REPAIR OF POTENTIALLY LETHAL DAMAGE IN X-IRRADIATED HELA CELLS
REPAIR OF POTENTIALLY LETHAL DAMAGE IN X-IRRADIATED HELA CELLS
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DOI：
10.2307/3572022
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发表时间：
1966-01-01
影响因子：
3.4
通讯作者：
TOLMACH, LJ
中科院分区：
文献类型：
--
作者：
PHILLIPS, RA;TOLMACH, LJ
在剂量范围为300至600拉德的220千伏x射线照射后立即用DNA抑制剂氟脱氧urtdine或羟基脲处理HeLa S3细胞的同步种群，可导致存活细胞比例下降。在29℃的辐射后孵育产生类似的结果。细胞在G1期对这些治疗表现出数量上相似的反应，它们的反应能力持续约5小时。辐照后。温度和羟基脲的作用随着治疗时间的延长而增加，至少可达12小时。这些处理都不会影响未辐照细胞的生存能力。据推测，这些治疗抑制了一个过程，通常在辐照细胞中操作，从而修复潜在的致命损伤。这个修复过程可能涉及某种类型的DNA合成。推定的潜在致死损害与亚致死损害的关系尚不清楚。相反，环己亚胺，一种蛋白质合成抑制剂，在辐照后给予培养物时增加了存活率；它显然增强了修复过程，可能是通过抑制竞争过程，潜在的致命损伤通常在细胞中表达。此外，与G1早期暴露的细胞相比，在Gl晚期照射的细胞中，环己亚胺治疗带来的存活增加更大。这表明，与修复过程相比，该菌株细胞在G1期的放射敏感性增加是表达过程越来越有利的结果。
Treatment of synchronous populations of HeLa S3 cells with the DNA inhibitors fluorodeoxyurtdine or hydroxyurea immediately after irradiation with 220-kv X-rays in the dose range 300 to 600 rads causes a decrease in the fraction of surviving cells. Postirradiation incubation at 29[degree] C produces a similar result. Cells show quantitatively similar responses to these treatments throughout G1, their capacity to respond persisting for about 5 hr. after irradiation. The effect of temperature and hydroxyurea increases with the duration of treatment up to at least 12 hr. None of the treatments affects the viability of unirradiated cells. It is postulated that these treatments inhibit a process, ordinarily operating in irradiated cells, whereby potentially lethal damage is repaired. This repair process may involve some type of DNA synthesis. The relation of the presumptive potentially lethal damage to sublethal damage is unknown. In contrast, cyclo-heximide, an inhibitor of protein synthesis, increases survival when administered to cultures after irradiation; it apparently enhances the repair process, perhaps by inhibiting a competing process by which the potentially lethal damage is ordinarily expressed in the cell. In addition, the increase in survival brought about by treatment with cycloheximide is greater in cells irradiated in late Gl than in cells exposed in early G1. This suggests that the increase in radiation sensitivity accompanying progression of cells of this strain through G1 is the result of an increasingly favorable outcome of the expression process as compared to the repair process.