Abstract
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 CdCl2 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.
Highlights
Further analysis showed that the rate of fetal growth restriction (FGR) per litter was markedly elevated in the Cd group (Table 2)
The previous results showed that maternal exposure to cadmium (4.5 mg/kg, i.p.) on gestational day 9 induced forelimb ectrodactyly in fetal mice, caused oxidative stress and endoplasmic reticulum stress in mouse placenta [8]
We further explored the effects of maternal Cd exposure at the third trimester on fetal growth and development in mice
Summary
The aim of the present study was to investigate whether NAC protects against Cd-induced placental ER stress and fetal growth restriction in mice
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