Thermal radiosensitization in heat- and radiation-sensitive mutants of CHO cells.

Thermal radiosensitization in heat- and radiation-sensitive mutants of CHO cells.
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CHO 细胞热和辐射敏感突变体的热放射增敏作用。

DOI:
10.1080/09553009314551331
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发表时间:
1993
影响因子:
2.6
通讯作者:
J. Bedford
J. Bedford
中科院分区:
医学3区
文献类型:
--
作者:
H. Kampinga;B. Kanon;A. Konings;M. Stackhouse;J. Bedford

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最近,人们假设(Iliakis和Seaner 1990)DNA双链断裂(dsb)修复能力是热辐射增敏的先决条件,这是基于以下发现:辐射敏感和dsb修复缺陷突变xrs-5细胞系未显示出显著的热诱导辐射增敏(即使在严重的热剂量下也未显示),而其野生型对应物(CHO)确实显示出这种效应。在当前研究中,将Stackhouse和贝德福德(1991)最近分离的新的γ辐射敏感细胞系irs-20和热敏感突变体hs-36(Harvey和贝德福德1988)的高温辐射增敏程度与其共同亲本CHO 10 B12细胞系的辐射增敏进行了比较。irs-20和CHO 10 B12细胞具有相当的热敏感性(43.5 ℃),而hs-36和CHO 10 B12对γ射线和X射线显示出相似的敏感性。对于所有三种细胞系,发现由于平台期培养物预暴露于43.5 ° C加热而引起的放射增敏,即使在相对温和的热处理后杀死< 20%的细胞。使用CHEF电泳的实验证实了irs-20细胞的dsb修复缺陷(Stackhouse和贝德福德1992),并表明热抑制所有三种细胞系中的dsb修复。这些数据表明,DNA修复缺陷(整体dsb修复)本身并不意味着缺乏热放射增敏的能力。
Recently, it has been hypothesized (Iliakis and Seaner 1990) that DNA double-strand break (dsb) repair proficiency is a prerequisite for heat radiosensitization on the basis of the finding that the radiosensitive and dsb-repair-deficient mutant xrs-5 cell line shows no significant heat-induced radiosensitization (not even for severe heat doses), whereas their wildtype counterpart (CHO) did show such an effect. In the current study, the extent of hyperthermic radiosensitization in a new gamma-radiation-sensitive cell line, irs-20, recently isolated by Stackhouse and Bedford (1991) and a heat-sensitive mutant hs-36 (Harvey and Bedford 1988) was compared with the radiosensitization of their mutual parent CHO 10B12 cell line. The irs-20 and CHO 10B12 cells have comparable heat (43.5 degrees C) sensitivities, whereas hs-36 and CHO 10B12 show a similar sensitivity to gamma- and X-rays. Radiosensitization due to pre-exposure to 43.5 degrees C heating of plateau phase cultures was found for all three cell lines, even after relatively mild heat treatment killing < 20% of cells. Experiments using CHEF electrophoresis confirmed the dsb repair deficiency of the irs-20 cells (Stackhouse and Bedford 1992) and showed that heat inhibited dsb repair in all three cells lines. These data indicate that DNA repair deficiency (overall dsb repair) per se does not imply an absence of the ability for heat radiosensitization.
辐射敏感 CHO 突变细胞 xrs-5 中核结构的变化。
DOI: --
发表时间: 1991
期刊: Radiation research
影响因子: 3.4
作者:
Yasui,LS;Ling-Indeck,L;Johnson-Wint,B;Fink,TJ;Molsen,D
通讯作者: Molsen,D
xrs-5 细胞中碱性条件下 DNA 解旋速度加快可能反映了染色质结构的改变。
DOI: 10.1016/0165-7992(92)90067-r
发表时间: 1992
期刊: Mutation research
影响因子: --
作者:
Schwartz,JL;Moan,E;Mustafi,R;Fink,L;Yasui,LS
通讯作者: Yasui,LS
热和辐射的相互作用影响核 DNA 发生超螺旋变化的能力。
DOI: --
发表时间: 1988
期刊: Radiation research
影响因子: 3.4
作者:
Kampinga,HH;Wright,WD;Konings,AW;RotiRoti,JL
通讯作者: RotiRoti,JL
DOI: --
发表时间: 1988
期刊: Radiation research
影响因子: 3.4
作者:
Harvey,WF;Bedford,JS
通讯作者: Bedford,JS