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Text
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URL Address
<a href="http://doi.org/10.1016/j.etap.2017.11.005" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2017.11.005</a>
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Pages
46-52
Volume
57
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Title
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Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans
Publisher
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Environmental Toxicology and Pharmacology
Date
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2018
2018-01
Subject
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C. elegans; Glyphosate; Hydrogen peroxide; Mitochondrial inhibition; oxidative stress; Toxicology; Environmental Sciences & Ecology; Pharmacology & Pharmacy; parkinsons-disease; brain; alzheimers-disease; mechanisms; degeneration; species; neurodegenerative diseases; 6-ohda; C. elegans; complex-i; Herbicide; Reactive oxygen
Creator
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Bailey D C; Todt C E; Burchfield S L; Pressley A S; Denney R D; Snapp I B; Negga R; Traynor W L; Fitsanakis V A
Description
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Glyphosate-containing herbicides are among the most widely-used in the world. Although glyphosate itself is relatively non-toxic, growing evidence suggests that commercial herbicide formulations may lead to increased oxidative stress and mitochondrial inhibition. In order to assess these mechanisms in vivo, we chronically (24 h) exposed Caenorhabditis elegans to various concentrations of the glyphosate-containing herbicide TouchDown (TD). Following TD exposure, we evaluated the function of specific mitochondrial electron transport chain complexes. Initial oxygen consumption studies demonstrated inhibition in mid- and high-TD concentration treatment groups compared to controls. Results from tetramethylrhodamine ethyl ester and ATP assays indicated reductions in the proton gradient and ATP levels, respectively. Additional studies were designed to determine whether TD exposure resulted in increased reactive oxygen species (ROS) production. Data from hydrogen peroxide, but not superoxide or hydroxyl radical, assays showed statistically significant increases in this specific ROS. Taken together, these data indicate that exposure of Caenorhabditis elegans to TD leads to mitochondrial inhibition and hydrogen peroxide production.
Identifier
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<a href="http://doi.org/10.1016/j.etap.2017.11.005" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2017.11.005</a>
Format
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Journal Article or Conference Abstract Publication
2018
6-ohda
alzheimers-disease
Bailey D C
Brain
Burchfield S L
C. elegans
complex-i
degeneration
Denney R D
Department of Pharmaceutical Sciences
Environmental Sciences & Ecology
Environmental toxicology and pharmacology
Fitsanakis V A
Glyphosate
Herbicide
Hydrogen peroxide
Journal Article or Conference Abstract Publication
mechanisms
Mitochondrial inhibition
Negga R
NEOMED College of Pharmacy
Neurodegenerative Diseases
Oxidative Stress
parkinsons-disease
Pharmacology & Pharmacy
Pressley A S
Reactive oxygen
Snapp I B
SPECIES
Todt C E
Toxicology
Traynor W L