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Environ Res. 2017 Oct;158:233-244. doi: 10.1016/j.envres.2017.06.016. Epub 2017 Jul 3.

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

Author information

1
Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA.
2
Department of Environmental Medicine and Public Health, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
3
Department of Genome Sciences, Icahn School of Medicine at Mount Sinai, New York, NY, USA.
4
Department of Earth Sciences, Dartmouth College, Hanover, NH, USA.
5
Department of Biological Sciences, Dartmouth College, Hanover, NH, USA.
6
Department of Epidemiology, Geisel School of Medicine, Dartmouth College, Hanover, NH, USA.
7
Department of Environmental Health, Rollins School of Public Health, Emory University, Atlanta, GA, USA. Electronic address: Carmen.J.Marsit@emory.edu.

Abstract

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.

PMID:
28662449
PMCID:
PMC5554457
DOI:
10.1016/j.envres.2017.06.016
[Indexed for MEDLINE]
Free PMC Article

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