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Gunapala Shetty1 , Gene Wilson1 , Marvin L Meistrich1 *
University of Texas, MD Anderson Cancer Center, Houston, Texas. 1
Previous studies have shown that suppression of testosterone (T) production by GnRH-analogues stimulates recovery of spermatogenesis in rats after irradiation and other toxic exposures. To determine whether the inhibition of spermatogenesis following irradiation was mediated through T or its metabolites, particularly estrogen (E), the effects of T, estradiol (E2) and an aromatase inhibitor (AI) on the GnRH-antagonist stimulated recovery of spermatogenesis was examined. Rats were given 5 Gy of irradiation and treated during weeks 3-7 after irradiation with a GnRH-antagonist Cetrorelix. This treatment restored the percent of repopulating seminiferous tubules (RI) and sperm head count (SHC) to 52% and 4.1 × 106 respectively from the irradiation alone values of 0. Testosterone in 6-cm silastic capsules drastically inhibited the Cetrorelix stimulated repopulation (RI = 3.6%; SHC = 6.6 × 103). Treatment with the AI (CGP 47645) alone did not affect the recovery of spermatogenesis. However, AI enhanced the Cetrorelix stimulated spermatogenic recovery (RI = 98%; SHC = 5.9 × 106) but could not reverse the T-induced inhibition of spermatogenic recovery (RI = 0.5%; SHC < 6.6 × 103). Although these results indicated that estrogens might have an inhibitory role in the recovery of spermatogenesis after irradiation, E2 itself given in 0.5-cm silastic capsules did not suppress and may even have enhanced the spermatogenic stimulatory effect of GnRH-antagonist (RI = 79%) . We conclude that T or its metabolites other than E2 inhibit spermatogenic recovery after irradiation. The mechanisms will be further discussed based on measurements of levels of the above hormones present during the treatment period.
This abstract is being presented on Monday, August 2 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.