Journal of Clinical Endocrinology & Metabolism, Vol 50, 938-948, Copyright © 1980 by Endocrine Society

ARTICLES

Estrogen receptors in the human prostate, seminal vesicle, epididymis, testis, and genital skin: a marker for estrogen-responsive tissues?

JB Murphy, RC Emmott, LL Hicks and PC Walsh

In an effort to identify those human male sex accessory tissues that may be under the physiological influence of estrogen, cytosolic and nuclear estrogen receptors were measured with two ligand systems that used either [3H]R2858 [moxesterol(11 beta-methoxy-17-ethynyl-1,3,5,(10)- estratriene-3,17 beta-diol)] or [3H]estradiol plus 1 microM dihydrotestosterone with diethylstilbestrol to correct for nonspecific binding. In seminal vesicles, high affinity binding was identified in cytosol (6 of 7 determinations) and nuclear extract (4 of 7 determinations); in the epididymis, high affinity binding was also present in the cytosol (10 of 12 determinations) and nuclear extract (10 of 11 determinations). In contrast, no high affinity binding was demonstrated in cytosol from the testis (0 of 5 determinations) or genital skin (0 of 7 determinations), and only low levels of nuclear receptor (80 fmol/g tissue) were present in the testis (3 of 5 determinations) and genital skin (1 of 7 determinations). In nonhyperplastic prostatic tissue, high affinity binding was present [in the cytosol of periurethral zone tissue (3 of 7 determinations) and nuclear extract (1 of 7 determinations), in cytosol of peripheral zone tissue (7 of 8 determinations) and nuclear extract (4 of 7 determinations), and in prostatic carcinoma cytosol (5 of 12 determinations) and nuclear extract (10 of 13 determinations)]. In contrast, no high affinity binding was present in either cytosol or nuclear extract from benign hyperplastic prostatic tissue. The finding of estrogen receptors in the human epididymis, seminal vesicle, and prostatic carcinoma suggests that estrogen, in addition to androgen, may act in the physiological regulation of these organs. However, the direct role of estrogen in the induction and maintenance of benign prostatic hyperplasia remains to be defined.

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