Bradley M O, Taylor V I
Proc Natl Acad Sci U S A. 1981 Jun;78(6):3619-23. doi: 10.1073/pnas.78.6.3619.
DNA double-strand breaks (DSBs) are formed in normal human IMR-90 cells during repair incubation after 100 and 300 J.m-2 of ultraviolet light. By contrast, no DSBs are formed after exposure to ultraviolet light in human XPA cells (from a patient with xeroderma pigmentosum complementation group A), which are unable to excise pyrimidine dimers. The DSBs are not due to immediate cell death, because all the cells excluded trypan blue at the time of assay and because XPA cells, which are much more sensitive to ultraviolet light than are IMR-90 cells, did not form DSBs after exposure to ultraviolet light. The DSBs do not appear to be due to either DNA synthesis or cellular single-strand endonucleases. We suggest that repair-induced DSBs would be potent lesions that might lead to cytotoxicity, chromosome aberrations, deletion mutations, and perhaps cellular transformation.
在正常人类IMR - 90细胞中，在100和300 J.m-2紫外线照射后的修复孵育过程中会形成DNA双链断裂（DSB）。相比之下，人类XPA细胞（来自一名色素沉着干皮病A互补组患者）在暴露于紫外线后不会形成DSB，这些细胞无法切除嘧啶二聚体。DSB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，并且因为对紫外线比IMR - 90细胞敏感得多的XPA细胞在暴露于紫外线后未形成DSB。DSB似乎既不是由DNA合成也不是由细胞单链内切核酸酶引起的。我们认为修复诱导的DSB可能是导致细胞毒性、染色体畸变、缺失突变以及可能的细胞转化的潜在损伤。
