Tebufenpyrad induces cell cycle arrest and disruption of calcium homeostasis in porcine trophectoderm and luminal epithelial cells

Tebufenpyrad is classified as a pyrazole acaricide and insecticide. It is widely used for several crops, especially in greenhouses, in several countries. While its unfavorable effects on non-target organisms have already been established, relatively little is known about its reproductive toxicity. Therefore, we demonstrated the biochemical effects of tebufenpyrad using porcine trophectoderm and porcine luminal epithelial cells, which are involved in implantation. We found that tebufenpyrad had antiproliferative effects and reduced cell viability. Tebufenpyrad also triggered apoptosis and excessive reactive oxygen species production. Furthermore, it induced cell cycle arrest in the G1 phase and disrupted calcium homeostasis in the cytosol and mitochondria. MAPK signaling pathways and the crosstalk among them were altered following tebufenpyrad treatment. In addition, the migration ability of cells was reduced after treatment with tebufenpyrad. Lastly, tebufenpyrad influenced the expression of genes related to pregnancy. Collectively, these results reveal the mechanism of the biochemical and physiological effects of tebufenpyrad to both trophectoderm and uterine cells and suggest that tebufenpyrad reduces the potential of successful implantation.

Automated summary

Tebufenpyrad, a pyrazole acaricide and insecticide, has been widely used in several countries for various crops. This study investigated the biochemical and physiological effects of tebufenpyrad on porcine trophectoderm and luminal epithelial cells, revealing its antiproliferative effects, apoptosis induction, reactive oxygen species production, cell cycle arrest, disrupted calcium homeostasis, altered MAPK signaling pathways, reduced cell migration ability, and influence on gene expression related to pregnancy.