Maternal nutrient supplementation counteracts bisphenol A-induced DNA hypomethylation in early development

By Dana C. Dolinoy, Dale H. Huang, R. Jirtle. Proceedings of the National Academy of Sciences of the United States of America, 2007

1,348 citations recorded by the source corpus.

Subfields: Health, Toxicology and Mutagenesis, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/120891e75feb79e99ce0abf309fc46a886a222a5

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Citations in the corpus

Prenatal environmental exposures, epigenetics, and disease (2011, neutral): “The early developmental period is thought to be the most susceptible to epigenetic insults because the DNA synthesis rate is high and the elaborate DNA methylation patterning and chromatin structure required for normal tissue development is established at that time [28].”
Ten Putative Contributors to the Obesity Epidemic (2009, positive): “Maternal exposure to bisphenol A (a synthetic estrogen and ubiquitous industrial contaminant) before and during pregnancy has the opposite effect, inducing DNA hypomethylation at Avy and another metastable epiallele, CabpIAP (Dolinoy et al., 2007).”
Influence of Metabolism on Epigenetics and Disease (2013, positive): “Studies in rodents and sheep have confirmed that the availability of nutrients required for one-carbon metabolism (for example, folate, choline, methionine, and betaine, as well as selected B vitamins) at the time of conception and during pregnancy can induce epigenetically driven phenotypes in thei”
Child health, developmental plasticity, and epigenetic programming. (2011, background): “For example, maternal nutrition can influence gene expression of the growing fetus in utero and in the developing progeny after its birth (170, 382, 417, 418), and DNA methylation can be prenatally manipulated by hormonal stimuli (168).”
Nutrition and epigenetics: An interplay of dietary methyl donors, one-carbon metabolism, and DNA methylation (2012, positive): “Furthermore, using the A model, we have demonstrated that maternal diet supplemented with methyl donors negated a shift towards hypomethylation due to bisphenol A exposure, restoring normal stochastic methylation in offspring [25].”
450K Epigenome-Wide Scan Identifies Differential DNA Methylation in Newborns Related to Maternal Smoking during Pregnancy (2012, background): “Data from animal models demonstrate that maternal exposures, such as dietary methyl donors (Hollingsworth et al. 2008) and bisphenol A (Dolinoy et al. 2007) can impact offspring phenotypes via DNA methylation.”
Endocrine Disrupting Chemicals and Disease Susceptibility (2011, background): “For example, Bouskine et al. reported that BPA stimulates JKT-1 cell proliferation in vitro in an inverse U-shape dose-response curve [30].”
EDC-2: The Endocrine Society's Second Scientific Statement on Endocrine-Disrupting Chemicals. (2015, background): “Evidence that BPA induces changes in DNA methylation, primarily hypomethylation, was first shown for the agouti viable (A) mouse (104) and in prostate cancer cells (105).”
Epigenetics and the environment: emerging patterns and implications (2012, background): “Maternal food supplementation with bisphenol A (BPA) — a compound that is widely used in the manufacturing of polycarbonate plastics — led to decreased CpG methylation at the A vy allele in the offspring, along with an increased frequency of yellow coat colour, obesity and diabete”