PRODUCTION OF DNA DOUBLE-STRAND BREAKS BY INTERACTIONS BETWEEN CARBOPLATIN AND RADIATION - A POTENTIAL MECHANISM FOR RADIOPOTENTIATION
PRODUCTION OF DNA DOUBLE-STRAND BREAKS BY INTERACTIONS BETWEEN CARBOPLATIN AND RADIATION - A POTENTIAL MECHANISM FOR RADIOPOTENTIATION
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DOI：
10.2307/3579218
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发表时间：
1995-09-01
影响因子：
3.4
通讯作者：
WANG, HJ
中科院分区：
文献类型：
--
作者：
YANG, LX;DOUPLE, EB;WANG, HJ
在联合辐射与卡铂增强细胞杀伤（放射增敏和放射增强）的条件下，研究了4种CHO细胞系细胞中DNA双链断裂（DSB）的产生。这些细胞系包括修复熟练（AA 8和K1）、切除修复缺陷（UV 41）和DSB修复缺陷（xrs-5）细胞。在低氧条件下给予单次55-戈伊辐射剂量后立即或4小时，通过中性洗脱分析双链断裂。在AA 8、UV 41和xrs-5细胞中，与照射后立即单独照射相比，卡铂（1 mM）联合照射产生了DSB的小幅增加。然而，在AA 8，K1和xrs-5细胞中的DSB产量显着较高的卡铂辐射处理后4小时，在UV 41细胞中没有发现这样的增加在4小时。链断裂因子（SSF）计算为SSF = -log [在8小时洗脱时保留在过滤器上的DNA百分比（处理的细胞）/在8小时洗脱时保留的DNA百分比（未处理的细胞）]。照射后4 h与0 h的SSF比值分别为K1 13.7、xrs-5 4.9、AA 8 2.5和UV 41 1.2。这些结果支持了一个可能的解释增强杀伤照射细胞的铂化疗剂，即增强生产的DSB。(C)1995年，辐射研究学会
The production of DNA double-strand breaks (DSBs) was studied in cells of four CHO cell lines under conditions where combining radiation with carboplatin enhanced cell killing (radiosensitization and radiopotentiation). The cell lines included repair-proficient (AA8 and K1), excision repair-deficient (UV41) and DSB repair-deficient (xrs-5) cells. Double-strand breaks were analyzed by neutral elution either immediately after or 4 h after a single 55-Gy radiation dose delivered under hypoxic conditions. Carboplatin (1 mM) combined with radiation produced a small increase in DSBs compared to radiation alone immediately after irradiation in AA8, UV41 and xrs-5 cells. However, the yield of DSBs in AA8, K1 and xrs-5 cells was significantly higher 4 h after carboplatin-radiation treatment; no such increase was found at 4 h in UV41 cells. Strand scission factors (SSFs) were calculated as SSF = -log [percentage DNA remaining on filter at 8 h elution (treated cells)/percentage DNA remaining at 8 h elution (untreated cells)]. The ratios of the SSF at 4 h to 0 h postirradiation for carboplatin-treated cells were 13.7 for K1, 4.9 for xrs-5, 2.5 for AA8 and 1.2 for UV41 cells. These results support a possible explanation for the enhanced killing of irradiated cells by platinum chemotherapeutic agents, namely enhanced production of DSBs. (C) 1995 by Radiation Research Society