Ohnishi T, Iwata K, Hamada N, Nozu K
Department of Biology, Nara Medical University, Japan.
Int J Radiat Biol. 1988 Oct;54(4):651-8. doi: 10.1080/09553008814552081.
DNA repair of a lower eukaryote, Dictyostelium discoideum, has been investigated through the analysis of heat effects on cell mortality and DNA repair of UV-irradiated amoeboid cells. In a wild-type strain (NC4), an increase in temperature immediately after UV irradiation resulted in an increase in cell mortality, though similar heat treatment before UV irradiation had no such effect. Similar results were obtained in another wild-type strain, HPS83. In NC4, heat treatment after UV irradiation did not inhibit the nicking of DNA strands during excision repair processes, but did inhibit the rejoining of the DNA strand breaks. Removal of thymine-containing pyrimidine dimers from DNA molecules was also depressed by heat treatment after UV irradiation. In contrast, heat treatment before UV irradiation had no effect on any stage of the nicking process, the excision of the dimers or the rejoining. On the other hand, a radiation-sensitive mutant (TW8) defective in an incision step of the excision repair process did not show an increase in cell mortality in response to heat treatment administered either before or after UV irradiation. Though the optimum temperature for cell growth of the amoebae was 23 degrees C, the critical temperature for effective enhancement of cell killing was ca. 30 degrees C. Hence we assume that the excision repair of UV-damaged DNA is selectively sensitive to heat treatment.
通过分析热对紫外线照射的变形虫细胞死亡率和DNA修复的影响,对低等真核生物盘基网柄菌的DNA修复进行了研究。在野生型菌株(NC4)中,紫外线照射后立即升温会导致细胞死亡率增加,而在紫外线照射前进行类似的热处理则没有这种效果。在另一个野生型菌株HPS83中也得到了类似的结果。在NC4中,紫外线照射后的热处理并不抑制切除修复过程中DNA链的切口,但会抑制DNA链断裂的重新连接。紫外线照射后的热处理也会抑制从DNA分子中去除含胸腺嘧啶的嘧啶二聚体。相比之下,紫外线照射前的热处理对切口过程、二聚体切除或重新连接的任何阶段都没有影响。另一方面,在切除修复过程的切口步骤有缺陷的辐射敏感突变体(TW8),在紫外线照射前后进行热处理时,细胞死亡率没有增加。虽然变形虫细胞生长的最适温度是23℃,但有效增强细胞杀伤的临界温度约为30℃。因此我们认为,紫外线损伤DNA的切除修复对热处理具有选择性敏感性。