Since dihydrotestosterone rather than testosterone is the principal intracellular androgen in the prostate and since dihydrotestosterone concentration is increased in hypertrophie prostate of dog and man, long term studies were undertaken to test the possibility that unregulated production of dihydrotestosterone is the cause of prostatic hypertrophy. Control and castrated two year-old dogs were given triolein or pharmacological doses of testosterone or dihydrotestosterone (75 mg/week) for 18-24 months. Although two control dogs developed prostatic hypertrophy (15.5 and 19.4 g in weight), none of the castrated animals developed prostatic hypertrophy, despite the fact that prostate dihydrotestosterone content was as high in testosterone and dihydrotestosterone-treated dogs (1.0 and 0.7 μg dihydrotestosterone/100g tissue) as in the controls with benign prostatic hypertrophy (0.6 μg/100 g tissue). This suggested that mode of delivery of the hormone to the gland was critical or that some testicular hormone other than testosterone or dihydrotestosterone is required for the development of prostatic hypertrophy. Therefore, six aged male dogs with prostatic hypertrophy were subjected to vas duct ligation and followed for six months. No change occurred in prostate weight or the tissue content of testosterone and dihydrotestosterone. Thus, some testicular hormone other than testosterone or dihydrotestosterone is required for the development of prostatic hypertrophy.
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