Interaction between cadmium (Cd), selenium (Se) and oxidative stress biomarkers in healthy mothers and its impact on birth anthropometric measures

Al‐Saleh, Iman; Al-Rouqi, Reem; Obsum, Cercilia Angela; Shinwari, Neptune; Mashhour, Abdullah; Billedo, Grisellhi; Al-Sarraj, Yasser; Rabbah, Abdullah

doi:10.1016/j.ijheh.2014.08.001

Cited by 64 publications

(36 citation statements)

References 162 publications

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“…Johnston et al reported that the mothers with high blood Cd levels (≥ 0.50 μg/L) had 1.98-fold (95% CI: 1.30, 3.02) increased odds of having a SGA infant compared to those with low blood Cd levels (≤0.28 μg/L) (Johnston et al, 2014). Another study conducted in Saudi Arabia (n = 250) reported a significant increased association of SGA with maternal blood Cd (OR = 5.94; 95% CI: 2.07, 17.01), but no significant association with Cd in cord blood and placental tissue (Al-Saleh et al, 2015).…”

Section: Nomentioning

confidence: 98%

Maternal urinary cadmium concentrations in relation to preterm birth in the Healthy Baby Cohort Study in China

Yang

Huo

Zhang

et al. 2016

Environment International

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Section: Nomentioning

confidence: 98%

Maternal urinary cadmium concentrations in relation to preterm birth in the Healthy Baby Cohort Study in China

Yang

Huo

Zhang

et al. 2016

Environment International

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“…These are comparable to other investigations of Cd on growth restriction and pregnancy outcomes, and similar to a previous study from our lab utilizing a larger sample size (n = 242), which applied different statistical methods and did not adjust for Se exposure, that did observe a significant Cd-SGA association (Everson et al, 2016). Other investigations have observed associations between increasing placental, maternal or fetal Cd concentrations with increased odds of preeclampsia (PE) (Laine et al, 2015) and odds of SGA (Al-Saleh et al, 2015; Johnston et al, 2014; Wang et al, 2016b), and with decreased birth weights (Kippler et al, 2012; Llanos and Ronco, 2009; Menai et al, 2012), birth weight percentiles (Johnston et al, 2014), head circumference (Kippler et al, 2012), Apgar 5-min scores and with placental size (Al-Saleh et al, 2015). Some of these associations were dependent on low maternal Se concentrations (Laine et al, 2015) or varied by infant sex (Kippler et al, 2013, 2012; Romano et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…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). Furthermore, Cd may influence the distribution of Se across maternal, fetal and placental tissues, and vice versa (Al-Saleh et al, 2015; Kantola et al, 2004). …”

Section: Introductionmentioning

confidence: 99%

“…Epidemiologic studies have observed increasing concentrations of placental, maternal or fetal Cd to be associated with various measures of restricted fetal growth or pregnancy complications (Al-Saleh et al, 2015, 2014; Kippler et al, 2013, 2012; Johnston et al, 2014; Laine et al, 2015; Llanos and Ronco, 2009; Wang et al, 2016b; Menai et al, 2012). Alternatively, many studies have found that maternal, fetal or placental Se concentrations positively correlate with fetal growth and successful pregnancies (Bogden et al, 2006; Klapec et al, 2008; Negi et al, 2012; Sun et al, 2014; Rayman et al, 2011, 2015, 2003).…”

Section: Introductionmentioning

confidence: 99%

“…While Cd-Se antagonism has been demonstrated at the cellular level with redox and apoptotic activity, only a handful of epidemiologic studies have investigated these responses, and these have produced mixed results. Laine et al (2015) found that the odds of Cd-associated preeclampsia (PE) were higher among mothers with lower placental concentrations of Se (Laine et al, 2015), while Al-Saleh et al (2015) observed no antagonism between Se and Cd on birth anthropomorphic measurements (Al-Saleh et al, 2015). …”

Section: Introductionmentioning

confidence: 99%

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

Everson

Kappil

Hao

et al. 2017

Environmental Research

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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.

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Selenium attenuates the cadmium‐induced placenta glucocorticoid barrier damage by up‐regulating the expression of specificity protein 1

Chen

et al. 2022

J Biochem & Molecular Tox

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Cadmium (Cd) is an environmental pollutant and pregnant women are especially susceptible to the effects of exposure to Cd. Our previous study found Cd can be accumulated in the placenta and causes fetal growth restriction (FGR) through damage the placental glucocorticoid barrier. Selenium (Se), as an essential micronutrient, can allivate Cd-induced toxicity. In this study, we aim to explore the protective mechanism of Se against Cd-induced the placental glucocorticoid barrier damage and FGR. Pregnant Sprague Dawley (SD) rats were exposed to CdCl 2 (1 mg/kg/day) and Na 2 SeO 3 (0.1-0.2-0.3 mg/kg/day) by gavage from gestational day (GD) 0 to GD 19. The results showed that reduced fetal weight, increased corticosterone concentrations in the maternal and fetal serum, and impaired placental labyrinth layer blood vessel development, appeared in pregnant rats after Cd exposure and improved after treated with Se. In cell experiments, we confirmed that Se reduces Cd-induced apoptosis. Moreover, Se can abolish Cd-induced 11β-HSD2 and specificity protein 1 (Sp1) decreasing in vivo and vitro. In human JEG-3 cells, the knockdown of Sp1 expression by small interfering RNA can suppressed the protective effect of Se on Cd-induced 11β-HSD2 decreasing. In general, our results demonstrated that Se is resistant to Cd-induced FGR through upregulating the placenta barrier via activation of the transcription factor Sp1.

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Interaction between cadmium (Cd), selenium (Se) and oxidative stress biomarkers in healthy mothers and its impact on birth anthropometric measures

Cited by 64 publications

References 162 publications

Maternal urinary cadmium concentrations in relation to preterm birth in the Healthy Baby Cohort Study in China

Maternal urinary cadmium concentrations in relation to preterm birth in the Healthy Baby Cohort Study in China

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

Selenium attenuates the cadmium‐induced placenta glucocorticoid barrier damage by up‐regulating the expression of specificity protein 1

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