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Regular Article |
b Department of Urology, Osaka University Medical School, Suita, Osaka 565-0871, Japan
c Department of Science for Laboratory Animal Experimentation, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan
d Department of Food Science and Nutrition, Mukogawa Women's University, Nishinomiya 663-8558, Japan
ABSTRACT
Male juvenile spermatogonial depletion (jsd/jsd) mice are sterile because of a failure of spermatogonial differentiation. We have previously reported the recovery of spermatogonial differentiation by suppressing the levels of gonadotropins and testosterone with Nal-Glu, a GnRH antagonist. To determine whether suppression of testosterone or the gonadotropins was responsible for spermatogenic recovery, we examined the effect of supplementation of LH or FSH along with Nal-Glu treatment. Systemic administration of flutamide, an androgen receptor antagonist, was also examined. LH supplementation elevated both serum and intratesticular testosterone levels and suppressed the recovery of spermatogonial differentiation in a dose-dependent manner. Supplementation with FSH did not affect either testosterone levels or spermatogonial differentiation. Furthermore, the mice treated with flutamide showed some recovery of spermatogonial differentiation. The overall findings revealed that testosterone action mediated by androgen receptors suppressed the spermatogonial differentiation in jsd/jsd mice and suggested that spermatogonial differentiation in the jsd mutant is highly sensitive to testosterone suppression.
First decision: 13 February 2001.
1 Correspondence: Kiyomi Matsumiya, Department of Urology, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan. FAX: 81 6 6879 3539; kmatsu{at}uro.med.osaka-u.ac.jp
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