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Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation

Hormones and endocrine-disrupting chemicals are generally thought to have permanent “organizational” effects when exposures occur during development but not adulthood. Yet, an increasing number of studies have shown that pregnant females are disrupted by endocrine-disrupting chemical exposures, with...

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Autores principales: LaPlante, Charlotte D, Bansal, Ruby, Dunphy, Karen A, Jerry, D Joseph, Vandenberg, Laura N
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Endocrine Society 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057512/
https://www.ncbi.nlm.nih.gov/pubmed/30057971
http://dx.doi.org/10.1210/js.2018-00024
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author LaPlante, Charlotte D
Bansal, Ruby
Dunphy, Karen A
Jerry, D Joseph
Vandenberg, Laura N
author_facet LaPlante, Charlotte D
Bansal, Ruby
Dunphy, Karen A
Jerry, D Joseph
Vandenberg, Laura N
author_sort LaPlante, Charlotte D
collection PubMed
description Hormones and endocrine-disrupting chemicals are generally thought to have permanent “organizational” effects when exposures occur during development but not adulthood. Yet, an increasing number of studies have shown that pregnant females are disrupted by endocrine-disrupting chemical exposures, with some effects that are permanent. Here, we examined the long-term effects of exposure to oxybenzone, an estrogenic chemical found in sunscreen and personal care products, on the morphology of the mammary gland in mice exposed during pregnancy and lactation. Female mice were exposed to vehicle or 30, 212, or 3000 µg oxybenzone/kg/d, from pregnancy day 0 until weaning. A nulliparous group, receiving vehicle treatment, was also evaluated. Mammary glands were collected 5 weeks after involution for whole-mount, histological, immunohistochemical, and molecular analyses. Exposure to 3000 µg oxybenzone/kg/d induced permanent changes to ductal density that was significantly different from both the nulliparous and vehicle groups. The two highest doses of oxybenzone similarly induced an intermediate phenotype for expression of progesterone receptor. A monotonic, dose-dependent increase in cell proliferation was also observed in the oxybenzone-treated females, becoming statistically significant at the highest dose. Finally, oxybenzone exposure induced an intermediate phenotype for Esr1 expression in all oxybenzone-treated groups. These data suggest that oxybenzone, at doses relevant to human exposures, produces long-lasting alterations to mammary gland morphology and function. Further studies are needed to determine if exposure to this chemical during pregnancy and lactation will interfere with the known protection that pregnancy provides against breast cancer.
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spelling pubmed-60575122018-07-27 Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation LaPlante, Charlotte D Bansal, Ruby Dunphy, Karen A Jerry, D Joseph Vandenberg, Laura N J Endocr Soc Research Articles Hormones and endocrine-disrupting chemicals are generally thought to have permanent “organizational” effects when exposures occur during development but not adulthood. Yet, an increasing number of studies have shown that pregnant females are disrupted by endocrine-disrupting chemical exposures, with some effects that are permanent. Here, we examined the long-term effects of exposure to oxybenzone, an estrogenic chemical found in sunscreen and personal care products, on the morphology of the mammary gland in mice exposed during pregnancy and lactation. Female mice were exposed to vehicle or 30, 212, or 3000 µg oxybenzone/kg/d, from pregnancy day 0 until weaning. A nulliparous group, receiving vehicle treatment, was also evaluated. Mammary glands were collected 5 weeks after involution for whole-mount, histological, immunohistochemical, and molecular analyses. Exposure to 3000 µg oxybenzone/kg/d induced permanent changes to ductal density that was significantly different from both the nulliparous and vehicle groups. The two highest doses of oxybenzone similarly induced an intermediate phenotype for expression of progesterone receptor. A monotonic, dose-dependent increase in cell proliferation was also observed in the oxybenzone-treated females, becoming statistically significant at the highest dose. Finally, oxybenzone exposure induced an intermediate phenotype for Esr1 expression in all oxybenzone-treated groups. These data suggest that oxybenzone, at doses relevant to human exposures, produces long-lasting alterations to mammary gland morphology and function. Further studies are needed to determine if exposure to this chemical during pregnancy and lactation will interfere with the known protection that pregnancy provides against breast cancer. Endocrine Society 2018-05-22 /pmc/articles/PMC6057512/ /pubmed/30057971 http://dx.doi.org/10.1210/js.2018-00024 Text en Copyright © 2018 Endocrine Society https://creativecommons.org/licenses/by-nc-nd/4.0/ This article has been published under the terms of the Creative Commons Attribution Non-Commercial, No-Derivatives License (CC BY-NC-ND; https://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Research Articles
LaPlante, Charlotte D
Bansal, Ruby
Dunphy, Karen A
Jerry, D Joseph
Vandenberg, Laura N
Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title_full Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title_fullStr Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title_full_unstemmed Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title_short Oxybenzone Alters Mammary Gland Morphology in Mice Exposed During Pregnancy and Lactation
title_sort oxybenzone alters mammary gland morphology in mice exposed during pregnancy and lactation
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6057512/
https://www.ncbi.nlm.nih.gov/pubmed/30057971
http://dx.doi.org/10.1210/js.2018-00024
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