Abstract
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.
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