Department of Physiology, Royal Veterinary College, Royal College Street, London, NW1 OTU
(Received 19 February 1976)
Administration of testosterone to newborn female rats suppresses cyclic gonadotrophin secretion and sexual receptivity in adulthood (Barraclough, 1961). This effect probably depends upon the conversion of testosterone to oestrogen in the brain (Reddy, Naftolin & Ryan, 1974; Doughty, Booth, McDonald & Parrott, 1975). Hydroxylation of the androgen molecule at carbon-19 is the initial step in aromatization (Gual, Morato, Hayano, Gut & Dorfman, 1962), and injecting 19-hydroxytestosterone (17β-hydroxy-4-androsten-19-ol-3-one; 19HT) into neonatal female rats prevents cyclic ovulation in adulthood (McDonald & Doughty, 1974). On the other hand, 5α-reduction of testosterone blocks conversion to oestrogen as the product, dihydrotestosterone (17β-hydroxy-5α-androstan-3-one; DHT), cannot be aromatized. Since DHT does not affect sexual differentiation of the brain (McDonald & Doughty, 1974), the non-aromatizable 5α-reduced form of 19HT (17β-hydroxy-5α-androstan-19-ol-3-one; 5α-19HT) should similarly be ineffective. This study compares the defeminization induced in
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