PROTECTION FROM PROCARBAZINE-INDUCED TESTICULAR DAMAGE BY HORMONAL PRETREATMENT DOES NOT INVOLVE ARREST OF SPERMATOGONIAL PROLIFERATION

Hormone treatments that suppress sperm production enhance the recovery of spermatogenesis after gonadal exposure to various cytotoxic agents , It has generally been assumed that the mechanism of protection invol ved an arrest of spermatogonial kinetics. To test this hypothesis crit ically, we examined spermatogonial kinetics and numbers in rats in whi ch the completion of spermatogenesis was suppressed with a 6-week test osterone plus 17 beta-estradiol treatment that protected the testis fr om procarbazine-induced damage. Histological examination showed that t he numbers of A-aligned, intermediate, and B spermatogonia and prelept otene spermatocytes and their mitoses were unaffected by testosterone plus 17 beta-estradiol treatment. Flow cytometric analysis of bromodeo xyuridine-labeled cells showed that the percentage of diploid cells un dergoing DNA synthesis, the progression of B spermatogonia and prelept otene spermatocytes through S-phase, the division of intermediate and B spermatogonia, the entry of intermediate spermatogonia into their ne xt S-phase as type B cells, and the progression of cells through meiot ic prophase were either unchanged or very slightly increased, Thus, ch anges in spermatogonial numbers or suppression of their proliferation cannot account for protection of spermatogenesis from exposure to cyto toxic agents.