Cadmium-induced teratogenicity: Association with ROS-mediated endoplasmic reticulum stress in placenta

Wang, Zhen; Wang, Hua; Xu, Zhiyong; Ji, Yan-Li; Chen, Yuan-Hua; Zhang, Zhihui; Zhang, Cheng; Meng, Xiu-Hong; Zhao, Mingqiu; D, Xu

doi:10.1016/j.taap.2012.01.001

Cited by 93 publications

(50 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The dose of CdCl 2 used in the current study referred to our previous study [25]. Forty dams were sacrificed at different time points (0, 2, 12 and 24 h) after Cd injection.…”

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Wang

et al. 2016

Reproductive Toxicology

Self Cite

View full text Add to dashboard Cite

“…The dose of CdCl 2 used in the current study referred to our previous study [25]. Forty dams were sacrificed at different time points (0, 2, 12 and 24 h) after Cd injection.…”

Section: Methodsmentioning

confidence: 99%

“…In mice, maternal Cd exposure in mid-gestation resulted in a relatively specific forelimb ectrodactyly [20][21][22][23][24][25]. Moreover, maternal Cd exposure in middle and late gestational age induced FGR in mice [15,26,27].…”

Section: Introductionmentioning

confidence: 99%

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Wang

et al. 2016

Reproductive Toxicology

Self Cite

View full text Add to dashboard Cite

“…In human pregnancy, apoptosis is increased in placentas subjected to IUGR or other disorders [30,31,34,35]. In mice and rats, several developmental toxicants including cadmium induced excessive placental apoptosis as well as impaired fetal growth [36]. Apoptosis can be triggered by an increase in apoptosis-inducing signals and/or suppression of apoptosis-inhibiting signaling [37].…”

Section: Introductionmentioning

confidence: 99%

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Banu

Stanley

Sivakumar

et al. 2017

Reproductive Toxicology

View full text Add to dashboard Cite

Environmental contamination with hexavalent chromium (CrVI) is a growing problem both in the U.S and developing countries. CrVI is a heavy-metal endocrine disruptor; women working in Cr industries exhibit an increased incidence of premature abortion and infertility. The current study was designed to understand the mechanism of CrVI toxicity on placental cell survival/death pathways. Pregnant mothers were treated with or without CrVI (50 ppm K2Cr2O7) through drinking water from gestational day (GD) 9.5–14.5, and placentas were analyzed on GD 18.5. Results indicated that CrVI increased apoptosis of trophoblasts, vascular endothelium of the metrial glands and yolk sac epithelium through caspase-3 and p53-dependent pathways. CrVI increased apoptosis in labyrinth and basal zones in a caspase-3-independent manner via AIF, and through an ATM-p53-NOXA-PUMA-p27 network. CrVI downregulated cell survival proteins Bcl-2, Bcl-XL and XIAP in the placenta. CrVI disrupts placental histoarchitecture and increases cell death by spatiotemporal modulation of apoptotic signaling.

show abstract

“…Animal models and in vitro studies have shown that Cd induces preeclampsia-like symptoms, restricts fetal growth (Wang et al, 2014, 2016a), may interfere with placental steroidogenesis (Kawai et al, 2002; Stasenko et al, 2010), inhibits trophoblast proliferation while promoting apoptosis (Wang et al, 2012; Erboga and Kanter, 2016), increases placental oxidative stress (Wang et al, 2012) and interferes with maternal-fetal nutrient transfer across the placenta (Wang et al, 2016a; Mikolić et al, 2015), demonstrating the placenta is a likely target tissue for Cd-associated reproductive toxicity. Indeed, excess ROS generation in the placenta has also been associated with altered placental function and negative pregnancy outcomes (Min et al, 2009; Scifres and Nelson, 2009; Vanderlelie et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes

Everson

Kappil

Hao

et al. 2017

Environmental Research

View full text Add to dashboard Cite

Background Cadmium (Cd) and selenium (Se) antagonistically influence redox balance and apoptotic signaling, with Cd potentially promoting and Se inhibiting oxidative stress and apoptosis. Alterations to placental redox and apoptotic functions by maternal exposure to Cd and Se during pregnancy may explain some of the Cd and Se associations with fetal development. Objectives Investigate associations between Cd and Se concentrations in maternal toenails with placental expression patterns of tumor necrosis factor (TNF) and steroidogenic genes involved in redox reactions and test associations with fetal growth. Methods In a sub-sample from the Rhode Island Child Health Study (n = 173), we investigated the relationships between: (1) maternal toenail Cd and Se concentrations and fetal growth using logistic regression, (2) Cd and Se interactions with factor scores from placental TNF and steroidogenic expression patterns (RNAseq) using linear models, and (3) TNF and steroidogenic expression factors with fetal growth via analysis of covariance. Results Se was associated with decreased odds of intrauterine growth restriction (IUGR) (OR = 0.27, p-value = 0.045). Cd was associated with increased odds of IUGR (OR = 1.95, p-value = 0.13) and small for gestational age (SGA) births (OR = 1.46, p-value = 0.11), though not statistically significant. Cd and Se concentrations were antagonistically associated with placental TNF and steroidogenic expression patterns, which also differed by birth size. Conclusions Se may act as an antagonist to Cd and as a modifiable protective factor in fetal growth restriction, and these data suggest these effects may be due to associated variations in the regulation of genes involved in placental redox balance and/or apoptotic signaling.

show abstract

Cadmium-induced teratogenicity: Association with ROS-mediated endoplasmic reticulum stress in placenta

Cited by 93 publications

References 52 publications

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Maternal cadmium exposure reduces placental zinc transport and induces fetal growth restriction in mice

Chromium VI − Induced developmental toxicity of placenta is mediated through spatiotemporal dysregulation of cell survival and apoptotic proteins

Maternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes

Contact Info

Product

Resources

About