Bradley M O
J Supramol Struct Cell Biochem. 1981;16(4):337-43. doi: 10.1002/jsscb.1981.380160404.
DNA DSBs are formed in normal human IMR-90 cells during repair incubation after 100 and 300 J.m-2 of UVL. By contrast, no DSBs are formed after UVL in human XPA cells that are unable to excise pyrimidine dimers. The DSBs are not due to immediate cell death since all the cells excluded trypan blue at the time of assay and because XPA cells, which are much more UVL-sensitive than IMR-90, did not form DSBs after UVL. We suggest that these repair-induced DSBs should be potent lesions that might lead to cytotoxicity, chromosome aberrations, deletion mutations, and perhaps cellular transformation. transformation.
在100和300 J.m-2紫外线照射后的修复培养过程中，正常人IMR-90细胞会形成DNA双链断裂（DSBs）。相比之下，在无法切除嘧啶二聚体的人XPA细胞中，紫外线照射后不会形成DSBs。这些DSBs并非由细胞立即死亡所致，因为在检测时所有细胞都排斥台盼蓝，而且比IMR-90对紫外线更敏感的XPA细胞在紫外线照射后并未形成DSBs。我们认为，这些修复诱导的DSBs应该是可能导致细胞毒性、染色体畸变、缺失突变以及或许细胞转化的强效损伤。 转化。
