PMID- 36724846
OWN - NLM
STAT- MEDLINE
DCOM- 20230223
LR  - 20231213
IS  - 1873-6351 (Electronic)
IS  - 0278-6915 (Linking)
VI  - 173
DP  - 2023 Mar
TI  - Maternal exposure to a glyphosate-based herbicide impairs placental development 
      through endoplasmic reticulum stress in mice.
PG  - 113640
LID - S0278-6915(23)00042-X [pii]
LID - 10.1016/j.fct.2023.113640 [doi]
AB  - Glyphosate-based herbicides (GBHs) are the most widely used agrochemicals 
      worldwide, increasing the risk of their occurrence in the environment. This study 
      aimed to explore effects and mechanisms of GBH exposure on placental development 
      in vivo during pregnancy in mice. Pregnant mice received GBH by gavage at 0, 5, 
      and 50 mg⋅kg(-1)⋅day(-1) doses from gestational day (GD) 1 to GD 13 and were 
      sacrificed on GD 13 or GD19. Our data indicated that GBH administration 
      significantly increased the number of resorbed fetuses, reduced the weight of 
      fetuses and placentas, and inhibited placental growth, as evident from decreased 
      placental total area and spongiotrophoblast area on GD 19. GBH treatment also 
      inhibited proliferation and induced apoptosis of placenta via upregulation of 
      Bax, cleaved caspase-3 and -12 expression, and downregulation of B cell lymphoma 
      (Bcl)-2 expression. Further study showed that GBH exposure significantly 
      increased expression levels of glucose-regulated protein 78 (GRP78), protein 
      kinase RNA-like endoplasmic reticulum kinase (PERK), and C/EBP homologous protein 
      (CHOP) mRNAs and proteins and triggered oxidative stress in placenta on GD 13 and 
      GD 19. In conclusion, our findings suggest that maternal exposure to GBH can 
      impair placental development through the endoplasmic reticulum stress-mediated 
      activation of GRP78/PERK/CHOP signaling pathway in mice.
CI  - Copyright (c) 2023 Elsevier Ltd. All rights reserved.
FAU - Liu, Mengling
AU  - Liu M
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China; Nursing School of Jiujiang University, Jiujiang, 
      Jiangxi, 332000, PR China. Electronic address: 304916968@qq.com.
FAU - Lu, Siying
AU  - Lu S
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: 892403767@qq.com.
FAU - Yang, Chuanzhen
AU  - Yang C
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: yangczhen@126.com.
FAU - Zhang, Dalei
AU  - Zhang D
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China; Jiangxi Provincial Key Laboratory of Reproductive 
      Physiology and Pathology, Nanchang University, Nanchang, Jiangxi, 330006, PR 
      China. Electronic address: zhangdalei@ncu.edu.cn.
FAU - Zhu, Jun
AU  - Zhu J
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: zj78_12@163.com.
FAU - Yin, Jiting
AU  - Yin J
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: 314885850@qq.com.
FAU - Zhao, Hongru
AU  - Zhao H
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: zhaohongru2019@163.com.
FAU - Yang, Bei
AU  - Yang B
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China. Electronic address: yangbei@ncu.edu.cn.
FAU - Kuang, Haibin
AU  - Kuang H
AD  - Department of Physiology, Basic Medical College, Nanchang University, Nanchang, 
      Jiangxi, 330006, PR China; Jiangxi Provincial Key Laboratory of Reproductive 
      Physiology and Pathology, Nanchang University, Nanchang, Jiangxi, 330006, PR 
      China. Electronic address: kuanghaibin@ncu.edu.cn.
LA  - eng
PT  - Journal Article
DEP - 20230129
PL  - England
TA  - Food Chem Toxicol
JT  - Food and chemical toxicology : an international journal published for the British 
      Industrial Biological Research Association
JID - 8207483
RN  - 0 (Herbicides)
RN  - 0 (Endoplasmic Reticulum Chaperone BiP)
SB  - IM
MH  - Humans
MH  - Pregnancy
MH  - Mice
MH  - Animals
MH  - Female
MH  - *Placentation
MH  - Maternal Exposure/adverse effects
MH  - Placenta
MH  - *Herbicides/pharmacology
MH  - Endoplasmic Reticulum Chaperone BiP
MH  - Endoplasmic Reticulum Stress
MH  - Apoptosis
MH  - Glyphosate
OTO - NOTNLM
OT  - Apoptosis
OT  - Endoplasmic reticulum stress
OT  - Glyphosate-based herbicides
OT  - Placenta
OT  - Pregnancy
COIS- Declaration of competing interest The authors declare that they have no known 
      competing financial interests or personal relationships that could have appeared 
      to influence the work reported in this paper.
EDAT- 2023/02/02 06:00
MHDA- 2023/02/25 06:00
CRDT- 2023/02/01 19:13
PHST- 2022/12/14 00:00 [received]
PHST- 2023/01/14 00:00 [revised]
PHST- 2023/01/25 00:00 [accepted]
PHST- 2023/02/02 06:00 [pubmed]
PHST- 2023/02/25 06:00 [medline]
PHST- 2023/02/01 19:13 [entrez]
AID - S0278-6915(23)00042-X [pii]
AID - 10.1016/j.fct.2023.113640 [doi]
PST - ppublish
SO  - Food Chem Toxicol. 2023 Mar;173:113640. doi: 10.1016/j.fct.2023.113640. Epub 2023 
      Jan 29.