Jenssen D
Mutat Res. 1986 May;165(3):185-90. doi: 10.1016/0167-8817(86)90053-2.
The mutagenicity of MNU, EMS, BMS and UV light was compared by analyzing the dose-response curve just before and after the replicative process of the HGPRT gene in synchronized V79 Chinese hamster cells. This system makes it possible to compare a 10-h period for repair of different mutagenic lesions with no time for repair. Additional time for repair in synchronized V79 cells resulted in a reduced response for MNU and UV, but not for EMS and BMS. This result suggests that an error-free repair process operates on mutagenic lesions in methylated DNA and on thymine dimers, but not on ethylated and butylated DNA. Based on these results, it is concluded that the repair capacity of V79 cells to remove mutagenic lesions is characterized as low for UV, moderate for MNU and not detectable for the mutagenic lesions induced by EMS and BMS.
通过分析同步化的V79中国仓鼠细胞中HGPRT基因复制过程前后的剂量反应曲线，比较了N-甲基-N-亚硝基脲（MNU）、甲基磺酸乙酯（EMS）、丁磺酸丁酯（BMS）和紫外线（UV）的致突变性。该系统使得能够比较不同诱变损伤修复的10小时时间段，且没有修复时间。同步化的V79细胞中额外的修复时间导致对MNU和UV的反应降低，但对EMS和BMS则不然。该结果表明，无差错修复过程作用于甲基化DNA中的诱变损伤和胸腺嘧啶二聚体，但不作用于乙基化和丁基化DNA。基于这些结果，可以得出结论，V79细胞去除诱变损伤的修复能力对于UV而言较低，对于MNU而言中等，而对于EMS和BMS诱导的诱变损伤则无法检测到。
