2. Academic Validation
  3. Exposure to etoxazole induces mitochondria-mediated apoptosis in porcine trophectoderm and uterine luminal epithelial cells

Exposure to etoxazole induces mitochondria-mediated apoptosis in porcine trophectoderm and uterine luminal epithelial cells

  • Environ Pollut. 2020 Feb;257:113480. doi: 10.1016/j.envpol.2019.113480.
Wonhyoung Park 1,  Whasun Lim 2,  Sunwoo Park 1,  Kwang-Youn Whang 3,  Gwonhwa Song 4
Affiliations

Affiliations

  • 1 Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea.
  • 2 Department of Food and Nutrition, Kookmin University, Seoul, 02707, Republic of Korea.
  • 3 Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea. Electronic address: kwhang@korea.ac.kr.
  • 4 Institute of Animal Molecular Biotechnology and Department of Biotechnology, College of Life Sciences and Biotechnology, Korea University, Seoul, 02841, Republic of Korea. Electronic address: ghsong@korea.ac.kr.
PMID: 31744678 DOI: 10.1016/j.envpol.2019.113480
Abstract

Etoxazole is an organofluorine insecticide widely used in agriculture. Exposure to insecticides is a serious environmental problem owing to their cytotoxic effects in humans and Animals. Reproductive toxicity of various organofluorine insecticides have been shown in previous studies. However, few studies have evaluated the toxicity of etoxazole in mammals. We aimed to examine the toxic effects of etoxazole in porcine trophectoderm (pTr) and uterine luminal epithelial (pLE) cells. To estimate the effects of etoxazole, we conducted assays after treatment with multiple concentration of etoxazole (0, 2, 4, 6 and 9 μM) to pTr and pLE cells for 0-72 h. Etoxazole decreased the cell proliferation, viability, and migration of pTr and pLE cells. Further, etoxazole induced Apoptosis via cell cycle arrest and disruption of mitochondrial membrane potential. We also found that pro-apoptotic proteins and endoplasmic reticulum (ER) stress-response proteins were activated in response to etoxazole. Finally, we observed that etoxazole altered the PI3K/Akt and MAPK signaling pathways and the mRNA expression of genes associated with implantation. Collectively, these results suggest that etoxazole disrupts normal cellular physiology and might cause early implantation failure.

Keywords

Apoptosis; Endometrium; Etoxazole; Pregnancy; Trophectoderm.

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