Long-term effects of early-life exposure to environmental oestrogens on ovarian function: role of epigenetics
Author
dc.contributor.author
Cruz, G.
Author
dc.contributor.author
Forest, W.
es_CL
Author
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Paredes, A.
es_CL
Author
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Yi, K. D.
es_CL
Author
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Uzumcu, M.
es_CL
Admission date
dc.date.accessioned
2015-01-08T19:21:39Z
Available date
dc.date.available
2015-01-08T19:21:39Z
Publication date
dc.date.issued
2014
Cita de ítem
dc.identifier.citation
Journal of Neuroendocrinology, 2014, 26, 613–624
en_US
Identifier
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DOI: 10.1111/jne.12181
Identifier
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https://repositorio.uchile.cl/handle/2250/121981
General note
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Artículo de publicación ISI
en_US
Abstract
dc.description.abstract
Oestrogens play an important role in development and function of the brain and reproductive
tract. Accordingly, it is considered that developmental exposure to environmental oestrogens
can disrupt neural and reproductive tract development, potentially resulting in long-term alterations
in neurobehaviour and reproductive function. Many chemicals have been shown to have
oestrogenic activity, whereas others affect oestrogen production and turnover, resulting in the
disruption of oestrogen signalling pathways. However, these mechanisms and the concentrations
required to induce these effects cannot account for the myriad adverse effects of environmental
toxicants on oestrogen-sensitive target tissues. Hence, alternative mechanisms are assumed to
underlie the adverse effects documented in experimental animal models and thus could be
important to human health. In this review, the epigenetic regulation of gene expression is
explored as a potential target of environmental toxicants including oestrogenic chemicals. We
suggest that toxicant-induced changes in epigenetic signatures are important mechanisms
underlying the disruption of ovarian follicular development. In addition, we discuss how exposure
to environmental oestrogens during early life can alter gene expression through effects on
epigenetic control potentially leading to permanent changes in ovarian physiology.
en_US
Patrocinador
dc.description.sponsorship
This work was supported in part by National Institute of Environmental Health
Science grant ES017847 and ES017059 and NIEHS Center grant ES005022 to
MU, Fondecyt grant 1120147 to AP and Fondecyt grant 11130707 to GC.