Bifenthrin reduces pregnancy potential via induction of oxidative stress in porcine trophectoderm and uterine luminal epithelial cells.

Exposure to pesticides has become a serious concern for the environment and human health. Bifenthrin, a synthetic pyrethroid pesticide, is one of the most frequently used pesticides worldwide. Despite the toxic potential of bifenthrin, no studies have elucidated the cytotoxic response of bifenthrin in maternal and fetal cells that are involved in the implantation process. In this study, the cytotoxic effect of bifenthrin was investigated using porcine trophectoderm (pTr) and uterine luminal epithelial (pLE) cells. The results showed that bifenthrin suppressed cell proliferation and viability in pTr and pLE cells. In particular, bifenthrin induced cell cycle arrest, resulting in apoptosis in both cell lines. We found that bifenthrin damaged the mitochondria and induced the production of reactive oxygen species, causing endoplasmic reticulum stress and calcium dysregulation in pTr and pLE cells. Finally, bifenthrin altered the MAPK/PI3K signaling pathway and pregnancy-related gene expression. Collectively, our results suggest that bifenthrin reduces the implantation potential of embryos and may help elucidate the mechanisms underlying toxin-derived cytotoxicity in maternal and fetal cells.