| Project/Area Number |
17510055
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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 |
Risk sciences of radiation/Chemicals
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| Research Institution | Japan Atomic Energy Agency |
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Principal Investigator |
KOBAYASHI Yasuhiko Japan Atomic Energy Agency, Quantum Beam Science Directorate, Senior Principle Researcher, 量子ビーム応用研究部門, 研究主幹 (50354957)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2005: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | heavy-ion microbeam / high-LET radiation / apoptosis / bystander effect / DNA damage / track structure / non-homologous end joining / Ku |
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| Research Abstract |
Differences in track structure of radiation are thought to result in different biological effects, and therefore we investigated the biological effects of the track structure generated by different particles with the same LET values. CHO-K1 cells were irradiated with different charged-particle beams (^<12>C ions and ^<20>Ne ions) with the same LET value (about 437 keV/4m), and cell killing was evaluated in a colony-formation assay. Cells were attached to a CR-39 ion-track detector to visualize ion-hit sites, and the amount of DNA double strand breaks (DSBs) was evaluated using a comet assay. The spatial distribution of DNA damage around the sites of individual particle traversals was detected with immunofluorescence techniques using exo III and TdT, and phosphorylated histone H2AX (γH2AX). Despite the ions having the same LET values, C ions were more effective than Ne ions in cell killing and induction of DSBs. The spatial distribution of-γH2AX induced by C ions and Ne ions did not differ significantly ; however, DNA damage, including single strand breaks, DSBs and AP sites, induced by Ne ions was threefold larger than that induced by C ions. These results indicate that a difference in track structure influences cell killing and induction of DNA damage.
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