Doherty A T, Ellard S, Parry E M, Parry J M
School of Biological Sciences, University of Wales, Swansea, UK.
Mutat Res. 1996 Dec;372(2):221-31. doi: 10.1016/s0027-5107(96)00142-x.
The potential of the pesticide trichlorfon to induce mitotic aneuploidy has been investigated in genetically engineered human lymphoblastoid cell lines. Trichlorfon failed to induce micronuclei in the AHH-1 and MCL-5 cell lines when treated in media at normal cell culture pH (pH 7.3). Under a treatment pH of 5.5, trichlorfon exposures resulted in the induction of both chromosome loss and chromosome non-disjunction as measured by fluorescence in situ hybridisation (FISH) using a pan-centromeric probe for all human centromeres and centromere probes specific for chromosomes 2, 7 and 18. At treatment concentrations greater than 20 micrograms/ml trichlorfon also induced structural chromosome damage resulting in the production of centromere negative micronuclei.
已在基因工程改造的人类淋巴母细胞系中研究了农药敌百虫诱导有丝分裂非整倍体的潜力。当在正常细胞培养pH值（pH 7.3）的培养基中处理时，敌百虫未能在AHH - 1和MCL - 5细胞系中诱导微核形成。在pH 5.5的处理条件下，通过使用针对所有人类着丝粒的泛着丝粒探针以及针对染色体2、7和18的特异性着丝粒探针进行荧光原位杂交（FISH）检测，发现敌百虫暴露导致了染色体丢失和染色体不分离。在处理浓度大于20微克/毫升时，敌百虫还诱导了结构性染色体损伤，导致产生着丝粒阴性微核。
