Trichlorfon inhibits proliferation and promotes apoptosis of porcine trophectoderm and uterine luminal epithelial cells
- Authors
- Lim, Whasun; An, Yikyung; Yang, Changwon; Bazer, Fuller W.; Song, Gwonhwa
- Issue Date
- 11월-2018
- Publisher
- ELSEVIER SCI LTD
- Keywords
- Trichlorfon; Pig; Trophoblast; Uterine luminal epithelium; Apoptosis; Cell cycle arrest
- Citation
- ENVIRONMENTAL POLLUTION, v.242, pp.555 - 564
- Indexed
- SCIE
SCOPUS
- Journal Title
- ENVIRONMENTAL POLLUTION
- Volume
- 242
- Start Page
- 555
- End Page
- 564
- URI
- https://scholar.korea.ac.kr/handle/2021.sw.korea/72053
- DOI
- 10.1016/j.envpol.2018.07.032
- ISSN
- 0269-7491
- Abstract
- Trichlorfon is an organophosphate insecticide widely used in agriculture. Additionally, it is applied to pigs for control of endo- and ectoparasites. Previous studies have shown the effects of trichlorfon in pigs during late stages of gestation; however, little is known about its effects during early pregnancy, including implantation and placentation. We investigated whether trichlorfon affects proliferation and apoptosis of porcine trophectoderm (pTr) and uterine luminal epithelial (pLE) cells. Trichlorfon inhibited the proliferation of pTr and pLE cells, as evidenced by cell cycle arrest, and altered the expression of proliferation-related proteins. In addition, trichlorfon induced cell death and apoptotic features, such as loss of mitochondrial membrane potential and DNA fragmentation, in pTr and pLE cells. Moreover, trichlorfon treatment decreased concentrations of Ca2+ in the cytoplasm in both cell lines and increased concentrations of Ca2+ in mitochondria of pTr cells. Trichlorfon inhibited the activation of phosphoinositide 3-kinase/AKT and mitogen-activated protein kinase signaling pathways in pTr and pLE cells. Therefore, we suggest that trichlorfon-treated pTr and pLE cells exhibited abnormal cell physiology which might lead to early pregnancy failure. (C) 2018 Elsevier Ltd. All rights reserved.
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