Snyder R D, Regan J D
Carcinogenesis. 1982;3(1):7-14. doi: 10.1093/carcin/3.1.7.
Excision repair of DNA in normal and xeroderma pigmentosum complementation group A fibroblasts were examined following treatment with methyl-, ethyl-, and isopropyl methanesulfonate. Studies utilizing repair synthesis methods and inhibition with arabinofuranosyl cytosine revealed two distinct phases of repair; one commencing and terminating within the first 3-5 h after the treatment, and a second much longer phase extending from 9-35 h post-treatment. Both phases of repair have a long-patch (u.v.-like) component, which establishes for the first time the existence of this mode of repair in response to alkane sulfonate damage. While xeroderma cells display somewhat fewer alkaline labile sites in their DNA following alkylation treatment than do their normal counterparts (consistent with earlier observations suggesting a deficiency in a glycosylase or apurinic endonuclease), we are unable to demonstrate a deficiency of these cells in either of the two phases of repair.
在用甲基磺酸甲酯、甲基磺酸乙酯和甲基磺酸异丙酯处理后,对正常和着色性干皮病A互补组成纤维细胞中的DNA切除修复进行了检测。利用修复合成方法和阿拉伯糖胞苷抑制作用的研究揭示了两个不同的修复阶段;一个阶段在处理后的最初3 - 5小时内开始并结束,另一个阶段长得多,从处理后9 - 35小时开始。两个修复阶段都有一个长片段(类似紫外线的)成分,这首次证实了在烷烃磺酸盐损伤后存在这种修复模式。虽然着色性干皮病细胞在烷基化处理后其DNA中的碱性不稳定位点比正常细胞略少(这与早期观察结果一致,表明存在糖基化酶或脱嘌呤内切酶缺陷),但我们无法证明这些细胞在两个修复阶段中的任何一个阶段存在缺陷。