Altamirano-Dimas M, Sklar R, Strauss B
Mutat Res. 1979 Apr;60(2):197-206. doi: 10.1016/0027-5107(79)90184-2.
Lymphoblastoid cell derived from a complementation group C xeroderma patient were unable to remove 06-methyl guanine residues formed in DNA by treatment of cells with low concentration of N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). The xeroderma cells were competent in their ability to excise 3-methyl adenine adducts. MNNG treatment induced excision repair in the xeroderma line and in addition the treatment resulted in the presence of numerous single-strand breaks in the DNA. The single gene, UV-excision-defective mutants of Escherichia coli, uvrA and uvrB, are able to excise MNNG-induced 06-methyl guanine adducts indicating that excision of this compound is not due to operation of UV endonuclease system.
从一名互补组C型着色性干皮病患者身上获取的淋巴母细胞,在经低浓度的N-甲基-N'-硝基-N-亚硝基胍(MNNG)处理细胞后,无法去除DNA中形成的06-甲基鸟嘌呤残基。着色性干皮病细胞在切除3-甲基腺嘌呤加合物的能力方面是正常的。MNNG处理诱导了着色性干皮病细胞系中的切除修复,此外,该处理还导致DNA中出现大量单链断裂。大肠杆菌的单基因紫外线切除缺陷突变体uvrA和uvrB能够切除MNNG诱导的06-甲基鸟嘌呤加合物,这表明该化合物的切除并非由于紫外线内切酶系统的作用。