Rosenstein B S, Chao C C
Mutat Res. 1985 Sep;146(2):191-6. doi: 10.1016/0167-8817(85)90010-0.
The level of excision repair and the inhibition and recovery of semiconservative DNA synthesis were examined following the induction of non-dimer DNA damages by solar ultraviolet radiation in a mutant cell line, DRP 36, derived from ICR 2A frog cells that is hypersensitive to these lesions. A relatively pure population of non-dimer photoproducts was produced by exposure of cells to the Mylar-filtered solar UV wavelengths produced by a fluorescent sunlamp followed by treatment with photoreactivating light (PRL) which removes most of the small yield of dimers induced by the irradiation. Using a modification of the bromodeoxyuridine (BrdUrd) photolysis assay, that enhances the sensitivity of this assay, it was found that DRP 36 cells perform a significantly lower level of excision repair following the induction of non-dimer DNA damages compared with the ICR 2A cells. In contrast, the level of excision repair of 254-nm-induced dimers was similar in the two cell lines. In addition, the induction of non-dimer damages caused a greater inhibition of DNA synthesis that persisted for a longer period of time in the mutant compared with the parental cells. Hence, these results indicate that the DRP 36 cells are deficient in the repair of at least one type of solar UV-induced non-dimer lesion.
在源自对这些损伤高度敏感的ICR 2A蛙细胞的突变细胞系DRP 36中，通过太阳紫外线辐射诱导非二聚体DNA损伤后，检测了切除修复水平以及半保留DNA合成的抑制和恢复情况。通过将细胞暴露于荧光太阳灯产生的经聚酯薄膜过滤的太阳紫外线波长下，然后用能去除大部分由辐射诱导产生的少量二聚体的光复活光（PRL）处理，产生了相对纯的非二聚体光产物群体。使用一种改进的溴脱氧尿苷（BrdUrd）光解测定法（该方法提高了该测定法的灵敏度），发现与ICR 2A细胞相比，DRP 36细胞在诱导非二聚体DNA损伤后进行的切除修复水平明显较低。相比之下，两种细胞系中254纳米诱导的二聚体的切除修复水平相似。此外，与亲代细胞相比，非二聚体损伤的诱导对DNA合成造成的抑制更大，且在突变细胞中持续时间更长。因此，这些结果表明DRP 36细胞在修复至少一种类型的太阳紫外线诱导的非二聚体损伤方面存在缺陷。
