Trichloropyridinol (TCP); 3, 5, 6-trichloro-2-pyridinol is the primary metabolites of the organophosphorus pesticide chlorpyrifos. It is more highly persistent than parent compounds in the environment and might represent serious risks to human health. In this study, we investigated the toxicological effects and mechanism of TCP on HepG2 cells. The results revealed that TCP induced DNA damage and apoptosis on HepG2 cells. Besides, up-regulating the expression level of Bax /Bcl-2, a reduction in mitochondrial membrane potential, caspase-9/-3 activation and the release of cytochrome-c are contributed to the toxicological effects of TCP on HepG2 cells. These data indicated that the cytotoxic effects of TCP might be associated with the activity of mitochondrial apoptotic pathways. In conclusion, the results demonstrated that TCP poses a potential threat to human health by inducing toxicological effects in the liver.

三氯吡啶醇 (TCP); 3, 5, 6-trichloro-2-pyridinol 是有机磷农药毒死蜱的主要代谢物。它比环境中的母体化合物具有更高的持久性，可能对人类健康构成严重威胁。在这项研究中，我们研究了 TCP 对 HepG2 细胞的毒理学作用和机制。结果显示TCP诱导HepG2细胞的DNA损伤和凋亡。此外，上调 Bax /Bcl-2 的表达水平、线粒体膜电位的降低、caspase-9/-3 的激活和细胞色素-c 的释放都有助于 TCP 对 HepG2 细胞的毒理学作用。这些数据表明 TCP 的细胞毒作用可能与线粒体凋亡通路的活性有关。综上所述，