| Project/Area Number |
23650304
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Medical systems
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| Research Institution | University of Toyama |
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Principal Investigator |
KONDO Takashi 富山大学, 大学院・医学薬学研究部(医学), 教授 (40143937)
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| Co-Investigator(Kenkyū-buntansha) |
TABUCHI Yoshiaki 富山大学, 生命科学先端研究センター, 准教授 (20322109)
ZHAO Qing-li 富山大学, 大学院・医学薬学研究部(医学), 助教 (90313593)
TAKASAKI Ichro 富山大学, 生命科学先端研究センター, 助教 (00397176)
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 超音波・DNA損傷 / 二本鎖切断 / リン酸化ヒストンH2AX / キャビテーション / フリーラジカル / DNA-PK / DNA損傷 / ATM / ATR / DNA二本鎖切断 |
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| Research Abstract |
A likely candidate process has been suggested to involve sonochemical activity, where reactive oxygen species mediate the generation of DNAsingle-strand breaks. Here however, we provide compelling new evidence that strongly supports a purely mechanical mechanism. Moreover, by a combination of specific assays （neutral comet tail and staining for γH2AX foci formation) we demonstrate for the first time that US exposure at even moderate intensities exhibits DNAdouble-strand breaks, through its facility to generate DNA damage across multiple cancer lines. Notably, colocalization assays highlight that ionizing radiation and ultrasound have distinctly different signatures to their respective γH2AX foci formation patterns, likely reflecting the different stress distributions that initiated damage formation.
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