EFFECTS OF HYPERTHERMIA ON THE REPAIR OF RADIATION-INDUCED DNA SINGLE-STRAND AND DOUBLE-STRAND BREAKS IN DNA DOUBLE-STRAND BREAK REPAIR-DEFICIENT AND REPAIR-PROFICIENT CELL-LINES

被引:44
作者
ILIAKIS, G
SEANER, R
OKAYASU, R
机构
[1] Thomas Jefferson University, Department of Radiation Oncology and Nuclear Medicine, Laboratory of Experimental Radiation Oncology, Philadelphia
[2] University of Texas, M.D. Anderson Cancer Center, Department of Medical Oncology, Houston, TX 77030
关键词
CHO cells; DNA double-strand breaks; DNA repair; DNA single-strand breaks; DNA unwinding technique; Hydroxy apatite chromatography; Hyperthermia; Non-unwinding DNA filter elution; Radiation; Xrs-5; cells;
D O I
10.3109/02656739009140828
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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 (45ċ5°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. © 1990 Informa UK Ltd All rights reserved: reproduction in whole or part not permitted.
引用
收藏
页码:813 / 833
页数:21
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