| Project/Area Number |
09480126
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
環境影響評価(含放射線生物学)
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| Research Institution | Nagasaki University |
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Principal Investigator |
WATANABE Masami Nagasaki University, Pharmaceutical Science, Professor, 薬学部, 教授 (20111768)
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| Co-Investigator(Kenkyū-buntansha) |
SUZUKI Keiji Nagasaki University, Pharmaceutical Science, Research Associate, 薬学部, 助手 (00196809)
KODAMA Seiji Nagasaki University, Pharmaceutical Science, Associate Professor, 薬学部, 助教授 (00195744)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥6,000,000 (Direct Cost: ¥6,000,000)
Fiscal Year 1999: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1998: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 1997: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | Low Dose Radiation / Human Embryonic Cells / Mutation / Chromosome Aberrations / Delayed Cell Death / Radiation Response / Genetical Instability / 遅廷型細胞死 |
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| Research Abstract |
Radiation induces genetic instability in the progeny of cells that survive irradiation. To know the effect of adaptive response on the induction of genetic instability, we focused our study on delayed chromosome aberrations newly produced in surviving cells over 30 cell generations post-irradiation. Most of the delayed chromosome aberrations consists of dicentric chromosomes, where the majority of them is not accompanied with a fragment. Pre-irradiation of a low dose (2 cGy) results in 40% reduction (p<0.01) of the frequency of the delayed chromosome aberrations induced by a high-dose irradiation. Of particular interest is that reduction of dicentric chromosomes is observed in those with a fragment but not in those without a fragment (p<0.004). From these results, we purpose that the mechanism of the formation of the delayed chromosome aberrations by radiation is different from that of directly induced chromosome aberrations. To know the mechanism of the formation of the delayed-type aberrations further, we studied the delayed chromosome aberrations in scid mouse cells which defect in non-homologous end joining repair. The result shows that scid cells are more sensitive to the formation of the delayed chromosome aberrations than wild-type cells when they are exposed to an equivalent surviving dose, suggesting that non-homologous end joining repair may play a role in prevention of genetic instability by radiation.
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