课题基金 / 基金详情

Radiosensitivity of scid cells for heavy ion particles

Radiosensitivity of scid cells for heavy ion particles
scid细胞对重离子粒子的放射敏感性
批准号:
09670943
负责人:
OKUMURA Yutaka
金额:
$1.66万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1999

项目摘要

项目成果

OKUMURA Yutaka的其他基金

相似基金

相关文献

中文摘要
翻译
缺乏DNA-PK的Scid细胞对低LET辐射高度敏感。用含有DNA-PK结构基因的人类8号染色体片段引入杂交细胞后,放射敏感性恢复到野生亲本细胞水平。scid细胞对高LET辐射的辐射敏感性尚未研究。本研究研究了细胞对重离子的辐射敏感性,以阐明LET辐射对DNA损伤的修复过程。采用x射线(200 kV)和碳离子作为重离子粒子(290MeV/u, 50 keV/μm)。x射线照射下杂交细胞DNA双链断裂(DNA-dsb)的修复呈双相性,而scid细胞DNA双链断裂的修复呈单相性。对碳离子的辐照显示出与x射线相同的结果,表明DNA-dsb的修复是与let无关的。对碳离子进行了RBE分析。scid细胞RBE为1.30,杂交细胞RBE为1.47。scid细胞的放射敏感性值减去杂交细胞的放射敏感性值表明DNA-PK修复损伤,DNA-PK贡献。DNA-PK贡献的RBE为1.02。这些结果表明,在scid细胞和杂交细胞中,不可修复的致死性DNA损伤是依赖于let的,而DNA- pk对DNA损伤的修复是不依赖于let的。
英文摘要
Scid cells deficient in DNA-PK are highly sensitive to low LET radiations. Hybrid cells introduced by a fragment of human chromosome 8 which contains the structural gene of DNA-PK recover radiosensitivity to the level of wild parental cells. Radiosensitivity of scid cells to high LET radiations has not been investigated. In this study radiosensitivity of scid cells to heavy ion particles was investigated in order to elucidate the process how DNA damages induced by LET radiation were repaired.X-rays (200 kV) and carbon ions as heavy ion particles (290MeV/u, 50 keV/μm) were used. Repair of DNA double strand breaks (DNA-dsb) in hybrid cells irradiated to X-rays showed bi-phasic, but mono-phasic in scid cells. Irradiation to carbon ions showed the same result as X-rays, indicating that repair of DNA-dsb was LET-independent. RBE for carbon ions was analyzed. RBE of scid cells was 1.30, and 1.47 for hybrid cells. The value of radiosensitivity of scid cells subtracted that of hybrid cells indicates damages repaired by DNA-PK, DNA-PK contribution. RBE of DNA-PK contribution was 1.02. These results indicate that lethal DNA damages unrepairable in scid cells and hybrid cells are LET-dependent, and that DNA damages repairable by DNA-PK contribution by LET-independent.
期刊论文(26)
专著(0)
科研奖励(0)
会议论文
K OKAICHI, L WANG, J. SAKAI, M. TADA AND Y. OKUMURA: "A point mutation of p53, which was not detected as a mutation by a yeast functional assay, led to apoptosis not p21 expression"INT. J. RADIAT.ONCOL. BIOL.PHYS.. 45. 975-980 (1999)
K OKAICHI、L WANG、J. SAKAI、M. TADA 和 Y. OKUMURA​​:“p53 的点突变未通过酵母功能测定检测为突变,导致细胞凋亡而不是 p21 表达”INT。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
岡市協生: "p53と発癌" 現代医療. 30(7). 1851-1857 (1998)
Kyosei Okaichi:“P53 和致癌作用”现代医学 30(7)(1998)。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
林 靖之: "Linac radiosurgery system を用いた stereotactic radiationtherapy の試み" 癌の臨床. 43(2). 139-143 (1997)
Yasuyuki Hayashi:“使用直线加速器放射外科系统的立体定向放射治疗的试验”癌症诊所 43(2) (1997)。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
M. IHARA, A. SUWA, K. KOMATSU, K. OKASAKI AND Y. OKUMURA: "Heat sensitivity of double-stranded DNA-dependent protein kinase (dna-pk) activity"INT. J. RADIAT. BIOL.. 75. 253-258 (1999)
M. IHARA、A. SUWA、K. KOMATSU、K. OKASAKI 和 Y. OKUMURA​​:“双链 DNA 依赖性蛋白激酶 (dna-pk) 活性的热敏感性”INT。
DOI: --
发表时间:
期刊:
影响因子: --
作者: []
通讯作者:
共 26 条
    Combined effects of light and naphthalene on marine microalgae
    • 批准号:
      17510034
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.44万
    • 财政年份:
      2005
    • 负责人:
      OKUMURA Yutaka
    • 依托单位:
    Radiosensitivity of Scid Cells Deficient in Repair of DNA Damages Induced by High LET Irradiation
    • 批准号:
      12670885
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.66万
    • 财政年份:
      2000
    • 负责人:
      OKUMURA Yutaka
    • 依托单位:
    Analysis of Thermotolerance of Cancer by Introduction of Oncogeges
    • 批准号:
      07671015
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $1.47万
    • 财政年份:
      1995
    • 负责人:
      OKUMURA Yutaka
    • 依托单位:
    国内基金
    海外基金
    H2AX、STAT1蛋白表达调控体内外食管癌细胞放射敏感性的研究
    • 批准号:
      30870743
    • 项目类别:
      面上项目
    • 资助金额:
      32.0万元
    • 批准年份:
      2008
    • 负责人:
      祝淑钗
    • 依托单位: