Rosenstein B S, Chao C C, Ducore J M
Radiat Res. 1985 Aug;103(2):286-92.
The excision repair of solar uv-induced nondimer DNA damage was examined in ICR 2A frog cells through the use of the bromodeoxyuridine (BrdUrd) photolysis assay. A relatively pure population of nondimer DNA photoproducts was induced by irradiation of ICR 2A cells with the Mylar-filtered solar ultraviolet (uv) wavelengths produced by a fluorescent sunlamp followed by exposure to photoreactivating light (PRL) which removes most of the small yield of pyrimidine dimers induced by this treatment. Cultures of cells were also exposed to 254 nm uv, which induces primarily dimers, and 60Co gamma rays. Through use of a modification of the BrdUrd photolysis assay possessing enhanced sensitivity, it was found that the solar uv-induced nondimer DNA damage was repaired by a short patch repair mechanism in which less than approximately 20 nucleotides are inserted into a repaired region. Similar results were also obtained for gamma-irradiated cells. In contrast, excision repair of 254-nm-induced dimers was accomplished by a long-patch process in which an average of about 180 nucleotides are inserted into the repaired sites.
通过使用溴脱氧尿苷（BrdUrd）光解试验，在ICR 2A蛙细胞中检测了太阳紫外线诱导的非二聚体DNA损伤的切除修复。用荧光太阳灯产生的聚酯薄膜过滤的太阳紫外线（uv）波长照射ICR 2A细胞，然后暴露于光复活光（PRL），从而诱导出相对纯的非二聚体DNA光产物群体，该光复活光可去除这种处理诱导产生的大部分少量嘧啶二聚体。细胞培养物还暴露于主要诱导二聚体的254 nm紫外线和60Coγ射线。通过使用具有更高灵敏度的改良BrdUrd光解试验，发现太阳紫外线诱导的非二聚体DNA损伤通过短片段修复机制进行修复，在该机制中，修复区域插入的核苷酸少于约20个。γ射线照射的细胞也获得了类似结果。相比之下，254 nm诱导的二聚体的切除修复是通过长片段过程完成的，在该过程中，平均约180个核苷酸插入到修复位点。
