Low dose bisphenol S or ethinyl estradiol exposures during the perinatal period alter female mouse mammary gland development

Kolla, SriDurgaDevi; Morcos, Mary Attia; Martin, Brian J.; Vandenberg, Laura N.

doi:10.1016/j.reprotox.2018.03.003

Cited by 67 publications

(30 citation statements)

References 86 publications

(112 reference statements)

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“…BPA alters intracellular molecular mechanisms that may cause breast cancer by binding to estrogen-related receptors (ERRs) or G protein-coupled receptors (GPERs). Fetal exposure to low doses of BPA has long-term effects, increasing the risk of breast cancer in adulthood [60].…”

Section: Bisphenol Amentioning

confidence: 99%

Oestrogenic Endocrine Disruptors in the Placenta and the Fetus

Tang

Deng

et al. 2020

IJMS

124

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Endocrine disrupting chemicals (EDCs) are exogenous substances that interfere with the stability and regulation of the endocrine system of the body or its offspring. These substances are generally stable in chemical properties, not easy to be biodegraded, and can be enriched in organisms. In the past half century, EDCs have gradually entered the food chain, and these substances have been frequently found in maternal blood. Perinatal maternal hormone levels are unstable and vulnerable to EDCs. Some EDCs can affect embryonic development through the blood-fetal barrier and cause damage to the neuroendocrine system, liver function, and genital development. Some also effect cross-generational inheritance through epigenetic mechanisms. This article mainly elaborates the mechanism and detection methods of estrogenic endocrine disruptors, such as bisphenol A (BPA), organochlorine pesticides (OCPs), diethylstilbestrol (DES) and phthalates (PAEs), and their effects on placenta and fetal health in order to raise concerns about the proper use of products containing EDCs during pregnancy and provide a reference for human health.

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Section: Bisphenol Amentioning

confidence: 99%

Oestrogenic Endocrine Disruptors in the Placenta and the Fetus

Tang

Deng

et al. 2020

IJMS

124

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“…The low dose (2 μg BPS/kg/day) was selected to approximate human exposures; it is approximately 1–10x higher than typical human intake [3] . The mid dose (200 μg BPS/kg/day) was selected based on prior studies showing that this dose disrupted maternal behaviors, the lactating mother, and development of the mammary gland [2] , [4] , [5] . The highest dose (2000 μg BPS/kg/day) was selected based on results from a recent study at the National Toxicology Program which revealed significant effects of BPS on the female mammary gland at a similar dose (5000 μg/kg/day) [6] .…”

Section: Experimental Design Materials and Methodsmentioning

confidence: 99%

Data describing effects of perinatal exposure to bisphenol S on a peripubertal estrogen challenge in intact female CD-1 mice

Kolla

Vandenberg

2019

Data in Brief

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Bisphenol S (BPS) is an analogue of bisphenol A (BPA), used in consumer products including food packaging and thermal paper. Like BPA, BPS is an estrogen receptor agonist and exposures during perinatal development have been shown to alter growth and morphology of the mouse female mammary gland prior to puberty and in adulthood. Reported here are data describing the effect of exposure to low doses of BPS (2, 200 or 2000 μg/kg/day) during perinatal development on morphology and gene expression in the mammary gland of female CD-1 mice, with or without an additional estrogen exposure (1 μg/kg/day ethinyl estradiol) during the peripubertal period. Additional data document other estrogen-sensitive outcomes including timing of vaginal opening and uterine weight. The data suggest that low doses of BPS induce modest changes in the mammary gland at puberty, but do not appear to sensitize the female to an estrogenic challenge administered during the peripubertal period.

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“…Pregnant mice were exposed from E9.5-E18.5 with 100µg/kg • bodyweight DES, 25µg/kg • bodyweight BPS, or oil control via oral gavage. Doses were chosen to be consistent with previous literature in mouse studies or known human exposures (Hilakivi-Clarke et al 2013;Kolla et al 2018;LaPlante et al 2017;Tucker et al 2018). At 12 weeks of age, mice were subjected to our breast stiffness assay.…”

Section: In Utero Bpa Increases Collagen Matrix Density and Gland Stimentioning

confidence: 99%

“…However, BPS did not show any change in stiffness. Interestingly, BPS induces many of these developmental abnormalities in the mammary gland which are seen with BPA and are typically used as a measure of cancer risk (Kolla et al 2018). While no study has directly tested BPS in a cancer susceptibility model, such as DMBA, its association with these phenotypes has raised concerns.…”

Section: Bpa Alternatives and The Importance Of Estrogenic Activitymentioning

confidence: 99%

“…While BPA has been extensively studied for both developmental defects and cancer-associated phenotypes in rodent models, there is much less data on the BPA alternatives. However, BPS has been shown to drive many of the same developmental abnormalities in the mammary gland seen in BPA exposed animals (Kolla et al 2018). While no study has demonstrated cancer formation in BPS-exposed mice, a small number of mice did have mammary neoplasias in one study (Tucker et al 2018).…”

Section: Introductionmentioning

confidence: 99%

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In uteroestrogenic endocrine disruption alters the stroma to increase extracellular matrix density and mammary gland stiffness

Wormsbaecher

Hindman

Avendano

et al. 2019

Preprint

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AbstractIn utero endocrine disruption is linked to increased risk of breast cancer later in life. Despite numerous studies establishing this linkage, the long-term molecular changes that predispose mammary cells to carcinogenic transformation are unknown. Several lines of evidence indicate the stroma mediates endocrine disruption following early-life (or in utero) exposure. Herein, we utilized BPA as a model of estrogenic endocrine disruption to analyze the long-term consequences in the stroma. Using RNA-seq transcriptional profiling of adult primary fibroblasts isolated from female mice exposed to BPA in utero, we identified deregulated genes associated with the extracellular matrix. Specifically, multiple collagen genes had increased expression in exposed mice. In line with the transcriptional data, collagen deposition is increased in adult BPA-exposed mice. We further demonstrate in vitro that fibroblasts exposed to BPA in utero remodel a collagen matrix, thereby decreasing permeability of the collagen matrix. These alterations to the mammary gland resulted in increased gland stiffness in the adult mice. Our data connects early life endocrine disruption to breast density. Interestingly, increased collagen deposition and gland stiffness were not observed in the developing glands of younger mice, suggesting risk factors for breast cancer continue to develop throughout life following these exposures. Finally, we assessed whether in utero exposure to two other endocrine disruptors, BPS and DES, also increase breast stiffness in adult mice. While DES increased breast stiffness, BPS did not, suggesting this BPA alternative may in fact pose less breast cancer risk than its predecessor. As breast stiffness, extracellular matrix density, and collagen deposition have been directly linked to breast cancer risk, these data mechanistically link endocrine disruptor exposures and molecular alterations to increased disease susceptibility in the gland.

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Low dose bisphenol S or ethinyl estradiol exposures during the perinatal period alter female mouse mammary gland development

Cited by 67 publications

References 86 publications

Oestrogenic Endocrine Disruptors in the Placenta and the Fetus

Oestrogenic Endocrine Disruptors in the Placenta and the Fetus

Data describing effects of perinatal exposure to bisphenol S on a peripubertal estrogen challenge in intact female CD-1 mice

In uteroestrogenic endocrine disruption alters the stroma to increase extracellular matrix density and mammary gland stiffness

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