Jansson K, Jansson V
Department of Cell Biology, University of Jyväskylä, Finland.
Mutat Res. 1992;280(3):175-9. doi: 10.1016/0165-1218(92)90046-3.
The genotoxicity of the rodent carcinogen 2,4,6-trichlorophenol (TCP) was studied without exogenous metabolic activation in V79 Chinese hamster cells. TCP did not induce mutation at the hprt locus to 6-thioguanine resistance or structural chromosome aberrations. However, it produced statistically significant, dose-related increases in hyperdiploidy and micronuclei. From these results it appears that TCP causes chromosome malsegregation as its major mode of genotoxic action.
在V79中国仓鼠细胞中，对啮齿动物致癌物2,4,6-三氯苯酚（TCP）的遗传毒性进行了研究，实验中未添加外源性代谢激活剂。TCP未诱导次黄嘌呤磷酸核糖转移酶（hprt）基因座发生突变，使其对6-硫鸟嘌呤产生抗性，也未诱导结构性染色体畸变。然而，它导致超二倍体和微核在统计学上出现显著的剂量相关增加。从这些结果来看，TCP导致染色体错分是其主要的遗传毒性作用模式。
