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Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure

Biomarkers are frequently used in ecotoxicology as they allow to study toxicant effects happening at low concentrations of exposure. However, most sublethal studies only evaluate cellular biomarkers which lack evident ecological relevance. We used a multibiomarker approach to estimate the toxic effe...

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Autores principales: Sandoval-Herrera, Natalia, Mena, Freylan, Espinoza, Mario, Romero, Adarli
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642105/
https://www.ncbi.nlm.nih.gov/pubmed/31324839
http://dx.doi.org/10.1038/s41598-019-46804-6
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author Sandoval-Herrera, Natalia
Mena, Freylan
Espinoza, Mario
Romero, Adarli
author_facet Sandoval-Herrera, Natalia
Mena, Freylan
Espinoza, Mario
Romero, Adarli
author_sort Sandoval-Herrera, Natalia
collection PubMed
description Biomarkers are frequently used in ecotoxicology as they allow to study toxicant effects happening at low concentrations of exposure. However, most sublethal studies only evaluate cellular biomarkers which lack evident ecological relevance. We used a multibiomarker approach to estimate the toxic effects of ethoprophos, an organophosphate insecticide commonly used in banana plantations, on the tropical fish Astyanax aeneus (Characidae). We measured biomarkers at sub-individual (cellular) and individual (metabolism, behavior) levels and examined relationships among these responses. A sublethal exposure to ethoprophos caused a significant (54%) reduction of brain Cholinesterase (ChE) activity, reflecting the pesticide’s high neurotoxicity. However, other biomarkers like oxidative stress, biotransformation reactions, and resting metabolic rate were not affected. Exposure to ethoprophos modified antipredator behaviors such as escape response and detection avoidance (light/dark preference): exposed fish escaped slower from a simulated attack and preferred brighter areas in a novel tank. The relationship between ChE activity and reaction time suggests that pesticide-induced ChE inhibition reduces escape ability in fish. Our results provide evidence that impacts of organophosphate pesticides on fish ecological fitness can occur even with short exposures at very low concentrations.
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spelling pubmed-66421052019-07-25 Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure Sandoval-Herrera, Natalia Mena, Freylan Espinoza, Mario Romero, Adarli Sci Rep Article Biomarkers are frequently used in ecotoxicology as they allow to study toxicant effects happening at low concentrations of exposure. However, most sublethal studies only evaluate cellular biomarkers which lack evident ecological relevance. We used a multibiomarker approach to estimate the toxic effects of ethoprophos, an organophosphate insecticide commonly used in banana plantations, on the tropical fish Astyanax aeneus (Characidae). We measured biomarkers at sub-individual (cellular) and individual (metabolism, behavior) levels and examined relationships among these responses. A sublethal exposure to ethoprophos caused a significant (54%) reduction of brain Cholinesterase (ChE) activity, reflecting the pesticide’s high neurotoxicity. However, other biomarkers like oxidative stress, biotransformation reactions, and resting metabolic rate were not affected. Exposure to ethoprophos modified antipredator behaviors such as escape response and detection avoidance (light/dark preference): exposed fish escaped slower from a simulated attack and preferred brighter areas in a novel tank. The relationship between ChE activity and reaction time suggests that pesticide-induced ChE inhibition reduces escape ability in fish. Our results provide evidence that impacts of organophosphate pesticides on fish ecological fitness can occur even with short exposures at very low concentrations. Nature Publishing Group UK 2019-07-19 /pmc/articles/PMC6642105/ /pubmed/31324839 http://dx.doi.org/10.1038/s41598-019-46804-6 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Sandoval-Herrera, Natalia
Mena, Freylan
Espinoza, Mario
Romero, Adarli
Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title_full Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title_fullStr Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title_full_unstemmed Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title_short Neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
title_sort neurotoxicity of organophosphate pesticides could reduce the ability of fish to escape predation under low doses of exposure
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6642105/
https://www.ncbi.nlm.nih.gov/pubmed/31324839
http://dx.doi.org/10.1038/s41598-019-46804-6
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