Rosenstein B S, Murphy J T, Ducore J M
Cancer Res. 1985 Nov;45(11 Pt 1):5526-31.
The excision repair of nondimer DNA damages induced in normal human skin fibroblasts exposed to the Mylar-filtered UV produced by a fluorescent sunlamp was investigated. This work was accomplished through the development of a modification of the bromodeoxyuridine photolysis assay that greatly increases the sensitivity of this assay. This enhancement in sensitivity was achieved through use of alkaline elution to measure the DNA strand breakage produced by the photolysis of bromodeoxyuridine incorporated into the DNA through excision repair. Using this modified bromodeoxyuridine photolysis assay, it was found that the solar UV-induced nondimer DNA damages appear to have been repaired by a short patch repair mechanism in which a small number of nucleotides (two to four) were inserted into the repaired site. This is in contrast to the long patch repair process involved in the excision of cyclobutane pyrimidine dimers in which approximately 40 nucleotides were inserted into each repaired region.
研究了暴露于荧光太阳灯产生的聚酯薄膜过滤紫外线下的正常人皮肤成纤维细胞中诱导产生的非二聚体DNA损伤的切除修复。这项工作是通过对溴脱氧尿苷光解测定法进行改进来完成的，该改进极大地提高了该测定法的灵敏度。灵敏度的提高是通过使用碱性洗脱来测量通过切除修复掺入DNA中的溴脱氧尿苷光解产生的DNA链断裂来实现的。使用这种改进的溴脱氧尿苷光解测定法，发现太阳紫外线诱导的非二聚体DNA损伤似乎是通过短片段修复机制修复的，在该机制中少量核苷酸（两到四个）被插入到修复位点。这与切除环丁烷嘧啶二聚体所涉及的长片段修复过程形成对比，在长片段修复过程中每个修复区域大约插入40个核苷酸。
