Kuo M L, Lin J K
Institute of Toxicology, College of Medicine, National Taiwan University, Taipei.
Mutat Res. 1993 Aug;300(3-4):223-9. doi: 10.1016/0165-1218(93)90054-h.
The genotoxic potencies of waste water condensate from paraquat manufacturing and its pyridyl components on V79 cells were evaluated using the alkaline elution assay and 6-thioguanine resistance mutation assay. Although 2,2'-dipyridyl and 2,2',2"-tripyridyl both were highly cytotoxic to the cells, only 2,2'-dipyridyl induced moderate DNA-cleaving activity and a low frequency of thioguanine resistance mutation in V79 cells. However, equally toxic doses of waste water condensate exhibited highly DNA-damaging and mutagenic activities in the same cell system. After chelation of ferrous ions, the number of DNA lesions and frequency of 6-TGr mutations induced by waste water condensate were slightly suppressed, whereas by contrast those induced by 2,2'-dipyridyl were significantly potentiated. These results indicate that the coordination compound formation of pyridyl derivatives of waste water with metal ions, especially ferrous ions, in biological systems may be closely related to these genotoxic mechanisms. Finally, it was found that DMSO (a scavenger of hydroxyl radical) and catalase could remarkably protect cells from genotoxic damage induced by waste water condensate, 2,2'-dipyridyl and their ferrous complexes, but this protection was not observed in cells which were treated with SOD (superoxide dismutase). This suggests that the generation of some unknown active oxygen species may be involved in the genotoxic mechanisms of waste water condensate and its constituent 2,2'-dipyridyl.
使用碱性洗脱试验和6-硫鸟嘌呤抗性突变试验,评估了百草枯生产废水冷凝物及其吡啶基成分对V79细胞的遗传毒性潜力。尽管2,2'-联吡啶和2,2',2''-三联吡啶对细胞均具有高度细胞毒性,但只有2,2'-联吡啶在V79细胞中诱导了中等程度的DNA切割活性和低频率的硫鸟嘌呤抗性突变。然而,相同毒性剂量的废水冷凝物在同一细胞系统中表现出高度的DNA损伤和诱变活性。在螯合亚铁离子后,废水冷凝物诱导的DNA损伤数量和6-TGr突变频率略有抑制,而相比之下,2,2'-联吡啶诱导的则显著增强。这些结果表明,废水中吡啶基衍生物与金属离子,尤其是亚铁离子,在生物系统中形成的配位化合物可能与这些遗传毒性机制密切相关。最后,发现二甲基亚砜(一种羟基自由基清除剂)和过氧化氢酶可以显著保护细胞免受废水冷凝物、2,2'-联吡啶及其亚铁络合物诱导的遗传毒性损伤,但在用超氧化物歧化酶(SOD)处理的细胞中未观察到这种保护作用。这表明某些未知活性氧物种的产生可能参与了废水冷凝物及其成分2,2'-联吡啶的遗传毒性机制。