de Moraes E C, Tyrrell R M
Mutat Res. 1981 Feb;80(2):229-38. doi: 10.1016/0027-5107(81)90095-6.
The mutagenic interaction between near-ultraviolet (365 nm) radiation and the alkylating agents ethyl methanesulphonate (EMS) and methyl methanesulphonate (MMS) was studied in a repair-competent and an excision-deficient strain of Escherichia coli. Near-UV radiation modified the metabolic response of exposure to these chemicals and either reduced or increased their mutagenic efficiency. Based on these results, an experimental model was formulated to explain the mutagenic interactions that occur between near-UV and various agents that induce prototrophic revertants via error-prone repair of DNA. According to this model, low doses of near-UV provoke conditions for mutation frequency decline (MFD) and lead to a mutagenic antagonism. With increasing near-UV doses, damage to constitutive error-free repair systems increases, favouring the error-prone system and inhibiting the MFD. Under these conditions there will be a progressive decrease in antagonism until at high doses an enhancement of mutation frequency (positive interaction) will occur.
在具有修复能力的和切除缺陷型的大肠杆菌菌株中，研究了近紫外线（365纳米）辐射与烷化剂甲磺酸乙酯（EMS）和甲磺酸甲酯（MMS）之间的诱变相互作用。近紫外线辐射改变了对这些化学物质暴露的代谢反应，要么降低要么提高它们的诱变效率。基于这些结果，构建了一个实验模型来解释近紫外线与通过DNA易错修复诱导原养型回复突变体的各种试剂之间发生的诱变相互作用。根据这个模型，低剂量的近紫外线引发突变频率下降（MFD）的条件并导致诱变拮抗作用。随着近紫外线剂量增加，对组成型无差错修复系统的损伤增加，有利于易错系统并抑制MFD。在这些条件下，拮抗作用将逐渐降低，直到在高剂量时发生突变频率增强（正向相互作用）。
