(207) Mitochondrial dysfunction induced by dipropetryn in porcine trophectoderm and uterine luminal epithelial cells causes programmed cell death

Mitochondrial dysfunction induced by dipropetryn in porcine trophectoderm and uterine luminal epithelial cells causes programmed cell death

Y. Kim¹, J. Song², T. Hong², J. Park², F.W. Bazer³, W. Lim^1,2

¹Department of MetaBioHealth, Sungkyunkwan University, Suwon, Republic of Korea

²Department of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea

³Department of Animal Science, Texas A&M University, College Station, TX, USA

Abstract Text:

Mitochondrial dysfunction induced by dipropetryn in porcine trophectoderm and uterine luminal epithelial cells causes programmed cell death

Y. Kim¹, J. Song², T. Hong², J. Park², F.W. Bazer³, W. Lim^1,2

¹Department of MetaBioHealth, Sungkyunkwan University, Suwon, Republic of Korea

²Department of Biological Sciences, Sungkyunkwan University, Suwon, Republic of Korea

³Department of Animal Science, Texas A&M University, College Station, TX, USA

Dipropetryn is a selective, systemic triazine herbicide that inhibits photosynthetic electron transport at photosystem II receptor site, thereby disrupting photosynthesis in target plants. While its primary use is in agricultural and aquatic environments, concerns have arisen regarding its potential impact on mammalian reproductive health due to environmental exposure. The trophectoderm and endometrial luminal epithelial cells play crucial roles in early implantation by blastocysts and uterine receptivity to implantation, making them valuable models for assessing reproductive toxicity of environmental contaminants. This study investigated the effects of dipropetryn on porcine trophectoderm (pTr) and uterine luminal epithelial (pLE) cells using various biochemical and molecular analyses. Dipropetryn exposure significantly reduced cell viability and induced mitochondrial dysfunction, as evidenced by increased mitochondrial depolarization and altered intracellular calcium levels. Apoptotic cell death was markedly elevated, with significant increases in early, late, and total populations of apoptotic cells. Metabolic analysis revealed declines in basal respiration, maximal respiration, and ATP production, indicating impaired cellular energy metabolism. Additionally, alterations in cell cycle progression and dysregulation of key signaling pathways, including MAPK and PI3K, were detected. Collectively, this research identified cytotoxic and metabolic disruptions caused by dipropetryn, suggesting its potential to impair functions of cells critical to the establishment of pregnancy in pigs. Further, the results provide new insights into the toxicological effects of a triazine herbicide and underscores the necessity for further research on their biological impacts.