1988 Fiscal Year Final Research Report Summary
Study on control mechanism of human testicular function
Project/Area Number |
62570724
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Research Category |
Grant-in-Aid for General Scientific Research (C)
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Allocation Type | Single-year Grants |
Research Field |
Urology
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Research Institution | Osaka University |
Principal Investigator |
MASAHIRO NAKAMURA Assistant Professor, Faculty of Medicine, Osaka University, 医学部, 助手 (60135689)
|
Co-Investigator(Kenkyū-buntansha) |
YUKITO KOKADO Assistant Professor, Faculty of Medicine, Osaka University, 医学部, 助手 (30186639)
AKIHIKO OKUYAMA Assistant Professor, Faculty of Medicine, Osaka University, 医学部, 助教授 (20093388)
|
Project Period (FY) |
1987 – 1988
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Keywords | Testis / FSH receptor / LH receptor / hMG / hCG / GnRH / エストローゲン |
Research Abstract |
1. Reduction of human testicular FSH receptors induced by hMG were estimated in vivo and in vitro. After a single injection of hMG, the number of FSH receptors were significantly reduced for 5 days. In experiments in vitro using organ culture technique, an exposure to hMG for 24 h induced a dose-related loss of FSH receptors for 7 days. 2. Changes of human testicular LH receptors induced by HCG were estimated in vivo and in vitro. After a single injection of HCG, the number of LH recweptors were significantly reduced for 5 days. In experimentfs in vitro using organ culture technique, an exposure to HCG for 24 h induced a dose-related loss LH receptors for 7 days. Results obtained from these two experiments (1,2) clarified that hMG and hCG induced down-regulation of human testicular FSH and LH receptors for several days. 3. Effect of estrogen treatment on testicular FSH and LH receptors were investigated. Testicular LH receptors were decreased after the treatment, while testicular FSH receptors were not changed after the treatment. 4. Effect of GnRH analog treatment on human testicular FSH and LH receptors were investigated in vivo and in vitro. Testicular FSH and LH receptors were not changed after the treatment. Results from above experiments (3,4), the mechanism of antiandrogen effect of prostatic cancer were clarified.
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