| Project/Area Number |
08457247
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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 |
Radiation science
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| Research Institution | National Institute of Radiological Sciences |
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Principal Investigator |
ANDO Koichi Natl Inst Radiol Sci, 3rd Research Group, head, 第3研究グループ, 研究員 (00159526)
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| Co-Investigator(Kenkyū-buntansha) |
MARCO DURANT 放射線医学総合研究所, 第3研究グループ, STAフェロー
MAEZAWA Hiroshi TOKAI University School of Medicine Dep.Radiology, Assistant Professor, 放射線科学, 講師 (00138653)
SUZUKI Masao Natl Inst Radiol Sci, 3rd Research Group, Senior Researcher, 第3研究グループ, 研究員 (70281673)
AKASHI Makoto Natl Inst Radiol Sci, Div.Radiation Health, head, 放射線障害医療部, 研究員 (10222514)
DURANTE Marco Natl Inst Radiol Sci, 3rd Research Group, head Visiting Scientist
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| Project Period (FY) |
1996 – 1997
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| Keywords | carbon ions / fractionation / skin / cultured epithelial cells / chromatin / TNF / NFkB |
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| Research Abstract |
We have investigated relationship between cell lethality and chromatin damage induced by ionizing radiation. Cultured normal cells derived from human skin were irradiated with X rays or carbon ions. Premature condensed chromosome (PCC) method indicated that residual chromatin damages increased with dose for X rays as well as carbon ions. RBE of carbon ions was similar between colony formation and the residual PCC.Cacyculin could efficiently induced PCC in human lymphocytes, suggesting the chemical would be valuable for clinical use in future. Radiosensitivity of immortalized human epithelial cells was stable during fractionated irradiations with carbon ions for 5 fractions with an interval time of 4 hours. Isoeffect doses for carbon ions depended on LET and the number of fractions in mouse skin reaction. Fe plot analysis suggested that either cellular repair or repopulation would be changed during fractionated irradiation. Irradiation with X rays to human monocytic leukemia HTP-1 induced TNF production, and also activated NFkB in nuclear protein. These results suggest that radiation-induced cell lethality stems from chromatin damages in critical cells whereas radiation-induced gene expression including also take place for repopulation and tissue repair. Further analyze of gene expression and chromatin damages is required for developing new predictive assays.
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