Effects of hyperthermia on the repair of radiation-induced DNA single- and double-strand breaks in DNA double-strand break repair-deficient and repair-proficient cell lines.

Effects of hyperthermia on the repair of radiation-induced DNA single- and double-strand breaks in DNA double-strand break repair-deficient and repair-proficient cell lines.
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热疗对 DNA 双链断裂修复缺陷和修复熟练细胞系中辐射诱导的 DNA 单链和双链断裂修复的影响。

DOI:
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发表时间:
1990
影响因子:
3.1
通讯作者:
R. Okayasu
R. Okayasu
中科院分区:
医学2区
文献类型:
--
作者:
G. Iliakis;R. Seaner;R. Okayasu

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热对DNA单链(SSB)和双链(DSB)断裂的诱导和修复的影响进行了研究,在辐射指数增长或平台期CHO细胞和他们的DNA DSB修复缺陷,辐射敏感的对应物,XRS-5细胞。通过碱性解旋技术测量DNA ssb的诱导和修复,而通过非解旋过滤器洗脱技术测量DNA dsb的诱导和修复。结果表明,在生长的指数期或平台期测试,细胞预暴露于热(45 × 5 ℃)8-30分钟不影响CHO或xrs-5细胞中每戈伊和道尔顿DNA的DNA ssb或DNA dsb的诱导。另一方面,预暴露于热抑制DNA修复过程,并增加未修复的辐射诱导的损伤的分数照射后2小时测量。在两种细胞系中,DNA双链断裂的修复比DNA单链断裂的修复更热敏感。辐射诱导的ssb或dsb修复在xrs-5细胞中受到抑制的程度比在类似的热暴露后的CHO细胞更大。这些结果补充了先前报道的热诱导的放射增敏在这些细胞系,并表明,减少热诱导的放射增敏观察xrs-5细胞在很大程度上是由于他们的缺陷修复DNA双链断裂,而不是减少热抑制DNA修复过程的能力一般。这里提出的数据提供了进一步的支持,假设DNA双链断裂修复能力是热诱导的放射增敏的先决条件。
The effect of heat on the induction and repair of DNA single (ssb) and double (dsb) strand breaks was studied in irradiated exponentially growing or plateau-phase CHO cells and their DNA dsb repair-deficient, radiation-sensitive counterpart, the xrs-5 cells. Induction and repair of DNA ssb was measured by the alkaline unwinding technique, whereas induction and repair of DNA dsb was measured by the non-unwinding filter elution technique. The results indicated that pre-exposure of cells to heat (45 x 5 degrees C) for 8-30 min did not affect the induction of DNA ssb or DNA dsb per Gy and dalton of DNA in CHO or xrs-5 cells, tested either in the exponential or in the plateau-phase of growth. On the other hand, pre-exposure to heat inhibited DNA repair processes and increased the fraction of unrepaired radiation-induced damage measured 2 h after irradiation. Repair of DNA dsb was more heat-sensitive than repair of DNA ssb in both cell lines. Repair of radiation-induced ssb or dsb was inhibited in xrs-5 cells to a larger extent than in CHO cells after a similar exposure to heat. These results complement those previously reported on heat-induced radiosensitization in these cell lines, and suggest that the reduction in heat-induced radiosensitization observed in xrs-5 cells is largely due to their deficiency in repairing DNA dsb, rather than to a reduction in the ability of heat to inhibit DNA repair processes in general. The data presented here provide further support to the hypothesis that DNA dsb repair proficiency is a prerequisite for heat-induced radiosensitization.
通过诱导间期哺乳动物细胞中的过早染色体浓缩来观察高温对染色质浓缩和核仁崩解的影响。
DOI: --
发表时间: 1989
期刊: Cancer research
影响因子: 11.2
作者:
Iliakis,GE;Pantelias,GE
通讯作者: Pantelias,GE
热与放疗和化疗的相互作用。
DOI: --
发表时间: 1984
期刊: Cancer research
影响因子: 11.2
作者:
Dewey,WC
通讯作者: Dewey,WC
辐射后未重新连接的 DNA 链断裂的高温增强。
DOI: --
发表时间: 1983
期刊: Radiation research
影响因子: 3.4
作者:
Mills,MD;Meyn,RE
通讯作者: Meyn,RE
核基质蛋白质量的变化与热诱导的 DNA 单链断裂修复抑制相关。
DOI: 10.1080/09553008714551761
发表时间: 1987
期刊: International journal of radiation biology and related studies in physics, chemistry, and medicine
影响因子: --
作者:
Warters,RL;Brizgys,LM;Lyons,BW
通讯作者: Lyons,BW
CHO 细胞从高温增强到 DNA 和染色质 X 射线修复的恢复。
DOI: --
发表时间: 1981
期刊: Radiation research
影响因子: 3.4
作者:
Clark,EP;Dewey,WC;Lett,JT
通讯作者: Lett,JT