Effects of androgen and antiandrogen treatment on canine prostatic arginine esterase

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Abstract
A series of experiments were conducted to investigate the regulation of the primary secretory protein of the canine prostate, arginine esterase, by androgens and/or new antiandrogens under development. In the first experiment, castration decreased (P2) or the i.m. injection of 25 mg 3α‐diol and 0.25 mg E2 for 12 weeks resulted in a dose‐dependent increase (P2 silastic capsules) of castrate dogs for 12 weeks resulted in prostatic arginine esterase activity of 17.8±2.3 μmole/min/mg. Co‐administration of the steroidal androgen receptor antagonist Win 49,596 (WIN) at doses of 0.625, 2.5, 10, or 40 mg/kg/day p.o., dose‐dependently inhibited (PPP<0.05) arginine esterase levels (17.0±1.0, 16.3±1.5, 10.2±1.2, and 3.9±2.5 μmole/min/mg, respectively) compared to intact controls (14.4±1.2 μmole/min/mg). Histomorphologic and ultrastructural evaluation of prostates from dogs indicated that antiandrogen treatment resulted in glandular epithelial atrophy as well as a reduction in the number of secretory granules. The results of these experiments support that canine prostatic arginine esterase activity is under androgenic control, can be inhibited by antiandrogen treatment and may serve as a functional marker of the androgenic state of the prostate. Whether the effects of androgen and antiandrogens on prostatic arginine esterase is direct or indirect due to a general inhibitory effect on secretory epithelial cell function requires additional study. Furthermore, subject to further evaluation, the steroidal androgen receptor antagonist, Win 49,596, may be useful in the treatment of androgen‐dependent disorders of the prostate.