Picolinafen exposure induces ROS accumulation and calcium depletion, leading to apoptosis in porcine embryonic trophectoderm and uterine luminal epithelial cells during the peri-implantation period

The global use of herbicides accounts for more than 48% of total pesticide usage. Picolinafen is a pyridine carboxylic acid herbicide that is predominantly used to control broadleaf weeds in wheat, barley, corn, and soybeans. Despite its widespread use in agriculture, its toxicity in mammals has rarely been studied. In this study, we first identified the cytotoxic effects of picolinafen on porcine trophectoderm (pTr) and luminal epithelial (pLE) cells, which are involved in the implantation process during early pregnancy. Picolinafen treatment significantly decreased the viability of pTr and pLE cells. Our results demonstrate that picolinafen increased the number of sub-G1 phase cells and early/late apoptosis. In addition, picolinafen disrupted mitochondrial function and resulted in the accumulation of intracellular ROS, leading to a reduction in calcium levels in both the mitochondria and cytoplasm of pTr and pLE cells. Moreover, picolinafen was found to significantly inhibit the migration of pTr. These responses were accompanied by the activation of the MAPK and PI3K signal transduction pathways by picolinafen. Our data suggest that the deleterious effects of picolinafen on the viability and migration of pTr and pLE cells might impair their implantation potential.(c) 2023 Elsevier Inc. All rights reserved.

Automated summary

This study found that picolinafen has a significant impact on the viability of porcine trophectoderm and luminal epithelial cells involved in the implantation process during early pregnancy. It increased apoptosis, disrupted mitochondrial function, and caused intracellular ROS accumulation, which led to a reduction in calcium levels. Furthermore, it inhibited the migration of porcine trophectoderm cells. These effects were mediated by the activation of the MAPK and PI3K signaling pathways.