Fox M, Carlton C M
Carcinogenesis. 1984 Nov;5(11):1531-2. doi: 10.1093/carcin/5.11.1531.
A reverse mutation assay HGPRT- to HGPRT+ has been used to demonstrate adaptation to the mutagenic effects of monofunctional alkylating agents. HGPRT- cells exposed to single doses of methylating or ethylating agents show maximum revertant frequencies immediately after treatment and these subsequently decline exponentially. Cells pre-treated with MNNG (1.0 microM) or MMS (0.27 mM) then challenged 6-168 h later with MNNG or EMS showed a consistent reduction in revertant frequencies. Pretreatment with EMS did not result in any reduction in EMS-induced reversion frequency. In parallel experiments no modifications in survival kinetics were observed. V79 cells do not remove O6-methylguanine and totally lack O6-methylguanine transferase activity, therefore other lesions and repair enzymes must be involved in the mutagenic adaptation observed.
已采用从次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶缺陷(HGPRT-)到次黄嘌呤 - 鸟嘌呤磷酸核糖转移酶正常(HGPRT+)的回复突变试验来证明对单功能烷化剂诱变作用的适应性。暴露于单剂量甲基化或乙基化试剂的HGPRT-细胞在处理后立即显示出最大回复频率,随后这些频率呈指数下降。先用N-甲基-N'-硝基-N-亚硝基胍(MNNG,1.0微摩尔)或甲基磺酸甲酯(MMS,0.27毫摩尔)预处理,然后在6至168小时后用MNNG或甲基磺酸乙酯(EMS)攻击的细胞,其回复频率持续降低。用EMS预处理并未导致EMS诱导的回复频率有任何降低。在平行实验中,未观察到存活动力学有任何改变。V79细胞不能去除O6-甲基鸟嘌呤且完全缺乏O6-甲基鸟嘌呤转移酶活性,因此,其他损伤和修复酶必定参与了所观察到的诱变适应性。