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Protection from Procarbazine-induced Testicular Damage by Hormonal Pretreatment Does Not Involve Arrest of Spermatogonial Proliferation¹

Department of Experimental Radiation Oncology, The University of Texas M. D. Anderson Cancer Center, Houston, Texas 77030

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 involved an arrest of spermatogonial kinetics. To test this hypothesis critically, we examined spermatogonial kinetics and numbers in rats in which the completion of spermatogenesis was suppressed with a 6-week testosterone plus 17ß-estradiol treatment that protected the testis from procarbazine-induced damage. Histological examination showed that the numbers of A-aligned, intermediate, and B spermatogonia and preleptotene spermatocytes and their mitoses were unaffected by testosterone plus 17ß-estradiol treatment. Flow cytometric analysis of bromodeoxyuridinelabeled cells showed that the percentage of diploid cells undergoing DNA synthesis, the progression of B spermatogonia and preleptotene spermatocytes through S-phase, the division of intermediate and B spermatogonia, the entry of intermediate spermatogonia into their next S-phase as type B cells, and the progression of cells through meiotic prophase were either unchanged or very slightly increased. Thus, changes in spermatogonial numbers or suppression of their proliferation cannot account for protection of spermatogenesis from exposure to cytotoxic agents.

¹ Supported by Research Grants ES-08075 and CA-17364, Core Grant CA-16672, and the Cobb Endowment for Cancer Research.

² To whom requests for reprints should be addressed, at Department of Experimental Radiation Oncology, Box 66, M. D. Anderson Cancer Center, 1515 Holcombe Boulevard, Houston, TX 77030. Phone: (713) 792-3424; Fax: (713) 794-5369.

³ Present address: Department of Radiation Oncology, Thomas Jefferson University, 111 South 11th Street, Philadelphia. PA 19107.

Received 10/ 7/96. Accepted 1/16/97.

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