Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a

Abstract Bisphenol chemicals are commonly used in the manufacturing of polycarbonate plastics, polyvinyl chloride plastics, resins, and thermal printing applications. Humans are inadvertently exposed to bisphenols through contact with consumer products and/or medical devices. Recent reports have sho...

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Autores principales:	Manelle Ramadan, Meredith Sherman, Rafael Jaimes, Ashika Chaluvadi, Luther Swift, Nikki Gillum Posnack
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2018
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/d3812031f3b741618154f6e005197fd2
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spelling	oai:doaj.org-article:d3812031f3b741618154f6e005197fd22021-12-02T11:40:17ZDisruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a10.1038/s41598-018-25719-82045-2322https://doaj.org/article/d3812031f3b741618154f6e005197fd22018-05-01T00:00:00Zhttps://doi.org/10.1038/s41598-018-25719-8https://doaj.org/toc/2045-2322Abstract Bisphenol chemicals are commonly used in the manufacturing of polycarbonate plastics, polyvinyl chloride plastics, resins, and thermal printing applications. Humans are inadvertently exposed to bisphenols through contact with consumer products and/or medical devices. Recent reports have shown a link between bisphenol-a (BPA) exposure and adverse cardiovascular outcomes; although these studies have been limited to adult subjects and models. Since cardiac physiology differs significantly between the developing and adult heart, we aimed to assess the impact of BPA exposure on cardiac function, using a neonatal cardiomyocyte model. Neonatal rat ventricular myocytes were monitored to assess cell viability, spontaneous beating rate, beat rate variability, and calcium-handling parameters in the presence of control or bisphenol-supplemented media. A range of doses were tested to mimic environmental exposure (10−9–10−8M), maximum clinical exposure (10−5M), and supraphysiological exposure levels (10−4M). Acute BPA exposure altered cardiomyocyte functionality, resulting in a slowed spontaneous beating rate and increased beat rate variability. BPA exposure also impaired intracellular calcium handling, resulting in diminished calcium transient amplitudes, prolonged calcium transient upstroke and duration time. Alterations in calcium handling also increased the propensity for alternans and skipped beats. Notably, the effect of BPA-treatment on calcium handling was partially reversible. Our data suggest that acute BPA exposure could precipitate secondary adverse effects on contractile performance and/or electrical alternans, both of which are dependent on intracellular calcium homeostasis.Manelle RamadanMeredith ShermanRafael JaimesAshika ChaluvadiLuther SwiftNikki Gillum PosnackNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 8, Iss 1, Pp 1-11 (2018)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Manelle Ramadan Meredith Sherman Rafael Jaimes Ashika Chaluvadi Luther Swift Nikki Gillum Posnack Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
description	Abstract Bisphenol chemicals are commonly used in the manufacturing of polycarbonate plastics, polyvinyl chloride plastics, resins, and thermal printing applications. Humans are inadvertently exposed to bisphenols through contact with consumer products and/or medical devices. Recent reports have shown a link between bisphenol-a (BPA) exposure and adverse cardiovascular outcomes; although these studies have been limited to adult subjects and models. Since cardiac physiology differs significantly between the developing and adult heart, we aimed to assess the impact of BPA exposure on cardiac function, using a neonatal cardiomyocyte model. Neonatal rat ventricular myocytes were monitored to assess cell viability, spontaneous beating rate, beat rate variability, and calcium-handling parameters in the presence of control or bisphenol-supplemented media. A range of doses were tested to mimic environmental exposure (10−9–10−8M), maximum clinical exposure (10−5M), and supraphysiological exposure levels (10−4M). Acute BPA exposure altered cardiomyocyte functionality, resulting in a slowed spontaneous beating rate and increased beat rate variability. BPA exposure also impaired intracellular calcium handling, resulting in diminished calcium transient amplitudes, prolonged calcium transient upstroke and duration time. Alterations in calcium handling also increased the propensity for alternans and skipped beats. Notably, the effect of BPA-treatment on calcium handling was partially reversible. Our data suggest that acute BPA exposure could precipitate secondary adverse effects on contractile performance and/or electrical alternans, both of which are dependent on intracellular calcium homeostasis.
format	article
author	Manelle Ramadan Meredith Sherman Rafael Jaimes Ashika Chaluvadi Luther Swift Nikki Gillum Posnack
author_facet	Manelle Ramadan Meredith Sherman Rafael Jaimes Ashika Chaluvadi Luther Swift Nikki Gillum Posnack
author_sort	Manelle Ramadan
title	Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
title_short	Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
title_full	Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
title_fullStr	Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
title_full_unstemmed	Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
title_sort	disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a
publisher	Nature Portfolio
publishDate	2018
url	https://doaj.org/article/d3812031f3b741618154f6e005197fd2
work_keys_str_mv	AT manelleramadan disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola AT meredithsherman disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola AT rafaeljaimes disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola AT ashikachaluvadi disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola AT lutherswift disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola AT nikkigillumposnack disruptionofneonatalcardiomyocytephysiologyfollowingexposuretobisphenola
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Disruption of neonatal cardiomyocyte physiology following exposure to bisphenol-a

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