Suri A, deBoer J, Kusser W, Glickman B W
Centre for Environmental Health, Department of Biology, University of Victoria, B.C., Canada.
Mutat Res. 1996 Nov 11;372(1):23-31. doi: 10.1016/S0027-5107(96)00105-4.
The mechanisms by which an electromagnetic field (EMF) influences biological material are poorly understood. One potentially important model suggests that a magnetic field can stabilize free radicals in such a way as to permit their dispersement rather than their return to the ground state (Okazaki et al., 1988; Scaiano, 1995). We have tested this hypothesis by examining mutagenesis in the E. coli lacI gene target carried in the Big Blue rat embryo fibroblast cell line, R2 lambda LIZ. Mutant frequencies were determined in cells exposed to a magnetic field, cells pretreated with the mutagens N-methylnitrosourea (MNU) or 2-methyl-1,4-naphthoquinone (menadione), prior to being held in a 60 Hz 3 milliTesla (mT) magnetic field and cells concurrently exposed to the mutagens and the magnetic field. Menadione was selected because its mutagenic mechanism involves the formation of free radicals, while MNU is an alkylating agent not thought to act through radical formation. According to the radical stabilization hypothesis the application of a magnetic field to menadione treated cells would accentuate the mutagenic effects. Our results failed to indicate that the magnetic field affects mutagenesis by the oxygen-radical mediated mutagen, menadione.
电磁场（EMF）影响生物材料的机制目前还知之甚少。一种潜在的重要模型表明，磁场能够以某种方式稳定自由基，使其得以扩散而非回到基态（冈崎等人，1988年；斯卡亚诺，1995年）。我们通过检测携带于大蓝大鼠胚胎成纤维细胞系R2 lambda LIZ中的大肠杆菌lacI基因靶点的诱变情况，对这一假说进行了验证。在暴露于磁场的细胞、在置于60赫兹3毫特斯拉（mT）磁场之前先用诱变剂N-甲基亚硝基脲（MNU）或2-甲基-1,4-萘醌（甲萘醌）预处理的细胞以及同时暴露于诱变剂和磁场的细胞中，测定了突变频率。选择甲萘醌是因为其诱变机制涉及自由基的形成，而MNU是一种烷基化剂，一般认为其作用并非通过自由基形成。根据自由基稳定假说，对经甲萘醌处理的细胞施加磁场会增强诱变效应。但我们的结果并未表明磁场会影响由甲萘醌这种氧自由基介导的诱变剂所引发的诱变作用。
