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The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)

[Image: see text] Due to the detection frequencies and measured concentrations in surface water, the type I pyrethroid insecticide, bifenthrin, has been of particular concern within the Sacramento-San Joaquin Delta in California. Concentrations have been detected above levels previously reported to...

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Autores principales: Magnuson, Jason T., Caceres, Leslie, Sy, Nathan, Ji, Chenyang, Tanabe, Philip, Gan, Jay, Lydy, Michael J., Schlenk, Daniel
Formato: Online Artículo Texto
Lenguaje:English
Publicado: American Chemical Society 2022
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9387103/
https://www.ncbi.nlm.nih.gov/pubmed/35876619
http://dx.doi.org/10.1021/acs.est.2c01542
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author Magnuson, Jason T.
Caceres, Leslie
Sy, Nathan
Ji, Chenyang
Tanabe, Philip
Gan, Jay
Lydy, Michael J.
Schlenk, Daniel
author_facet Magnuson, Jason T.
Caceres, Leslie
Sy, Nathan
Ji, Chenyang
Tanabe, Philip
Gan, Jay
Lydy, Michael J.
Schlenk, Daniel
author_sort Magnuson, Jason T.
collection PubMed
description [Image: see text] Due to the detection frequencies and measured concentrations in surface water, the type I pyrethroid insecticide, bifenthrin, has been of particular concern within the Sacramento-San Joaquin Delta in California. Concentrations have been detected above levels previously reported to impair neuroendocrine function and induce neurotoxicity to several species of salmonids. Metabolomic and transcriptomic studies indicated impairment of cellular signaling within the brain of exposed animals and potential alteration of lipid metabolism. To better understand the potential impacts of bifenthrin on brain lipids, juvenile rainbow trout (Oncorhynchus mykiss) were exposed to mean bifenthrin concentrations of 28 or 48 ng/L for 14 days, and non-targeted lipidomic profiling in the brain was conducted. Brain tissue sections were also assessed for histopathological insult following bifenthrin treatment. Bifenthrin-exposed trout had a concentration-dependent decrease in the relative abundance of triglycerides (TGs) with levels of phosphatidylcholines (PCs) and phosphatidylethanolamines (PEs) significantly altered following 48 ng/L bifenthrin exposure. An increased incidence of histopathological lesions, such as focal hemorrhages and congestion of blood vessels, was noted in the brains of bifenthrin-treated animals, suggesting an association between altered lipid metabolism and neuronal cell structure and integrity.
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spelling pubmed-93871032022-08-19 The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss) Magnuson, Jason T. Caceres, Leslie Sy, Nathan Ji, Chenyang Tanabe, Philip Gan, Jay Lydy, Michael J. Schlenk, Daniel Environ Sci Technol [Image: see text] Due to the detection frequencies and measured concentrations in surface water, the type I pyrethroid insecticide, bifenthrin, has been of particular concern within the Sacramento-San Joaquin Delta in California. Concentrations have been detected above levels previously reported to impair neuroendocrine function and induce neurotoxicity to several species of salmonids. Metabolomic and transcriptomic studies indicated impairment of cellular signaling within the brain of exposed animals and potential alteration of lipid metabolism. To better understand the potential impacts of bifenthrin on brain lipids, juvenile rainbow trout (Oncorhynchus mykiss) were exposed to mean bifenthrin concentrations of 28 or 48 ng/L for 14 days, and non-targeted lipidomic profiling in the brain was conducted. Brain tissue sections were also assessed for histopathological insult following bifenthrin treatment. Bifenthrin-exposed trout had a concentration-dependent decrease in the relative abundance of triglycerides (TGs) with levels of phosphatidylcholines (PCs) and phosphatidylethanolamines (PEs) significantly altered following 48 ng/L bifenthrin exposure. An increased incidence of histopathological lesions, such as focal hemorrhages and congestion of blood vessels, was noted in the brains of bifenthrin-treated animals, suggesting an association between altered lipid metabolism and neuronal cell structure and integrity. American Chemical Society 2022-07-25 2022-08-16 /pmc/articles/PMC9387103/ /pubmed/35876619 http://dx.doi.org/10.1021/acs.est.2c01542 Text en © 2022 The Authors. Published by American Chemical Society https://creativecommons.org/licenses/by/4.0/Permits the broadest form of re-use including for commercial purposes, provided that author attribution and integrity are maintained (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Magnuson, Jason T.
Caceres, Leslie
Sy, Nathan
Ji, Chenyang
Tanabe, Philip
Gan, Jay
Lydy, Michael J.
Schlenk, Daniel
The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title_full The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title_fullStr The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title_full_unstemmed The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title_short The Use of Non-targeted Lipidomics and Histopathology to Characterize the Neurotoxicity of Bifenthrin to Juvenile Rainbow Trout (Oncorhynchus mykiss)
title_sort use of non-targeted lipidomics and histopathology to characterize the neurotoxicity of bifenthrin to juvenile rainbow trout (oncorhynchus mykiss)
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9387103/
https://www.ncbi.nlm.nih.gov/pubmed/35876619
http://dx.doi.org/10.1021/acs.est.2c01542
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