PMID- 34331232
OWN - NLM
STAT- MEDLINE
DCOM- 20211203
LR  - 20230914
IS  - 1614-7499 (Electronic)
IS  - 0944-1344 (Linking)
VI  - 28
IP  - 46
DP  - 2021 Dec
TI  - Perfluorooctanoic acid exposure in early pregnancy induces oxidative stress in 
      mice uterus and liver.
PG  - 66355-66365
LID - 10.1007/s11356-021-15453-6 [doi]
AB  - This study aimed to explore the mechanism of perfluorooctanoic acid (PFOA) 
      toxicity on the uterus and liver of mice during early pregnancy. Pregnant mice 
      were given 0, 1, 5, 10, 20, and 40 mg/kg PFOA daily by gavage from gestational 
      day (GD) 1-7 and sacrificed on GD 9. Subsequently, several toxicity parameters 
      were evaluated, including the uterus and liver weights, liver and uterine 
      indexes, histopathological changes of the liver and uterus, and levels of 
      malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase 
      (GSH-Px) in the liver. We also determined the expressions of FAS, FASL, Bax, 
      Bcl-2, and Caspase-3 in decidual cells by immunohistochemistry and the TUNEL 
      assay to detect apoptosis uterine cells. The results showed that PFOA increased 
      the liver weights and reduced the uterus index in a dose-dependent manner. With 
      increasing doses of PFOA, the levels of SOD and GSH-Px were significantly 
      decreased, and MDA increased substantially in liver tissue. 20 mg/kg and 40 mg/kg 
      of PFOA caused more substantial harm to the uterus, thus a higher probability for 
      congestion and resorption. The expression of FAS, FASL, Bax, and Caspase-3 in 
      decidual cells of the uterus in the PFOA treatment groups significantly increased 
      in a dose-dependent manner. The expression of Bcl-2 was downregulated, decreasing 
      the Bcl-2/Bax ratio. At gestation day 9, the control group had significantly 
      fewer apoptotic cells in the uterus and shallower staining than the 40 mg/kg PFOA 
      group. The findings of this study suggest that oxidative damage may be one of the 
      mechanisms by which PFOA induces liver toxicity, and a subsequent increase in 
      uterine cell apoptosis may cause embryo loss or damage.
CI  - (c) 2021. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, 
      part of Springer Nature.
FAU - Zhang, Yan
AU  - Zhang Y
AD  - College of Traditional Chinese Veterinary Medicine, Hebei Agricultural 
      University, Baoding, 071001, China.
FAU - Zhang, Linchao
AU  - Zhang L
AD  - College of Traditional Chinese Veterinary Medicine, Hebei Agricultural 
      University, Baoding, 071001, China.
FAU - Bao, Jialu
AU  - Bao J
AD  - College of Traditional Chinese Veterinary Medicine, Hebei Agricultural 
      University, Baoding, 071001, China.
FAU - Liu, Liantao
AU  - Liu L
AD  - College of Agronomy, Hebei Agricultural University, Baoding, 071001, China.
FAU - Wang, Xiaodan
AU  - Wang X
AD  - College of Traditional Chinese Veterinary Medicine, Hebei Agricultural 
      University, Baoding, 071001, China. wangxiaodan_wxd@126.com.
LA  - eng
GR  - 32072910/National Natural Science Foundation of China/
PT  - Journal Article
DEP - 20210731
PL  - Germany
TA  - Environ Sci Pollut Res Int
JT  - Environmental science and pollution research international
JID - 9441769
RN  - 0 (Caprylates)
RN  - 0 (Fluorocarbons)
RN  - 947VD76D3L (perfluorooctanoic acid)
SB  - IM
MH  - Animals
MH  - Apoptosis
MH  - *Caprylates/metabolism/toxicity
MH  - Female
MH  - Fluorocarbons
MH  - Liver/metabolism
MH  - Mice
MH  - *Oxidative Stress
MH  - Pregnancy
MH  - Uterus
OTO - NOTNLM
OT  - Early pregnancy
OT  - Liver
OT  - Perfluorooctanoic acid
OT  - Toxic effect
OT  - Uterus
EDAT- 2021/08/01 06:00
MHDA- 2021/12/15 06:00
CRDT- 2021/07/31 08:34
PHST- 2021/01/13 00:00 [received]
PHST- 2021/07/11 00:00 [accepted]
PHST- 2021/08/01 06:00 [pubmed]
PHST- 2021/12/15 06:00 [medline]
PHST- 2021/07/31 08:34 [entrez]
AID - 10.1007/s11356-021-15453-6 [pii]
AID - 10.1007/s11356-021-15453-6 [doi]
PST - ppublish
SO  - Environ Sci Pollut Res Int. 2021 Dec;28(46):66355-66365. doi: 
      10.1007/s11356-021-15453-6. Epub 2021 Jul 31.