Administration of testosterone inhibits initiation of seminal tubule growth and decreases Sertoli cell number in the earliest period of rat's postnatal development.

摘要

Sertoli cell (SC) number determines testes size and their capacity to produce spermatozoa. In the rat SC proliferate until 15th postnatal day (PND). Their proliferation is stimulated by FSH and inhibited by estradiol, but the role for androgens is uncertain. In this study we analyzed the effects of testosterone administration on testes growth and SC number in relation to timing of the treatment. Male rats were injected with 2.5 mg of testosterone propionate (TP) from birth until 5th PND and autopsied either on 6th PND [TP1-5(6)] or on 16th PND [TP1-5(16)] (transient administration). Other rats received TP from birth until 15th PND [TP1-15] or between 5th and 15th PND [TP5-15] continuously and were autopsied on day 16th. Control groups (C) received vehicle. In the Cs serum level of estradiol was 20-fold higher (p<0.001) and FSH was 1,7-fold higher (p<0.05) on 6th PND than on 16th PND, while testosterone did not change. After TP blood level of testosterone increased 2200-fold on 6th PND (p<0.05), and 8-fold on 16th PND. In turn, continuous TP administrations resulted on 16th PND in the increase in testosterone serum level by 2000-times of C without influence on FSH. While the treatment from birth either during initial 5 days or continuously until 15th day decreased testicular weight (p<0.001), tubule length (p<0.05) and SC number (p<0.001), the treatment initiated on 5th PND had no effects. TP reduced serum estradiol level on 6th PND by 13-fold (p<0.01), but doubled it on 16th PND. Conclusion: Neonatal rats secrete estradiol and FSH in the amounts greatly extending those presented during further development. Testosterone inhibits testicular growth and SC number acting during first 5 neonatal days by decreasing FSH secretion, but is not effective during further development. Direct inhibitory influence of testosterone or trough its increased aromatisation to estradiol beyond neonatal period may be responsible for sustained inhibition of testes growth and SC number during infancy.