Exposure to iprodione induces ROS production and mitochondrial dysfunction in porcine trophectoderm and uterine luminal epithelial cells, leading to implantation defects during early pregnancy

This study demonstrated a series of cytotoxic responses of iprodione along with the alteration of implantation-related gene expression in porcine trophectoderm (pTr) and luminal epithelium (pLE) cells. In this study, iprodione suppressed cell viability, proliferation, and migration of these cells. Iprodione induced G1 phase arrest and attenuated spheroid formation by pTr and pLE cells. Furthermore, iprodione caused mitochondrial dysfunction and excessive reactive oxygen species generation, which resulted in an increase in mitochondrial calcium levels. Consequently, DNA damage and apoptotic cell death were induced by iprodione treatment in pTr and pLE cells. This stress-induced cell death was mediated by alterations in intracellular signal transduction, including the PI3K/AKT and MAPK signaling pathways. This finding suggests the potential of iprodione to impair the implantation capacity by exerting cytotoxic effects on fetal and maternal cells.PMID:35926749 | DOI:10.1016/j.chemosphere.2022.135894
Source: Chemosphere - Category: Chemistry Authors: Source Type: research