ArticleEnvironmental and molecular mutagenesis2014
Bisphenol A-associated alterations in the expression and epigenetic regulation of genes encoding xenobiotic metabolizing enzymes in human fetal liver.
Article in Environmental and molecular mutagenesis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
29 citing papers in PubMed, 61 citations in OpenAlex.
- Complex roles for sulfation in the toxicities of polychlorinated biphenyls.Critical reviews in toxicology · 2024Review
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- Probing prenatal bisphenol exposures and tissue-specific DNA methylation responses in cord blood, cord tissue, and placenta.Reproductive toxicology (Elmsford, N.Y.) · 2023Article
- Bisphenol A is a carcinogen that induces lipid accumulation, peroxisome proliferator‑activated receptor‑γ expression and liver disease.Experimental and therapeutic medicine · 2022Article
- Endocrine-Disrupting Effects of Bisphenol A on the Cardiovascular System: A Review.Journal of xenobiotics · 2022Review
- Impact of Neonatal Activation of Nuclear Receptor CAR (Nr1i3) on Cyp2 Gene Expression in Adult Mouse Liver.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- Effects of Prenatal Exposure to Titanium Dioxide Nanoparticles on DNA Methylation and Gene Expression Profile in the Mouse Brain.Frontiers in toxicology · 2021Article
- Fetal-Maternal Exposure to Endocrine Disruptors: Correlation with Diet Intake and Pregnancy Outcomes.Nutrients · 2020Review
- Epigenome environment interactions accelerate epigenomic aging and unlock metabolically restricted epigenetic reprogramming in adulthood.Nature communications · 2020Article
- Long noncoding RNA LINC00844-mediated molecular network regulates expression of drug metabolizing enzymes and nuclear receptors in human liver cells.Archives of toxicology · 2020Article
- Developmental programming: Sex-specific programming of growth upon prenatal bisphenol A exposure.Journal of applied toxicology : JAT · 2019Article
- MicroRNAs hsa-miR-495-3p and hsa-miR-486-5p suppress basal and rifampicin-induced expression of human sulfotransferase 2A1 (SULT2A1) by facilitating mRNA degradation.Biochemical pharmacology · 2019Article
- An epigenome-wide analysis of cord blood DNA methylation reveals sex-specific effect of exposure to bisphenol A.Scientific reports · 2019Article
- Prenatal epigenetics diets play protective roles against environmental pollution.Clinical epigenetics · 2019Review
- Prenatal Bisphenol A Exposure in Mice Induces Multitissue Multiomics Disruptions Linking to Cardiometabolic Disorders.Endocrinology · 2019Article
- Maternal levels of endocrine disrupting chemicals in the first trimester of pregnancy are associated with infant cord blood DNA methylation.Epigenetics · 2018Article
- Small-Magnitude Effect Sizes in Epigenetic End Points are Important in Children's Environmental Health Studies: The Children's Environmental Health and Disease Prevention Research Center's Epigenetics Working Group.Environmental health perspectives · 2017Article
- Tris(1,3-dichloro-2-propyl)phosphate Induces Genome-Wide Hypomethylation within Early Zebrafish Embryos.Environmental science & technology · 2016Article
- Adolescent epigenetic profiles and environmental exposures from early life through peri-adolescence.Environmental epigenetics · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Alterations in xenobiotic metabolizing enzyme (XME) expression across the life course, along with genetic, nutritional, and environmental regulation, can influence how organisms respond to toxic insults. In this study, we investigated the hypothesis that in utero exposure to the endocrine active compound, bisphenol A (BPA), influences expression and epigenetic regulation of phase I and II XME genes during development. Using healthy 1st to 2nd trimester human fetal liver specimens quantified for internal BPA levels, we examined XME gene expression using PCR Array (n = 8) and RNA-sequencing (n = 12) platforms. Of the greater than 160 XME genes assayed, 2 phase I and 12 phase II genes exhibited significantly reduced expression with higher BPA levels, including isoforms from the carboxylesterase, catechol O-methyltransferase, glutathione S-transferase, sulfotransferase, and UDP-glucuronosyltransferase families. When the promoters of these candidate genes were evaluated in silico, putative binding sites for the E-twenty-six (ETS) and activator protein1 (AP1) related transcription factor families were identified and unique to 97% of all candidate transcripts. Interestingly, many ETS binding sites contain cytosine-guanine dinucleotides (CpGs) within their consensus sequences. Thus, quantitative analysis of CpG methylation of three candidate genes was conducted across n = 50 samples. Higher BPA levels were associated with increased site-specific methylation at COMT (P < 0.005) and increased average methylation at SULT2A1 (P < 0.020) promoters. While toxicological studies have traditionally focused on high-dose effects and hormonal receptor mediated regulation, our findings suggest the importance of low-dose effects and nonclassical mechanisms of endocrine disruption during development.
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Registered trials
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