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The in-vitro metabolism of testosterone in benign and malignant prostatic tissue was examined and distinct quantitative differences between the two types of specimens were observed. The major metabolite of testosterone in the hyperplastic prostate was 5-dihydrotestosterone and a high 3(β)-hydroxysteroid dehydrogenase activity was also detected.

In the malignant tissue, 5-reductase activity was considerably reduced and there was little or no androstanediol formed; the 17β-dehydrogenase activity was, however, higher than in the benign tissue. The decrease in 5-reductase was always followed by a compensatory change in the 3(β)-hydroxysteroid dehydrogenase of the malignant prostate. The present study revealed that the ratio of the mean activities of 5-reductase to 3(β)-hydroxysteroid dehydrogenase in the two types of specimen always remained a constant.

Although the antioestrogen, tamoxifen, induced an inhibitory effect on the activities of 5-reductase and 17β-hydroxysteroid dehydrogenase in the gland, the present investigation also suggested that tamoxifen stimulated the activity of 3(3β)-hydroxysteroid dehydrogenase. In blood, the action of tamoxifen appeared to be confined to the displacement of androgens from the binding sites on the sex hormone binding globulin.