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Fluroxypyr-1-methylheptyl ester causes apoptosis of bovine mammary gland epithelial cells by regulating PI3K and MAPK signaling pathways and endoplasmic reticulum stress

Authors
An, GaramPark, WonhyoungLim, WhasunSong, Gwonhwa
Issue Date
1월-2022
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Keywords
Fluroxypyr-1-methylheptyl ester; MAC-T; Apoptosis; Endoplasmic reticulum stress; Signal transduction
Citation
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY, v.180
Indexed
SCIE
SCOPUS
Journal Title
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
Volume
180
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/135326
DOI
10.1016/j.pestbp.2021.105003
ISSN
0048-3575
Abstract
Fluroxypyr-1-methylheptyl ester (FPMH) is an auxin herbicide that is widely applied to crops and pastures to block growth of post-emergence weeds. Several studies have reported the toxicity of FPMH in aquatic vertebrates. However, the adverse impacts of FPMH on mammals, including domestic animals, have not been reported. The purpose of our current study is to assess the impact of FPMH on the bovine mammary system and milk production. To evaluate the toxicity of FPMH on the mammary glands of lactating cows, the bovine mammary gland epithelial cell line, MAC-T, was exposed to various concentrations (0, 5, 7.5, 10, 15, and 20 mu M) of FPMH for 24 h, and then various assessments were performed. The results showed that FPMH dose dependently reduced MAC-T cell viability following exposure to FPMH and induced mitochondrial depolarization and apoptosis. FPMH also modulated signaling through the PI3K and MAPK pathways. In addition, the expression levels of proteins related to endoplasmic reticulum (ER) stress were upregulated, indicating induction of ER stress, and calcium homeostasis was disrupted following FPMH treatment. In conclusion, our investigation suggests that FPMH may be toxic to the bovine mammary system and may decrease dairy production.
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