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Text
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URL Address
<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">http://doi.org/10.1016/j.etap.2018.12.019</a>
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Pages
36-42
Volume
66
Dublin Core
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Title
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Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
Publisher
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Environmental toxicology and pharmacology
Date
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2019
2019-02
Subject
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C. elegans; Glyphosate; *hydrogen peroxide; Mitochondrial inhibition; Oxygen Consumption; *Reactive oxygen species; Animals; Reactive Oxygen Species/metabolism; Adenosine Triphosphate/metabolism; Herbicides/*toxicity; Caenorhabditis elegans/*drug effects/metabolism; Electron Transport Complex II/*antagonists & inhibitors/metabolism; Glycine/*analogs & derivatives/toxicity
Creator
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Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Description
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Glyphosate-based herbicides, such as Touchdown (TD) and Roundup, are among the most heavily-used herbicides in the world. While the active ingredient is generally considered non-toxic, the toxicity resulting from exposure to commercially-sold formulations is less clear. In many cases, cell cultures or various model organisms exposed to glyphosate formulations show toxicity and, in some cases, lethality. Using Caenorhabditis elegans, we assessed potential toxic mechanisms through which a highly-concentrated commercial formulation of TD promotes neurodegeneration. Following a 30-min treatment, we assayed mitochondrial electron transport chain function and reactive oxygen species (ROS) production. Initial oxygen consumption studies indicated general mitochondrial inhibition compared to controls ((*)p < 0.05). When Complex II activity was further assessed, inhibition was observed in all TD-treated groups ((*)p < 0.05). Complex IV activity, however, was not adversely affected by TD. This electron transport chain inhibition also resulted in reduced ATP levels ((*)p < 0.05). Furthermore, hydrogen peroxide levels, but not other ROS, were increased ((*)p < 0.05). Taken together, these data indicate that commercially-available formulations of TD may exert neurotoxicity through Complex II (succinate dehydrogenase) inhibition, decreased ATP levels, and increased hydrogen peroxide production.
Identifier
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<a href="http://doi.org/10.1016/j.etap.2018.12.019" target="_blank" rel="noreferrer noopener">10.1016/j.etap.2018.12.019</a>
*hydrogen peroxide
*Reactive oxygen species
2019
Adenosine Triphosphate/metabolism
Animals
Bailey Denise C
Burchfield Shelbie L
C. elegans
Caenorhabditis elegans/*drug effects/metabolism
Denney Rachel D
Department of Pharmaceutical Sciences
Electron Transport Complex II/*antagonists & inhibitors/metabolism
Environmental toxicology and pharmacology
Fitsanakis Vanessa A
Glycine/*analogs & derivatives/toxicity
Glyphosate
Herbicides/*toxicity
Mitochondrial inhibition
Negga Rekek
NEOMED College of Pharmacy
Oxygen Consumption
Reactive Oxygen Species/metabolism
Todt Callie E