biostudies-literatureEverson TMNICHD NIH HHSNIEHS NIH HHSNIMH NIH HHSNCI NIH HHSNational Institutes of HealthUnited States Environmental Protection AgencyNIGMS NIH HHS233-244https://www.ebi.ac.uk/biostudies/studies/S-EPMC5554457biostudies-literatureUnknown158<h4>Background</h4>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.<h4>Objectives</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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.Environmental researchMaternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes.PMC5554457R01ES022223P30 CA023108RD83544201R01 ES022223P20 GM104416P30 ES023515R24 ES028507R01 MH094609T32 HD049311R25 CA134286P01 ES022832R01MH094609Marsit CJKaragas MRHao KPunshon TChen JKappil MJackson BPEverson TMfalseMaternal exposure to selenium and cadmium, fetal growth, and placental expression of steroidogenic and apoptotic genes.<h4>Background</h4>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.<h4>Objectives</h4>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.<h4>Methods</h4>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.<h4>Results</h4>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.<h4>Conclusions</h4>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.2017-01-01T00:00:00Z2017 Oct2024-11-12T17:58:01.081Z2019-03-26T23:57:49ZS-EPMC55544572866244910.1016/j.envres.2017.06.016