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目的:应用人类淋巴母细胞TK6研究微囊藻毒素Microcystin -LR (MCLR)的体外遗传毒性分子机理。方法:藻毒素MCLR (80 μg/ml)体外染毒TK6细胞2 4h后检测tk位点突变频率并进行TK基因缺失突变体LOH的分析。结果:MCLR染毒导致TK6细胞相对存活率下降,TK基因突变频率明显上升,达到对照的5 1倍。MCLR诱导产生半合子LOH(41 7% )的比例是对照(2 0 7% )的两倍。结论:体外2 4h染毒TK6细胞MCLR可致突变并表现出断裂剂特性,诱发杂合性丢失而非点突变。
OBJECTIVE: To study the molecular mechanism of in vitro genotoxicity of microcystin-LR (MCLR) using human lymphoblasts TK6. Methods: The frequency of tk locus mutation was detected after TKD cells were treated with MCLR (80 μg / ml) for 24 h and the LOH gene deletion mutant was analyzed. Results: The relative survival rate of TK6 cells decreased after MCLR exposure, and the frequency of TK gene mutation increased significantly, reaching 51 times of the control. The proportion of MCLR-induced production of hemizygous LOH (41 7%) was double that of the control (270%). CONCLUSION: MCLR of TK6 cells can be induced to mutate at 24 h in vitro and show the characteristics of fragmentation agent, inducing loss of heterozygosity but not point mutation.