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The difference between in vivo and in vitro inhibitory effects on epididymal 5 alpha-reductase was investigated by using epididymides obtained from patients treated with chlormadinone acetate (6-chloro-3,20-dioxo-4,6-pregnadien-17-yl acetate, CMA) or ethinylestradiol (17 alpha-ethynyl-1,3,5(10)-estratriene-3,17 beta-diol, EE2). In the in vitro study CMA exhibited competitive inhibition, whereas EE2 was a noncompetitive inhibitor of human epididymal 5 alpha-reductase. Their in vitro inhibitory effects were weak compared with the effect of finasteride ((-)-N-tert-butyl-3-oxo-4-aza-5 alpha-androst-1-ene-17 beta carboxamide), a steroidal 5 alpha-reductase inhibitor. The Ki values of CMA, EE2, and finasteride were 1.4 x 10(-5) M, 1.5 x 10(-5) M, and 1.3 x 10(-9) M, respectively. Despite their weak in vitro inhibitory potency, CMA and EE2 strongly inhibited testosterone 5 alpha-reductase in vivo. There were regional differences in inhibitions by CMA and EE2 on human epididymal 5 alpha-reductase activity depending on the site of the epididymis; the efferent ductules, the head, the body or the tail. In vivo administration of CMA reduced epididymal 5 alpha-reductase activity by 49.7% to 89.4%. In vivo administration of EE2 reduced epididymal 5 alpha-reductase activity by 82.7% to 96.3%. The apparent Km values for the enzyme in patients treated with CMA or EE2 and untreated patients did not differ significantly. The Vmax values were significantly decreased in treated patients. These findings suggest that the marked in vivo inhibition of 5 alpha-reductase induced by CMA and EE2 was not related to the direct action of these compounds, but resulted from a reduction in the amount of the enzyme.

Effects of Chlormadinone Acetate and Ethinylestradiol Treatment on Epididymal 5.ALPHA.-Reductase Activities in Patients with Prostate Cancer.