TY - CHAP
T1 - Is Environmental Epigenetics Relevant to Endocrine Disease?
AU - Fleisch, Abby F.
AU - Wright, Robert O.
AU - Baccarelli, Andrea A.
N1 - Funding Information:
Funding The authors have received support from the following grants from the US National Institutes of Health: P30ES000002, R21ES019773, R21ES020010, R01ES020268, R01ES013744, R01ES014930, R01ES021357, P42ES016454, and K12 DK094721-02; from the Agency of Healthcare Research and Quality: T32 HS00063; and from Harvard School of Public Health.
Publisher Copyright:
© 2015, Springer-Verlag London.
PY - 2015
Y1 - 2015
N2 - Endocrine disrupting chemicals that are structurally similar to steroid or amine hormones have the potential to mimic endocrine endpoints at the receptor level. Endocrine disrupting chemicals may dysregulate hormone-mediated gene expression through changes in signal transduction and through epigenetic changes. However, epigenetic-induced alteration in gene expression may occur outside of receptor-mediated effects and has emerged as an alternative way in which environmental compounds may exert endocrine effects. We discuss general implications of DNA methylation, histone modification, micro RNAs, and other more recently recognized epigenetic modifications for endocrinology, and we discuss potential for transgenerational inheritance of epigenetic marks. We also review concepts related to environmental epigenetics and relevance for endocrinology through three broad examples, (1) effect of prenatal and early-life under- and overnutrition on future metabolic disease, (2) effect of lifetime environmental exposures such as ionizing radiation on endocrine cancer risk, and (3) potential for compounds previously classified as endocrine disrupting to additionally or alternatively exert effects through epigenetic mechanisms. The field of environmental epigenetics is still nascent, and additional studies are needed to confirm and reinforce data derived from animal models and preliminary human studies. Current evidence suggests that environmental exposures may significantly impact expression of endocrine-related genes and thereby affect clinical endocrine outcomes.
AB - Endocrine disrupting chemicals that are structurally similar to steroid or amine hormones have the potential to mimic endocrine endpoints at the receptor level. Endocrine disrupting chemicals may dysregulate hormone-mediated gene expression through changes in signal transduction and through epigenetic changes. However, epigenetic-induced alteration in gene expression may occur outside of receptor-mediated effects and has emerged as an alternative way in which environmental compounds may exert endocrine effects. We discuss general implications of DNA methylation, histone modification, micro RNAs, and other more recently recognized epigenetic modifications for endocrinology, and we discuss potential for transgenerational inheritance of epigenetic marks. We also review concepts related to environmental epigenetics and relevance for endocrinology through three broad examples, (1) effect of prenatal and early-life under- and overnutrition on future metabolic disease, (2) effect of lifetime environmental exposures such as ionizing radiation on endocrine cancer risk, and (3) potential for compounds previously classified as endocrine disrupting to additionally or alternatively exert effects through epigenetic mechanisms. The field of environmental epigenetics is still nascent, and additional studies are needed to confirm and reinforce data derived from animal models and preliminary human studies. Current evidence suggests that environmental exposures may significantly impact expression of endocrine-related genes and thereby affect clinical endocrine outcomes.
KW - Bisphenol A (BPA)
KW - Cytosine-phosphate-guanine (CpG)
KW - DNA methyltransferase (DNMT)
KW - Diethylstilbestrol (DES)
KW - High fat diet (HFD)
KW - Histone deacetylases (HDACs)
KW - Methyl binding proteins (MBPs)
KW - Toxic Substances Control Act (TSCA)
UR - http://www.scopus.com/inward/record.url?scp=85091510639&partnerID=8YFLogxK
U2 - 10.1007/978-1-4471-6678-8_4
DO - 10.1007/978-1-4471-6678-8_4
M3 - Chapter
AN - SCOPUS:85091510639
T3 - Molecular and Integrative Toxicology
SP - 55
EP - 74
BT - Molecular and Integrative Toxicology
PB - Springer Science+Business Media B.V.
ER -