Effects of Estrogen Treatment on Human Testicular Unconjugated Steroid and Steroid Sulfate Production in Vivo*

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Abstract
To analyze the relationships between human testicular unconjugated and sulfate-conjugated steroids, we investigated the effects of estradiol [polyestradiol phosphate (E2)] and a synthetic estrogen [diethylstilbestrol diphosphate (DESDP)] on testicular, spermatic venous, and peripheral venous serum concentrations of these compounds. Six unconjugated steroids and 4 steroid sulfates were measured by specific RIAs after chromatography in 27 prostatic carcinoma patients without preceding endocrine therapy and in 29 patients castrated after E2 or DESDP treatment. E2 treatment decreased testicular concentrations of pregnenolone, testosterone (T), and 5 a-dihydrotestosterone (DHT). Testicular androstenedione concentrations were also decreased, whereas progesterone concentrations increased, and there were decreased testicular concentrations of dehydroepiandrosterone sulfate (DHEA-SO4) and 5-androstene-3β,17β-diol sulfate. Spermatic venous concentrations of 17a-hydroxyprogesterone (17-OHP), T, and DHT as well as those of DHEA-SO4 and T sulfate were decreased after E2 treatment, and in the case of T, DHEASO4, and 17-OHP, this change was also reflected in peripheral serum concentrations. In the doses used, DESDP treatment was clearly more efficient than E2, and it decreased testicular concentrations and the secretion of all unconjugated and sulfated steroids. However, the difference between the effects of E2 and DESDP on peripheral serum steroid concentrations was mainly limited to those most clearly of testicular origin (17-OHP, T, and DHT). These findings show that estrogen treatment has an inhibitory effect on human testicular steroid sulfate production in vivo in addition to the known depressing effect on unconjugated steroid production. The results from E2-treated patients suggest that the changes in steroid sulfates are secondary to those in unconjugated steroids. The most probable sites of inhibition are a step before pregnenolone and the enzymes 17α-hydroxylase and 17–20-desmolase in the biosynthetic chain leading to T synthesis.