Abstract
The mechanism of the antiandrogenic effect of 5,10-seco-19-norpregnane-4,5-diene-3,10,20-trione (secosteroid), reputedly an irreversible inhibitor of 5α -reductase, was investigated. Its addition (10 μM) to culture media effectively suppressed the synthesis of rat epididymal proteins specifically induced by 0.1 μM testosterone (T) or dihydrotestosterone (DHT). Under the same conditions, secosteroid did not change the rate at which labeled T was metabolized to 5α -reduced compounds. In a comparative study, secosteroid inhibited 5α -reductase in an isolated microsomal fraction while not affecting the enzyme activity in minced tissue. Secosteroid was shown to be a competitor of the binding of [ 3H]T and [ 3H]DHT (both at 4nM) to the epididymal cytosol androgen receptor, with ID 50 of 1 μM for the former and 4μM for the latter, thus explaining the mechanism involved in its antiandrogenic properties.
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