DNA methylation and copy number variation analyses of human embryonic stem cell–derived neuroprogenitors after low-dose decabromodiphenyl ether and/or bisphenol A exposure

Du, Lili; Sun, Wen; Li, X M; Li, X Y; Liu, W; Chen, D

doi:10.1177/0960327117710535

Cited by 21 publications

(18 citation statements)

References 51 publications

(60 reference statements)

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“…It was found that decabromodiphenyl ether (BDE-209) and bisphenol A decreased DNA methylation and reduced DNA methyltransferase (DNMTI and DNMT3A) expression in human embryonic stem cells. 29 Moreover, it was shown that TDCIPP exposure predominantly resulted in hypomethylation of positions outside of CpG islands and within intragenic (exon) regions of the zebrafish genome. 30 Aberrant DNA methylation patterns were also present in human sperm when the exposure to OPFRs was increased.…”

Section: Discussionmentioning

confidence: 99%

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

et al. 2019

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Phosphorus flame retardants are a group of chemicals that are used to slow or prevent the spread of fire. These compounds have been detected in different environments including human organism. In the present study, we have investigated DNA-damaging potential and effect on DNA methylation of tris(2-chloroethyl) phosphate (TCEP) and tris(1-chloro-2-propyl) phosphate (TCPP) in human peripheral blood mononuclear cells (PBMCs). In order to determine DNA damage and repair, the alkaline and neutral versions of the comet assay were used. The level of DNA methylation was determined with specific antibodies against methylated DNA. PBMCs were exposed to TCEP and TCPP at the concentrations in the range of 1–1000 µM for 24 h. We have observed that TCEP and TCPP induced DNA damage—DNA breaks and alkali-labile sites. All DNA damages were effectively repaired during 120-min repair incubation. The results have also shown that TCEP and TCPP decreased the level of DNA methylation in PBMCs. In the case of TCEP, this effect was observed at a very low concentration of 1 µM.

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Section: Discussionmentioning

confidence: 99%

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

et al. 2019

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“…PBDE‐209 causes copy number variants at the different regions on chromosomes. The demethylation activity by PBDE‐209 collapses genomic stability at the embryonic stage that may affect neurodevelopment (Du, Sun, et al, 2018). Another in vivo study using rat hippocampal neurons exposed to PBDE‐209 showed the increased apoptosis with improved P38 MAPK level and oxidative stress besides global DNA hypomethylation (J. Chen, Liufu, Sun, Sun, & Chen, 2010).…”

Section: Epigenetic Changes Link Ecs To Adverse Health Outcomesmentioning

confidence: 99%

“…TCC is able to bioaccumulate into the human tissues, for instance, maternal and umbilical cord sera, urine, toe and fingernails, as well as hypothalamus and white matter in the human brain, threatening the safety of human (Pycke et al, 2014;Van Der Meer et al, 2017;Wei et al, 2017). TCC is a novel endocrine disruptor (Chung, Genco, Megrelis, & Ruderman, 2011) and also exacerbates pathophysiological conditions of the central nervous system (CNS), including traumatic injury, stroke, neurodegenerative diseases, autoimmune inflammation (Lee & McEwen, 2001;Wise, 2002 development (Du, Sun, et al, 2018). Another in vivo study using rat hippocampal neurons exposed to PBDE-209 showed the increased apoptosis with improved P38 MAPK level and oxidative stress besides global DNA hypomethylation (J. Chen, Liufu, Sun, Sun, & Chen, 2010).…”

Section: Triclocarbanmentioning

confidence: 99%

Linking emerging contaminants exposure to adverse health effects: Crosstalk between epigenome and environment

Alam

Shapla

Shen

et al. 2020

J of Applied Toxicology

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Environmental epigenetic findings shed new light on the roles of epigenetic regulations in environmental exposure‐induced toxicities or disease susceptibilities. Currently, environmental emerging contaminants (ECs) are in focus for further investigation due to the evidence of human exposure in addition to their environmental occurrences. However, the adverse effects of these environmental ECs on health through epigenetic mechanisms are still poorly addressed in many aspects. This review discusses the epigenetic mechanisms (DNA methylation, histone modifications, and microRNA expressions) linking ECs exposure to health outcomes. We emphasized on the recent literature describing how ECs can dysregulate epigenetic mechanisms and lead to downstream health outcomes. These up‐to‐date research outputs could provide novel insights into the toxicological mechanisms of ECs. However, the field still faces a demand for further studies on the broad spectrum of health effects, synergistic/antagonistic effects, transgenerational epigenetic effects, and epidemiologic and demographic data of ECs.

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“…Neurons in the CA3 region of the hippocampus of these rats were also found to be undergoing significantly increased rates of apoptosis, with chromatin condensed and localized to the nuclear membrane [64]. Most recently, it was reported that BDE-209 exposures reduced hESC differentiation (although total induction was still greater than 90%) and also led to chromosomal copy number variants (CNVs), as well as decreased expression of DNMT1/3A [65].…”

Section: Relation Of Pbdes To Human Healthmentioning

confidence: 99%

Epigenetic Effects of Polybrominated Diphenyl Ethers on Human Health

Poston

Saha

2019

IJERPH

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Disruption of epigenetic regulation by environmental toxins is an emerging area of focus for understanding the latter’s impact on human health. Polybrominated diphenyl ethers (PBDEs), one such group of toxins, are an environmentally pervasive class of brominated flame retardants that have been extensively used as coatings on a wide range of consumer products. Their environmental stability, propensity for bioaccumulation, and known links to adverse health effects have evoked extensive research to characterize underlying biological mechanisms of toxicity. Of particular concern is the growing body of evidence correlating human exposure levels to behavioral deficits related to neurodevelopmental disorders. The developing nervous system is particularly sensitive to influence by environmental signals, including dysregulation by toxins. Several major modes of actions have been identified, but a clear understanding of how observed effects relate to negative impacts on human health has not been established. Here, we review the current body of evidence for PBDE-induced epigenetic disruptions, including DNA methylation, chromatin dynamics, and non-coding RNA expression while discussing the potential relationship between PBDEs and neurodevelopmental disorders.

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DNA methylation and copy number variation analyses of human embryonic stem cell–derived neuroprogenitors after low-dose decabromodiphenyl ether and/or bisphenol A exposure

Cited by 21 publications

References 51 publications

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

DNA damage and methylation induced by organophosphate flame retardants: Tris(2-chloroethyl) phosphate and tris(1-chloro-2-propyl) phosphate in human peripheral blood mononuclear cells

Linking emerging contaminants exposure to adverse health effects: Crosstalk between epigenome and environment

Epigenetic Effects of Polybrominated Diphenyl Ethers on Human Health

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