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Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout

Bisphenol A (BPA) is widely used in the manufacture of plastics and epoxy resins and is prevalent in the aquatic environment. BPA disrupts endocrine pathways in fish, but the long-term developmental implications are unknown. We demonstrate that BPA deposition in the eggs of rainbow trout (Oncorhynch...

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Autores principales: Sadoul, Bastien, Birceanu, Oana, Aluru, Neel, Thomas, Jith K., Vijayan, Mathilakath M.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658357/
https://www.ncbi.nlm.nih.gov/pubmed/29074850
http://dx.doi.org/10.1038/s41598-017-13301-7
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author Sadoul, Bastien
Birceanu, Oana
Aluru, Neel
Thomas, Jith K.
Vijayan, Mathilakath M.
author_facet Sadoul, Bastien
Birceanu, Oana
Aluru, Neel
Thomas, Jith K.
Vijayan, Mathilakath M.
author_sort Sadoul, Bastien
collection PubMed
description Bisphenol A (BPA) is widely used in the manufacture of plastics and epoxy resins and is prevalent in the aquatic environment. BPA disrupts endocrine pathways in fish, but the long-term developmental implications are unknown. We demonstrate that BPA deposition in the eggs of rainbow trout (Oncorhynchus mykiss), an ecologically and economically important species of fish, reprograms liver metabolism in the offspring and alters the developmental growth trajectory in two generations. Specifically, BPA reduces growth during early development, followed by a catch-up growth post-juveniles. More importantly, we observed a developmental shift in the liver transcriptome, including an increased propensity for protein breakdown during early life stages to lipid and cholesterol synthesis post- juveniles. The liver molecular responses corresponded with the transient growth phenotypes observed in the F1 generation, and this was also evident in the F2 generation. Altogether, maternal and/or ancestral embryonic exposure to BPA affects liver metabolism leading to development-distinct effects on growth, underscoring the need for novel risk assessment strategies for this chemical in the aquatic environment. This is particularly applicable to migratory species, such as salmon, where distinct temporal changes in growth and physiology during development are critical for their spawning success.
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spelling pubmed-56583572017-10-31 Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout Sadoul, Bastien Birceanu, Oana Aluru, Neel Thomas, Jith K. Vijayan, Mathilakath M. Sci Rep Article Bisphenol A (BPA) is widely used in the manufacture of plastics and epoxy resins and is prevalent in the aquatic environment. BPA disrupts endocrine pathways in fish, but the long-term developmental implications are unknown. We demonstrate that BPA deposition in the eggs of rainbow trout (Oncorhynchus mykiss), an ecologically and economically important species of fish, reprograms liver metabolism in the offspring and alters the developmental growth trajectory in two generations. Specifically, BPA reduces growth during early development, followed by a catch-up growth post-juveniles. More importantly, we observed a developmental shift in the liver transcriptome, including an increased propensity for protein breakdown during early life stages to lipid and cholesterol synthesis post- juveniles. The liver molecular responses corresponded with the transient growth phenotypes observed in the F1 generation, and this was also evident in the F2 generation. Altogether, maternal and/or ancestral embryonic exposure to BPA affects liver metabolism leading to development-distinct effects on growth, underscoring the need for novel risk assessment strategies for this chemical in the aquatic environment. This is particularly applicable to migratory species, such as salmon, where distinct temporal changes in growth and physiology during development are critical for their spawning success. Nature Publishing Group UK 2017-10-26 /pmc/articles/PMC5658357/ /pubmed/29074850 http://dx.doi.org/10.1038/s41598-017-13301-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Sadoul, Bastien
Birceanu, Oana
Aluru, Neel
Thomas, Jith K.
Vijayan, Mathilakath M.
Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title_full Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title_fullStr Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title_full_unstemmed Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title_short Bisphenol A in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
title_sort bisphenol a in eggs causes development-specific liver molecular reprogramming in two generations of rainbow trout
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5658357/
https://www.ncbi.nlm.nih.gov/pubmed/29074850
http://dx.doi.org/10.1038/s41598-017-13301-7
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