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Biology of Reproduction, Vol 14, 332-338, Copyright © 1976 by Society for the Study of Reproduction
Androstane 3
, 17
Diol on the Spermatogenesis of
Immature Rats
1 Centro de Investigaciones Endocrinológicas (C.E.D.I.E.),
División de Endocrinología and División de Patología,
Hospital Municipal de Niños, Gallo 1330.
Buenos Aires, Argentina The action of testosterone (T), dihydrotestosterone (DHT) and 5
-androstane 3
, 17
diol
(Diol) on the seminiferous epithelium of immature estrogen-treated rats was studied. Quantitative
histological evaluation was performed and testicular proteins and androgens contents were
determined. Estradiol benzoate (E2B) treatment resulted in a severe testicular atrophy with a
reduction of 50 percent in the testicular weight and protein content. In the estrogen treated rats
the levels of androgens in the testicular tissue were undetectable. Histologically, the germinal
epithelium showed a marked decrease of cell types, particularly the meiotic spermatocytes and
young spermatids. In E2B+T, E2B+DHT and E2B+Diol-treated animals testicular weight decreased
only 10 to 20 percent, with a normal concentration of testicular proteins. In E2B+T-treated
animals the three androgens were found in the testis, and in both E2B+DHT and E2B+Diol-treated
rats, high levels of these androgens were found, but testosterone was not detectable. In every case
the levels of Diol were higher than those of DHT. A diminution of spermatogonia, similar to that
found in E2B-treated animals was noted in all androgen-treated rats. Meiotic spermatocytes
showed, however, a significant increase in relation to E2B-treated rats, even though a decrease was
observed when compared with the normal controls. Spermatid diminution was only partially
prevented in E2B+DHT and E2B+Diol-treated groups, but not in E2B+T treated rats. It is
concluded that T, DHT and Diol, exert a meiotic stimulatory effect. In the case of DHT and
Diol-treated animals, absence of testicular testosterone indicates that both 5
reduced metabolites
are biologically active in the prevention of testicular atrophy induced by E2B at the time of
initiation of spermatogenesis.
Accepted on November 19, 1975
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