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* To whom correspondence should be addressed. E-mail: karen.porter{at}amedd.army.mil.
Irradiation of LBNF1 rat testes induces spermatogonial differentiation arrest, which can be reversed by GnRH-antagonist-induced suppression of intratesticular testosterone (ITT) and FSH. Although exogenous estrogen treatment also enhanced spermatogenic recovery, as measured by the tubule differentiation index (TDI), it was not clear whether estrogen stimulated spermatogonial differentiation only by further suppressing ITT or by an additional independent mechanism as well. To resolve this question, we performed the following experiments. At 15 weeks after irradiation, rats were treated with GnRH antagonist; some also received 17-
estradiol (E2) and were killed 4 weeks later. GnRH-antagonist treatment increased the TDI from 0% to 8%, and addition of E2 further increased TDI to 39%. However, E2 addition further reduced ITT from 7 ng/g-testis observed with GnRH-antagonist to 3 ng/g-testis, so decreased ITT levels may have contributed to recovery. Next GnRH-antagonist-treated rats were given exogenous testosterone and flutamide to stabilize ITT levels and block its action. This increased TDI slightly from 8% to 13%, but the further addition of E2 significantly raised the TDI to 27%, indicating it acted by a mechanism independent of ITT levels. Plots of TDI for all treatment groups versus ITT, FSH, or a linear combination of ITT and FSH showed that treatments including E2 produced higher TDI values than did treatments without E2. These results indicate that there was an effect of E2 on spermatogonial differentiation due to an additional direct action on the testis that is unrelated to its suppression of testosterone or gonadotropins.
Key words: Spermatogenesis •
Testis •
estrogen •
irradiation •
spermatogonial differentiation •
testosterone
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