Open AccessN-acetylcysteine alleviates cadmium-induced placental endoplasmic reticulum stress and fetal growth restriction in mice
Author(s) -
Min-Yin Guo,
Hua Wang,
Yuan-Hua Chen,
Mi-Zhen Xia,
Cheng Zhang,
Xu D
Publication year - 2018
Publication title -
plos one
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.99
H-Index - 332
ISSN - 1932-6203
DOI - 10.1371/journal.pone.0191667
Subject(s) - endoplasmic reticulum , placenta , endocrinology , medicine , fetus , biology , placental insufficiency , andrology , intervillous space , acetylcysteine , chemistry , microbiology and biotechnology , pregnancy , biochemistry , antioxidant , genetics
Cadmium (Cd) is a developmental toxicant that induces fetal growth restriction (FGR). Placental endoplasmic reticulum (ER) stress is associated with FGR. This study investigated the effects of N-acetylcysteine (NAC) on Cd-induced placental ER stress and FGR. Pregnant mice were intraperitoneally injected with CdCl 2 daily from gestational day (GD)13 to GD17. As expected, Cd reduced fetal weight and crown-rump length. Cd decreased the internal space of blood vessels in the placental labyrinth layer and inhibited placental cell proliferation. Several genes of growth factors, such as Vegf-a , placental growth factor , Igf1 and Igf1r , and several genes of nutrient transport pumps, such as Glut1 , Fatp1 and Snat2 , were down-regulated in placenta of Cd-treated mice. Moreover, Cd evoked placental ER stress. Of interest, NAC alleviated Cd-induced FGR. Additional experiment showed that NAC inhibited Cd-induced impairment of placental development and placental ER stress. Therefore, NAC may be exploited for prevention of Cd-induced placental insufficiency and FGR.