Jansson K, Hyttinen J M, Niittykoski M, Mäki-Paakkanen J
Division of Environmental Health, National Public Health Institute, Kuopio, Finland.
Environ Mol Mutagen. 1995;25(4):284-7. doi: 10.1002/em.2850250404.
The mutagenicity of chlorinated humic drinking waters is accounted for mainly by a single contaminant, 3-chloro-4-(dichloromethyl)-5-hydroxy-2(5H)-furanone (MX), as assessed in Salmonella typhimurium strain TA100. In the present study 3,4-dichloro-5-hydroxy-2(5H)-furanone (mucochloric acid, MA), another drinking water contaminant much less potent as a mutagen in TA100 than MX, was tested in Chinese hamster ovary (CHO) cells for the induction of mutation at the hypoxanthine phosphoribosyl transferase (hprt) locus to 6-thioguanine resistance (TGr). Unexpectedly, MA induced TGr mutants in CHO cells with a potency comparable to that reported previously for MX. In subsequent experiments with S. typhimurium, the presence of pKM101 plasmid in strain TA100 increased susceptibility to the mutagenicity of MA, but much less than to that of MX, relative to the parental strain TA1535 lacking pKM101. The difference between the two compounds in TA100 thus appears to be due to a higher enhancement of the mutagenicity of MX than that of MA by pKM101 mediated error-prone DNA repair.
通过鼠伤寒沙门氏菌TA100菌株评估发现，氯化腐殖酸类饮用水的致突变性主要由单一污染物3-氯-4-（二氯甲基）-5-羟基-2（5H）-呋喃酮（MX）引起。在本研究中，另一种饮用水污染物3,4-二氯-5-羟基-2（5H）-呋喃酮（粘氯酸，MA）在TA100菌株中的致突变性远低于MX，本研究在中华仓鼠卵巢（CHO）细胞中测试了MA诱导次黄嘌呤磷酸核糖转移酶（hprt）基因座发生突变产生6-硫鸟嘌呤抗性（TGr）的情况。出乎意料的是，MA在CHO细胞中诱导产生TGr突变体的效力与之前报道的MX相当。在随后对鼠伤寒沙门氏菌的实验中，相对于缺乏pKM101的亲本菌株TA1535，TA100菌株中pKM101质粒的存在增加了对MA致突变性的敏感性，但远低于对MX的敏感性。因此，TA100中这两种化合物之间的差异似乎是由于pKM101介导的易错DNA修复对MX致突变性的增强作用高于MA。
