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Epigenetic Effects of Bisphenol A (BPA): A Literature Review in the Context of Human Dietary Exposure

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Handbook of Nutrition, Diet, and Epigenetics

Abstract

Bisphenol A (BPA) is a high production volume industrial chemical used widely in the production of polycarbonate plastics and epoxy resins for manufacturing food and drink storage containers, the lining of food cans, dental sealants, medical devices, and thermal paper. Biomonitoring studies show that there is widespread exposure of the human population to BPA, mainly via the diet. The median daily intake of the overall US population is approximately 25 ng BPA/kg body weight (bw)/day, which is estimated to result in serum levels of BPA in the pM range. BPA is an endocrine-disrupting chemical, with known estrogenic activity; more recently, it has been reported to induce epigenetic changes in vitro and in vivo, including effects in DNA methylation, differential histone modifications, and modulation of the levels of noncoding RNAs. This chapter summarizes the studies reporting epigenetic effects associated with human exposure to BPA or induced by the in vitro or in vivo exposure to the chemical. The literature suggesting an association between human exposure to BPA and epigenetic changes is limited. Several studies have assessed the effects of BPA in in vitro cell systems and suggest treatment-related epigenetic effects; the lowest effective BPA dose in vitro was in the nM dose range and the dose-response in these studies tended to be linear. In vivo animal studies suggest epigenetic effects of BPA in a wide range of organs, dose levels, and epigenetic endpoints; however, many studies have limitations, including the use of a single dose level that precludes the characterization of the dose-response of the reported effects. Comprehensive well-designed and well-controlled studies, which include both sexes, multiple and properly spaced BPA doses, multiple time points, and integration of the epigenetic endpoints with other molecular, physiological, and morphological endpoints should provide a better understanding of the potential of BPA to act as an epigenetic modulator.

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Abbreviations

BPA:

Bisphenol A

bw:

Body weight

Casq2 :

Calsequestrin 2

CLARITY-BPA:

Consortium Linking Academic and Regulatory Insights on BPA Toxicity

DNMT:

DNA methyltransferase

EFSA:

European Food Safety Agency

ER:

Estrogen receptor

Esrrg :

Estrogen-related receptor-γ

Ezh2 :

Enhancer of zeste 2 polycomb repressive complex 2 subunit

FDA:

Food and Drug Administration

Fkbp5 :

FK506-binding protein 5

GCK:

Glucokinase

GD:

Gestational day

GPER:

G protein-coupled estrogen receptor

H19:

Imprinted maternally expressed transcript

Hdac1 :

Histone deacetylase 1

HOMA:

Homeostatic model assessment

HOTAIR:

HOX antisense intergenic RNA

HOX:

Homeobox

Hpcal1 :

Hippocalcin-like 1

IAP:

Intracisternal A particle

Igf1 :

Insulin-like growth factor 1

Igf2r :

Insulin-like growth factor 2 receptor

LAMP3:

Lysosomal-associated membrane protein 3

LINE-1:

Long interspersed nuclear elements-1

lncRNA:

Long noncoding RNA

miRNA:

microRNA

Nsbp1 :

Nucleosome-binding protein 1

Pde4d4 :

Phosphodiesterase type 4D variant 4

Peg3 :

Paternally expressed gene 3

Pgc-1α :

Peroxisome proliferator activated receptor-γ, coactivator 1α

PND:

Postnatal day

Scgb2a1 :

Secretaglobin family 2A member 1

SNORD:

Small nucleolar RNAs with C/D motif

Sox2 :

Sex determining region Y box 2

SREBF:

Sterol regulatory element-binding transcription factor

StAR :

Steroidogenic acute regulatory protein

Stra8 :

Stimulated by retinoic acid gene 8

Tpd52 :

Tumor protein D52

β–Cas :

β-casein

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Camacho, L., Pogribny, I.P. (2017). Epigenetic Effects of Bisphenol A (BPA): A Literature Review in the Context of Human Dietary Exposure. In: Patel, V., Preedy, V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham. https://doi.org/10.1007/978-3-319-31143-2_32-1

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