| Project/Area Number |
14571505
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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 |
Urology
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| Research Institution | Kyushu University |
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Principal Investigator |
YOSHIMURA Yasuhide Kyushu University, Faculty of medical Sciences, Graduate School, Research Associate (60263307)
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| Co-Investigator(Kenkyū-buntansha) |
TERUHISA Tsuzuki 九州大学, Faculty of Medical Sciences, Graduate School, professor (40155429)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2003: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2002: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | germ cell / spermatogenesis / oxidative DNA damage / DNA repair / fertility / 精巣 / ミスマッチ修復 / 放射線影響 |
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| Research Abstract |
We have studied about the relationship between fertility and mutation on genome caused by oxidative damage during spermatogenesis. We used C57BL/6 wild type mice as well as Msh2 deficient mice. We have observed the testis section according to the aging and also we performed irradiation. Irradiation should increase the oxidative DNA damage on the genome of germ cells. Testis was fixed with bouins solution and sectioned to 5μm. We also observed fertility of Msh2 deficient mice.
Results : The testis weight of Msh2 deficient mice was decreased according to the age. After 14 weeks old, the testis weight of Msh2 deficient mice become 60% of wild type one. The observation of section reveals degeneration of gonia and pre leptotene stage. Durin gonia and pre leptotene stage, we could observe significant apoptotic germ cells. We supposed the decrease of testis weight should be caused by the continuous apoptosis of germ cells. Although the apoptotic germ cell number increase after 14 weeks old Msh2 deficient mice and the weight of the testis decrease to 60% of wild type mice, they reveals normal fertility.
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