Herrera L A, Ostrosky-Wegman P, Schiffmann D, Chen Q Y, Ziegler-Skylakakis K, Andrae U
Instituto de Investigaciones Biomedicas, UNAM, Mexico, D.F., Mexico.
Mutat Res. 1993 Nov;303(3):121-5. doi: 10.1016/0165-7992(93)90024-p.
The insecticide buprofezin was examined for its genotoxicity in cultured Syrian hamster embryo cells in order to better understand the mechanisms underlying the genotoxicity of the compound in mammalian cells. Exposure to buprofezin concentrations of 12.5-100 microM did not significantly affect the colony-forming ability of the cells, but did result in increased frequencies of morphologically transformed colonies. Treatment with buprofezin did not cause a detectable induction of DNA repair synthesis, an indicator of DNA damage, but significantly increased the frequency of micronuclei. Immunostaining of the cells with antikinetochore antibody (CREST antibody) showed that essentially all of the buprofezin-induced micronuclei were kinetochore-positive. The results suggest that morphological transformation of Syrian hamster embryo cells by buprofezin results from an interaction of the compound or a metabolite of it with the mitotic apparatus rather than from DNA damage.
为了更好地理解该化合物在哺乳动物细胞中的遗传毒性机制,对杀虫剂噻嗪酮在培养的叙利亚仓鼠胚胎细胞中的遗传毒性进行了研究。暴露于浓度为12.5 - 100微摩尔的噻嗪酮中对细胞的集落形成能力没有显著影响,但确实导致形态转化集落的频率增加。用噻嗪酮处理并未引起可检测到的DNA修复合成诱导(DNA损伤的一个指标),但显著增加了微核的频率。用抗动粒抗体(CREST抗体)对细胞进行免疫染色显示,基本上所有噻嗪酮诱导的微核都是动粒阳性的。结果表明,噻嗪酮引起的叙利亚仓鼠胚胎细胞形态转化是该化合物或其代谢产物与有丝分裂装置相互作用的结果,而非DNA损伤所致。