Trichlorfon inhibits proliferation and promotes apoptosis of porcine trophectoderm and uterine luminal epithelial cells

A schematic diagram of mechanisms responsible for proapoptotic and antiproliferative effects of trichlorfon on pTr and pLE cells. Trichlorfon decreased the phosphorylation of PI3K/AKT and MAPK signaling proteins, which are normally activated during cell proliferation. Also, trichlorfon decreased the expression of PCNA and phosphorylation of cyclin D1 resulting in cell cycle arrest. In addition, a mitochondrial Ca2+ overload induced by trichlorfon in pTr cells may be responsible for the decrease in mitochondrial membrane potential (MMP, Δψm). Loss of Δψm subsequently promoted apoptosis in pTr and pLE cells. Overall, exposure to trichlorfon decreased the viability of pTr and pLE cells which may cause pregnancy failure.181