Effects of aphidicolin on cell proliferation, repair of potentially lethal damage and repair of DNA strand breaks in Ehrlich ascites tumour cells exposed to X-rays.
Effects of aphidicolin on cell proliferation, repair of potentially lethal damage and repair of DNA strand breaks in Ehrlich ascites tumour cells exposed to X-rays.
复制标题
阿菲迪霉素对暴露于 X 射线的艾利希腹水肿瘤细胞的细胞增殖、潜在致命损伤的修复和 DNA 链断裂的修复的影响。
DOI：
10.1080/09553008214551341
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
P. Bryant
中科院分区：
文献类型：
--
作者：
G. Iliakis;M. Nüsse;P. Bryant
阿非迪霉素，DNA α-聚合酶的特异性抑制剂，对各种细胞终点和DNA链断裂修复的影响进行了研究。在0.02-2 μ g/ml浓度范围内，DNA合成受到强烈抑制，导致伴随细胞增殖能力丧失; RNA和蛋白质合成在此范围内不受影响。在这些浓度下，即使在用阿非迪霉素处理7小时后，X照射的平台期细胞中的PLD修复也不受影响;然而，在更高浓度（大于2微克/毫升）下，PLD修复被抑制。我们表明，在低浓度范围内（小于2微克/毫升）PLD修复可以看到在指数生长的细胞和同步细胞的实验，我们建立的PLD修复观察到的可以归因于S-期人口，G1-细胞的生存不受aphidicolin的影响。PLD修复指数增长的细胞中的“促进”是超过相同的细胞中观察到的平衡盐溶液中，PLD修复通常观察到。在高浓度（大于2微克/毫升）的阿非迪霉素，X射线照射和对照S细胞被杀死越来越多的浓度增加。DNA链断裂（单链和双链）的修复在低浓度范围内不受影响，但在高浓度下观察到强烈抑制。从这些结果可以得出结论，α-聚合酶，这是强烈抑制在低浓度的阿非迪霉素证明了DNA合成的抑制，在修复DNA链断裂或在修复PLD中没有发挥重要作用。
The effects of aphidicolin, a specific inhibitor of DNA alpha-polymerase, have been studied on various cellular end-points and on DNA strand break repair. In the concentration range 0.02-2 micrograms/ml DNA synthesis was strongly inhibited resulting in a concomittant loss of cell proliferation ability; RNA and protein synthesis were unaffected in this range. At these concentrations PLD repair in X-irradiated plateau-phase cells was unaffected even after 7 hours treatment with aphidicolin; however, at higher concentrations (greater than 2 micrograms/ml) PLD repair was inhibited. We show that in the low concentration range (less than 2 micrograms/ml) PLD repair can be seen in exponentially growing cells and from experiments with synchronized cells we establish that the PLD repair observed can be attributed to the S-phase population, the survival of G1-cells not being affected by aphidicolin. The 'promotion' of PLD repair in exponentially growing cells was in excess of that observed for the same cells in balanced salt solution in which PLD repair is usually observed. At high concentrations (greater than 2 micrograms/ml) of aphidicolin, both X-irradiated and control S-cells were killed increasingly as concentration increased. The repair of DNA strand breaks (single and double) was unaffected in the low concentration range, but a strong inhibition was observed at high concentration. It is concluded from these results that alpha-polymerase, which is strongly inhibited at low concentrations of aphidicolin as evidenced by the inhibition of DNA synthesis, plays no major part in the repair of DNA strand breaks or in the repair of PLD.