Acute exposure to a glyphosate-containing herbicide formulation inhibits Complex II and increases hydrogen peroxide in the model organism Caenorhabditis elegans.
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
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.
Burchfield Shelbie L; Bailey Denise C; Todt Callie E; Denney Rachel D; Negga Rekek; Fitsanakis Vanessa A
Environmental toxicology and pharmacology
2019
2019-02
<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>
Changing the Channels: Nature's Remote Controlling in Health and Disease.
*coronary artery disease; *Editorials; *hydrogen peroxide; *potassium channels; *protein kinases; *vasodilation
Thodeti Charles K
Circulation research
2017
2017-02
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.1161/CIRCRESAHA.117.310442" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.117.310442</a>
Changing the Channels: Nature's Remote Controlling in Health and Disease.
Humans; *vasodilation; *Editorials; *Coronary Artery Disease; *hydrogen peroxide; *potassium channels; *protein kinases; *Coronary Artery Disease; Arterioles; Coronary Vessels; Dilatation; *hydrogen peroxide
Thodeti Charles K
Circulation research
2017
2017-02
<a href="http://doi.org/10.1161/CIRCRESAHA.117.310442" target="_blank" rel="noreferrer noopener">10.1161/CIRCRESAHA.117.310442</a>