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Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses
Ocean acidification (OA) is expected to indirectly impact biota living in contaminated coastal environments by altering the bioavailability and potentially toxicity of many pH-sensitive metals. Here, we show that OA (pH 7.71; pCO(2) 1480 μatm) significantly increases the toxicity responses to a glob...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761931/ https://www.ncbi.nlm.nih.gov/pubmed/26899803 http://dx.doi.org/10.1038/srep21554 |
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author | Lewis, Ceri Ellis, Robert P. Vernon, Emily Elliot, Katie Newbatt, Sam Wilson, Rod W. |
author_facet | Lewis, Ceri Ellis, Robert P. Vernon, Emily Elliot, Katie Newbatt, Sam Wilson, Rod W. |
author_sort | Lewis, Ceri |
collection | PubMed |
description | Ocean acidification (OA) is expected to indirectly impact biota living in contaminated coastal environments by altering the bioavailability and potentially toxicity of many pH-sensitive metals. Here, we show that OA (pH 7.71; pCO(2) 1480 μatm) significantly increases the toxicity responses to a global coastal contaminant (copper ~0.1 μM) in two keystone benthic species; mussels (Mytilus edulis) and purple sea urchins (Paracentrotus lividus). Mussels showed an extracellular acidosis in response to OA and copper individually which was enhanced during combined exposure. In contrast, urchins maintained extracellular fluid pH under OA by accumulating bicarbonate but exhibited a slight alkalosis in response to copper either alone or with OA. Importantly, copper-induced damage to DNA and lipids was significantly greater under OA compared to control conditions (pH 8.14; pCO(2) 470 μatm) for both species. However, this increase in DNA-damage was four times lower in urchins than mussels, suggesting that internal acid-base regulation in urchins may substantially moderate the magnitude of this OA-induced copper toxicity effect. Thus, changes in metal toxicity under OA may not purely be driven by metal speciation in seawater and may be far more diverse than either single-stressor or single-species studies indicate. This has important implications for future environmental management strategies. |
format | Online Article Text |
id | pubmed-4761931 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Nature Publishing Group |
record_format | MEDLINE/PubMed |
spelling | pubmed-47619312016-02-29 Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses Lewis, Ceri Ellis, Robert P. Vernon, Emily Elliot, Katie Newbatt, Sam Wilson, Rod W. Sci Rep Article Ocean acidification (OA) is expected to indirectly impact biota living in contaminated coastal environments by altering the bioavailability and potentially toxicity of many pH-sensitive metals. Here, we show that OA (pH 7.71; pCO(2) 1480 μatm) significantly increases the toxicity responses to a global coastal contaminant (copper ~0.1 μM) in two keystone benthic species; mussels (Mytilus edulis) and purple sea urchins (Paracentrotus lividus). Mussels showed an extracellular acidosis in response to OA and copper individually which was enhanced during combined exposure. In contrast, urchins maintained extracellular fluid pH under OA by accumulating bicarbonate but exhibited a slight alkalosis in response to copper either alone or with OA. Importantly, copper-induced damage to DNA and lipids was significantly greater under OA compared to control conditions (pH 8.14; pCO(2) 470 μatm) for both species. However, this increase in DNA-damage was four times lower in urchins than mussels, suggesting that internal acid-base regulation in urchins may substantially moderate the magnitude of this OA-induced copper toxicity effect. Thus, changes in metal toxicity under OA may not purely be driven by metal speciation in seawater and may be far more diverse than either single-stressor or single-species studies indicate. This has important implications for future environmental management strategies. Nature Publishing Group 2016-02-22 /pmc/articles/PMC4761931/ /pubmed/26899803 http://dx.doi.org/10.1038/srep21554 Text en Copyright © 2016, Macmillan Publishers Limited http://creativecommons.org/licenses/by/4.0/ This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/ |
spellingShingle | Article Lewis, Ceri Ellis, Robert P. Vernon, Emily Elliot, Katie Newbatt, Sam Wilson, Rod W. Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title | Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title_full | Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title_fullStr | Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title_full_unstemmed | Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title_short | Ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
title_sort | ocean acidification increases copper toxicity differentially in two key marine invertebrates with distinct acid-base responses |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4761931/ https://www.ncbi.nlm.nih.gov/pubmed/26899803 http://dx.doi.org/10.1038/srep21554 |
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