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喹乙醇作为一种抗菌促生长类兽药,能够通过环境转归和生物链富集作用危害人类健康。本文从构效关系和上下游通路角度出发,以细胞凋亡发生阶段为主线,对喹乙醇诱导细胞凋亡分子机制加以综述,综合分析了喹乙醇代谢产生ROS,诱导p53、Bax、Bcl、c-myc、p38MAPK蛋白表达和转录水平变化及对caspase酶系、细胞色素c的影响等过程。在此基础上提出了喹乙醇致细胞凋亡的可能途径,以期为喹乙醇健康损伤效应位点和方式的进一步研究提供依据。
Olaquindox, as an antimicrobial growth-promoting veterinary drug, can endanger human health through environmental conversion and bio-strand enrichment. Based on the structure-activity relationship and upstream and downstream pathways, the molecular mechanism of olaquindox-induced apoptosis was reviewed based on the stage of apoptosis. The molecular mechanism of olaquindox metabolism and the induction of p53, Bax, Bcl and c -myc, p38MAPK protein expression and transcriptional changes and the caspase enzyme, cytochrome c and other processes. On this basis, the possible pathways of olaquindox induced apoptosis were proposed in order to provide evidence for the further study of olaquindox’s healthy injury site and manner.