| Project/Area Number |
13670005
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General anatomy (including Histology/Embryology)
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| Research Institution | Chiba University |
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Principal Investigator |
KOMIYAMA Masatoshi Chiba University, Graduate School of Medicine, Lecturer, 大学院・医学研究院, 講師 (70175339)
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| Co-Investigator(Kenkyū-buntansha) |
ADACHI Tetsuya Chiba University, Graduate School of Medicine, Assistant, 大学院・医学研究院, 助手 (60345014)
MORI Chisato Chiba University, Graduate School of Medicine, Professor, 大学院・医学研究院, 教授 (90174375)
豊田 直二 千葉大学, 大学院・医学研究院, 講師 (00188822)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | GFP mouse / Spermatogenesis / Endocrine disruptors / Testis / Epididymis / Cell transplantation / Gene expression / DNA microarray / ホルモン受容体 / エストロゲン |
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| Research Abstract |
In order to clarify which are the target of toxicity of diethylstilbestrol (DBS), germ cells or somatic cells supporting the germ cells, in the disorder of spermatogenesis caused by neonatal exposure to DES, germ cells of GFP mice were transplanted to seminiferous tubules of C57BL/6 mice which were free of own germ cells by Busulfan treatment. First, it was confirmed that neonatal exposure to 0.5 μg/mouse/day of DES for 5 days causes spermatogenesis disorder in GFP mice as well as C57BL/6 mice. When DES-exposed germ cells were transplanted to the germ cell-free mice that were not exposed to DES, spermatogenesis occurred normally. On the other hand, when normal germ cells were transplanted to the germ cell-free mice that were neonatally exposed to DES, spermatogenesis was not normal and spermatozoa were rarely observed. From these results, it was concluded that the target of DES toxicity is not germ cells but somatic cells.
The effect of neonatal exposure to DES (5 μg/mouse/day) for 5 days on the epididymis was studied using ICR mice. By exposure to DES, (1) expression of androgen receptor protein was delayed ; (2) expression term of estrogen receptor α protein was widened and its distribution along the epididymal ductule was braodened ; (3) area of mRNA expression of lactoferrin, one of the estrogen-responsive genes, was proximally broadened ; and (4) various morphological changes, such as enlargement of interstitial space and lumen of epididymal tubule and thickening of the epithelium, occurred. Mechanisms of these effects will be analyzed using in-house mouse epididymis cDNA microarray.
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