Nevaldine B, Longo J A, Hahn P J
Department of Radiology, State University of New York Health Science Center at Syracuse 13210.
Int J Hyperthermia. 1994 May-Jun;10(3):381-8. doi: 10.3109/02656739409010282.
Hyperthermia is known to synergistically interact with X-rays to kill cells. We have used pulsed-field gel electrophoresis to investigate the effects of hyperthermia on cell survival and on repair of radiation-induced DNA double-strand breaks (dsbs). Combining hyperthermia (43 degrees C, 45 min) with radiation (7.5 Gy) resulted in a complete inhibition of dsb repair and a surviving fraction of 0.9%. Cells treated with hyperthermia alone resulted in a 55% cell survival with no increase in dsb levels over background. Cells treated with 7.5 Gy alone demonstrated 11% survival and exponential dsb repair. Dsb repair was equally inhibited by hyperthermia whether administered immediately before or after the radiation. We compared the rejoining of dsbs resulting from 7.5 Gy at 37 and 43 degrees C to determine whether dsbs were being repaired during hyperthermia. While repair occurred at 37 degrees C, no dsbs were repaired at 43 degrees C. Our results indicate that hyperthermia completely inhibits dsb repair.
已知热疗可与X射线协同作用杀死细胞。我们已使用脉冲场凝胶电泳来研究热疗对细胞存活以及对辐射诱导的DNA双链断裂(dsb)修复的影响。将热疗(43摄氏度,45分钟)与辐射(7.5 Gy)相结合导致dsb修复完全受到抑制,存活分数为0.9%。单独接受热疗的细胞存活率为55%,dsb水平未超过背景水平。单独接受7.5 Gy辐射的细胞存活率为11%,且dsb呈指数修复。无论在辐射之前还是之后立即进行热疗,dsb修复均受到同等程度的抑制。我们比较了在37摄氏度和43摄氏度下由7.5 Gy导致的dsb的重新连接情况,以确定在热疗期间dsb是否正在被修复。虽然在37摄氏度时发生了修复,但在43摄氏度时没有dsb得到修复。我们的结果表明热疗完全抑制了dsb修复。