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

Authors
Park, JunhoAn, GaramLim, WhasunSong, Gwonhwa
Issue Date
5-8월-2022
Publisher
ELSEVIER
Keywords
Dinitramine; Porcine trophectoderm; Porcine endometrial luminal epithelium; Mitochondrial dysfunction; Cell cycle arrest; Apoptosis
Citation
JOURNAL OF HAZARDOUS MATERIALS, v.435
Indexed
SCIE
SCOPUS
Journal Title
JOURNAL OF HAZARDOUS MATERIALS
Volume
435
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/141801
DOI
10.1016/j.jhazmat.2022.128927
ISSN
0304-3894
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.
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