2006International Journal of UrologyRequires access

Testosterone administration promotes regeneration of chemically impaired spermatogenesis in rats

Koichi Udagawa, Takehiko Ogawa, Takeshi Watanabe, Y Tamura, Kaoru Kita, Yoshinobu Kubota

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Abstract

AIM: It has been proposed that gonadotropin-releasing hormone (GnRH) analog administered after testicular damage stimulates the recovery of spermatogenesis. However, GnRH analogs suppress the function of sex accessory organs. In this study, we investigated whether testosterone also stimulates the regeneration of rat spermatogenesis after exposure to busulfan. METHODS: Male Fisher rats were divided into three groups of five each and all rats were treated with busulfan, 25 mg/kg, intraperitoneally at week 0. Group A served as the control. The other two groups received testosterone enanthate, 8 mg/kg, subcutaneous injections at 3 week intervals two times before (group B) or three times after (group C) busulfan. States of spermatogenesis were evaluated by histology and by the number of spermatid nuclei per testis at week 25. RESULTS: The mean percentage of 'recovered' seminiferous tubules plus or minus standard deviation was 10.3 +/- 7.8% in group A and 2.1 +/- 1.2% in group B. In both groups, more than 80% of the tubules remained degenerated. However, testes of group C rats showed an improvement of up to 37.1 +/- 20.5% (P < 0.05). The significant recovery of spermatogenesis was also demonstrated in group C by counting the number of spermatid nuclei per testis ([78.8 +/- 57.5] x 106). However, the count was only (7.6 +/- 13.5) x 106 and (0.52 +/- 1.0) x 106 in group A and B, respectively. CONCLUSIONS: Testosterone administration after severe testicular damage enhanced the regeneration of spermatogenesis in rats. We assumed that supplementary doses of testosterone would be more practical for clinical application than GnRH analogs, because exogenous testosterone maintains androgenicity.

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AIM: It has been proposed that gonadotropin-releasing hormone (GnRH) analog administered after testicular damage stimulates the recovery of spermatogenesis. However, GnRH analogs suppress the function of sex accessory organs. In this study, we investigated whether testosterone also stimulates the regeneration of rat spermatogenesis after exposure to busulfan. METHODS: Male Fisher rats were divided into three groups of five each and all rats were treated with busulfan, 25 mg/kg, intraperitoneally at week 0. Group A served as the control. The other two groups received testosterone enanthate, 8 mg/kg, subcutaneous injections at 3 week intervals two times before (group B) or three times after (group C) busulfan. States of spermatogenesis were evaluated by histology and by the number of spermatid nuclei per testis at week 25. RESULTS: The mean percentage of 'recovered' seminiferous tubules plus or minus standard deviation was 10.3 +/- 7.8% in group A and 2.1 +/- 1.2% in group B. In both groups, more than 80% of the tubules remained degenerated. However, testes of group C rats showed an improvement of up to 37.1 +/- 20.5% (P < 0.05). The significant recovery of spermatogenesis was also demonstrated in group C by counting the number of spermatid nuclei per testis ([78.8 +/- 57.5] x 106). However, the count was only (7.6 +/- 13.5) x 106 and (0.52 +/- 1.0) x 106 in group A and B, respectively. CONCLUSIONS: Testosterone administration after severe testicular damage enhanced the regeneration of spermatogenesis in rats. We assumed that supplementary doses of testosterone would be more practical for clinical application than GnRH analogs, because exogenous testosterone maintains androgenicity.

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Available abstract

AIM: It has been proposed that gonadotropin-releasing hormone (GnRH) analog administered after testicular damage stimulates the recovery of spermatogenesis. However, GnRH analogs suppress the function of sex accessory organs. In this study, we investigated whether testosterone also stimulates the regeneration of rat spermatogenesis after exposure to busulfan. METHODS: Male Fisher rats were divided into three groups of five each and all rats were treated with busulfan, 25 mg/kg, intraperitoneally at week 0. Group A served as the control. The other two groups received testosterone enanthate, 8 mg/kg, subcutaneous injections at 3 week intervals two times before (group B) or three times after (group C) busulfan. States of spermatogenesis were evaluated by histology and by the number of spermatid nuclei per testis at week 25. RESULTS: The mean percentage of 'recovered' seminiferous tubules plus or minus standard deviation was 10.3 +/- 7.8% in group A and 2.1 +/- 1.2% in group B. In both groups, more than 80% of the tubules remained degenerated. However, testes of group C rats showed an improvement of up to 37.1 +/- 20.5% (P < 0.05). The significant recovery of spermatogenesis was also demonstrated in group C by counting the number of spermatid nuclei per testis ([78.8 +/- 57.5] x 106). However, the count was only (7.6 +/- 13.5) x 106 and (0.52 +/- 1.0) x 106 in group A and B, respectively. CONCLUSIONS: Testosterone administration after severe testicular damage enhanced the regeneration of spermatogenesis in rats. We assumed that supplementary doses of testosterone would be more practical for clinical application than GnRH analogs, because exogenous testosterone maintains androgenicity.

Key concepts: Spermatogenesis, Testosterone (patch), Spermatid, Medicine, Busulfan, Endocrinology, Internal medicine, Andrology

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