Abstract
Selective uptake of H3-testosterone in human benign prostatic hypertrophy (BPH) has been demonstrated by in vitro and in vivo studies. 5α-dihydrotcstosteronc and 5α,3α-androstanediol are by far the major metabolites of testosterone. Progesterone and gestonorone capronate are competitive inhibitors of testosterone metabolism in BPH. These progestagens are taken up in preference to testosterone into prostatic cells. The subsequent formation of dihydrotestostcronc is inhibited, whereas cyproterone acetate does not influence the reduction of testosterone. Animal studies support the concept that this antiandrogcn acts by interfering with the binding of dihydrotestosterone to an intranuclear receptor.
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