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Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons
Bisphenol A (BPA) is one of the most widely used chemicals worldwide, e.g., as a component of plastic containers for food and water. It is considered to exert an estrogenic effect, by mimicking estradiol (E2) action. Because of this widespread presence, it has attracted the interest and concern of r...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539360/ https://www.ncbi.nlm.nih.gov/pubmed/31052388 http://dx.doi.org/10.3390/ijms20092160 |
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author | Ruffinatti, Federico Alessandro Gilardino, Alessandra Secchi, Valter Cottone, Erika Lovisolo, Davide Bovolin, Patrizia |
author_facet | Ruffinatti, Federico Alessandro Gilardino, Alessandra Secchi, Valter Cottone, Erika Lovisolo, Davide Bovolin, Patrizia |
author_sort | Ruffinatti, Federico Alessandro |
collection | PubMed |
description | Bisphenol A (BPA) is one of the most widely used chemicals worldwide, e.g., as a component of plastic containers for food and water. It is considered to exert an estrogenic effect, by mimicking estradiol (E2) action. Because of this widespread presence, it has attracted the interest and concern of researchers and regulators. Despite the vast amount of related literature, the potential adverse effects of environmentally significant doses of BPA are still object of controversy, and the mechanisms by which it can perturb endocrine functions, and particularly the neuroendocrine axis, are not adequately understood. One of the ways by which endocrine disruptors (EDCs) can exert their effects is the perturbation of calcium signaling mechanisms. In this study, we addressed the issue of the impact of BPA on the neuroendocrine system with an in vitro approach, using a consolidated model of immortalized Gonadotropin-Releasing Hormone (GnRH) expressing neurons, the GT1–7 cell line, focusing on the calcium signals activated by the endocrine disruptor. The investigation was limited to biologically relevant doses (nM–µM range). We found that BPA induced moderate increases in intracellular calcium concentration, comparable with those induced by nanomolar doses of E2, without affecting cell survival and with only a minor effect on proliferation. |
format | Online Article Text |
id | pubmed-6539360 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2019 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-65393602019-06-04 Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons Ruffinatti, Federico Alessandro Gilardino, Alessandra Secchi, Valter Cottone, Erika Lovisolo, Davide Bovolin, Patrizia Int J Mol Sci Article Bisphenol A (BPA) is one of the most widely used chemicals worldwide, e.g., as a component of plastic containers for food and water. It is considered to exert an estrogenic effect, by mimicking estradiol (E2) action. Because of this widespread presence, it has attracted the interest and concern of researchers and regulators. Despite the vast amount of related literature, the potential adverse effects of environmentally significant doses of BPA are still object of controversy, and the mechanisms by which it can perturb endocrine functions, and particularly the neuroendocrine axis, are not adequately understood. One of the ways by which endocrine disruptors (EDCs) can exert their effects is the perturbation of calcium signaling mechanisms. In this study, we addressed the issue of the impact of BPA on the neuroendocrine system with an in vitro approach, using a consolidated model of immortalized Gonadotropin-Releasing Hormone (GnRH) expressing neurons, the GT1–7 cell line, focusing on the calcium signals activated by the endocrine disruptor. The investigation was limited to biologically relevant doses (nM–µM range). We found that BPA induced moderate increases in intracellular calcium concentration, comparable with those induced by nanomolar doses of E2, without affecting cell survival and with only a minor effect on proliferation. MDPI 2019-05-01 /pmc/articles/PMC6539360/ /pubmed/31052388 http://dx.doi.org/10.3390/ijms20092160 Text en © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ruffinatti, Federico Alessandro Gilardino, Alessandra Secchi, Valter Cottone, Erika Lovisolo, Davide Bovolin, Patrizia Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title | Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title_full | Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title_fullStr | Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title_full_unstemmed | Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title_short | Bisphenol A Activates Calcium Influx in Immortalized GnRH Neurons |
title_sort | bisphenol a activates calcium influx in immortalized gnrh neurons |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6539360/ https://www.ncbi.nlm.nih.gov/pubmed/31052388 http://dx.doi.org/10.3390/ijms20092160 |
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