from this and other studies suggests that progestins may simulate the effects of androgens on some tissues by interaction with the androgen receptor directly or after biotransformation to C19 steroids: More importantly, however, progestins can modify androgen action by either potentiation or inhibition. It is possible that both the synandrogenic and the antiandrogenic activity of progestins may be explained by their interaction with the androgen receptor. To accommodate this hypothesis, it is necessary to postulate that the androgen receptor is an allosteric protein with multiple binding sites which will accept both androgens and progestins. (Endocrinology95: 1589 1974)" @default.
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- W2079083023 date "1974-12-01" @default.
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- W2079083023 title "Synandrogenic and Antiandrogenic Effect of Progestins: Comparison with Nonprogestational Antiandrogens<sup>1</sup>" @default.
- W2079083023 doi "https://doi.org/10.1210/endo-95-6-1589" @default.
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