| Project/Area Number |
09680520
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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 |
環境影響評価(含放射線生物学)
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| Research Institution | Kyoto University of Education |
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Principal Investigator |
IKUSHIMA Takaji Kyoto University of Education, Department of Science, Professor, 教育学部 (80027458)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | radiation / adaptive response / DNA repair |
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| Research Abstract |
The radioadaptive response is the phenomenon that cells pre-exposed to low doses of ionizing radiation can acquire the resistance to subsequent moderate or high doses of radiation for Induction of chromosomal aberrations, mutation and cell killing. To elucidate the molecular mechanism of radloadaptive response, a series of researches has been carried out In cultured mammalian cells which was previously proved to show cytogenetical adapative response.
A hypothesis that the Induction of a novel, efficient repair mechanism for chromosomal DNA damage may be involved In the radioadaptive response was tested by a neutral comet assay of repair kinetics of radiation-induced DNA damage in adapted Chinese hamster V79 cells. There were no indication of any difference In the initial yields of DNA damage (double-strand breaks) induced by challenging doses between non-adapted cells and cells adapted by priming exposure. The monitoring of the rejoining of DNA double-strand breaks induced by challenging doses has revealed that the rate of DNA damage repair in adapted cells was higher than that in non-adapted control cells, and the level of the residual damage was less In adapted cells. The enhanced repair rate was observed especially In the early stage of DNA repair process.
A cross-adaptive response was also demonstrated for enhanced repair of DNA damage induced by a radiomimetic agent, neocarzinostatin in radio-adapted cells. These results indicate that the radioadaptive response may result from the induction of a novel, efficient DNA repair mechanism which leads to less residual damage, but not from the induction of protective functions that reduce the initial damage, It Is suggested that the radioadaptive response may not be restricted to ionizing radiation. These fruitful results obtained in this study would be helpful to elucidate the molecular mechnism of radioadaptive response in more detail.
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