TY - JOUR
T1 - Fluroxypyr-1-methylheptyl ester induced ROS production and mitochondrial apoptosis through the MAPK signaling cascade in porcine trophectoderm and uterine luminal epithelial cells
AU - Kim, Miji
AU - An, Garam
AU - Lim, Whasun
AU - Song, Gwonhwa
N1 - Funding Information:
This research was supported by the National Research Foundation of Korea (NRF) grant funded by the Korea government (MSIT) (grant number: 2021R1A2C2005841 & 2021R1C1C1009807 ).
Publisher Copyright:
© 2022 Elsevier Inc.
PY - 2022/10
Y1 - 2022/10
N2 - FPMH (Fluroxypyr-1-methylheptyl ester) is a synthetic auxin herbicide used in agriculture. The mechanism by which FPMH induces adverse effects in porcine trophectoderm (pTr) and porcine uterine luminal epithelial (pLE) cells, which are involved in porcine implantation, have not been studied yet. Therefore, the present study investigates the toxicological effects of FPMH on pTr and pLE cells. We confirmed that FPMH induced cytotoxic effects on the cells, including apoptosis induction, mitochondrial membrane potential (MMP) depolarization, and ROS production. The phosphorylation of the MAPK pathway (ERK1/2, JNK, and p38) was dysregulated by FPMH administration. In addition, FPMH could suppress cell-cell adhesion and migration abilities of pTr and pLE, which are crucial for implantation. Therefore, exposure to FPMH induced adverse effects in pTr and pLE cells and could result in implantation failure.
AB - FPMH (Fluroxypyr-1-methylheptyl ester) is a synthetic auxin herbicide used in agriculture. The mechanism by which FPMH induces adverse effects in porcine trophectoderm (pTr) and porcine uterine luminal epithelial (pLE) cells, which are involved in porcine implantation, have not been studied yet. Therefore, the present study investigates the toxicological effects of FPMH on pTr and pLE cells. We confirmed that FPMH induced cytotoxic effects on the cells, including apoptosis induction, mitochondrial membrane potential (MMP) depolarization, and ROS production. The phosphorylation of the MAPK pathway (ERK1/2, JNK, and p38) was dysregulated by FPMH administration. In addition, FPMH could suppress cell-cell adhesion and migration abilities of pTr and pLE, which are crucial for implantation. Therefore, exposure to FPMH induced adverse effects in pTr and pLE cells and could result in implantation failure.
KW - Apoptosis
KW - Fluroxypyr
KW - Mitochondrial membrane potential
KW - ROS production
KW - Trophectoderm
KW - Uterine luminal epithelial
UR - http://www.scopus.com/inward/record.url?scp=85135723568&partnerID=8YFLogxK
U2 - 10.1016/j.pestbp.2022.105196
DO - 10.1016/j.pestbp.2022.105196
M3 - Article
C2 - 36127068
AN - SCOPUS:85135723568
VL - 187
JO - Pesticide Biochemistry and Physiology
JF - Pesticide Biochemistry and Physiology
SN - 0048-3575
M1 - 105196
ER -