Dinitramine induces implantation failure by cell cycle arrest and mitochondrial dysfunction in porcine trophectoderm and luminal epithelial cells

Junho Park, Garam An, Whasun Lim, Gwonhwa Song

Research output: Contribution to journalArticlepeer-review

Abstract

The herbicide market is growing rapidly, as weed control is a significant challenge in agriculture. Many studies have reported the toxicity of herbicides to non-target organisms. Dinitramine is a dinitroaniline herbicide that is particularly toxic to aquatic organisms. However, little is known about the effects of dinitramine on the female reproductive system. Therefore, in the present study, we utilized porcine trophectoderm (pTr) cells and porcine endometrial luminal epithelial (pLE) cells to verify the reproductive toxicity of dinitramine. Dinitramine reduced the viability of both cell types, by triggering cell cycle arrest, especially at the sub-G1 phase, and increasing apoptosis, inhibiting DNA replication. Dinitramine disrupted intracellular calcium homeostasis and induced oxidative stress by producing reactive oxygen species, leading to the loss of mitochondrial membrane potential and alteration of mitochondrial respiration. Mitogen-activated protein kinase pathways were altered, and migration decreased in pTr and pLE cells after dinitramine treatment; the expression of pregnancy-related genes in these cells was decreased. Thus, dinitramine reduced the viability and migratory capacity of both cell types, and this could interrupt the early stages of pregnancy.

Original languageEnglish
Article number128927
JournalJournal of hazardous materials
Volume435
DOIs
Publication statusPublished - 2022 Aug 5

Keywords

  • Apoptosis
  • Cell cycle arrest
  • Dinitramine
  • Mitochondrial dysfunction
  • Porcine endometrial luminal epithelium
  • Porcine trophectoderm

ASJC Scopus subject areas

  • Environmental Engineering
  • Environmental Chemistry
  • Waste Management and Disposal
  • Pollution
  • Health, Toxicology and Mutagenesis

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