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Environ Toxicol Pharmacol. 2018 Jan;57:46-52. doi: 10.1016/j.etap.2017.11.005. Epub 2017 Nov 20.

Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans.

Author information

1
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: dbailey@student.king.edu.
2
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: ctodt@student.king.edu.
3
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: sburchfield@student.king.edu.
4
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: adpressley@student.king.edu.
5
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: radonaldson@student.king.edu.
6
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: snapp@student.king.edu.
7
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: rnegga@student.king.edu.
8
King University, Department of Mathematics and Physics, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: wltrayno@king.edu.
9
King University, Department of Biology, 1350 King College Road, Bristol, TN 37620, USA. Electronic address: vfitsanakis@neomed.edu.

Abstract

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 (24h) 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.

KEYWORDS:

C. elegans; Glyphosate; Herbicide; Hydrogen peroxide; Mitochondrial inhibition; Reactive oxygen species

PMID:
29190595
PMCID:
PMC5803312
DOI:
10.1016/j.etap.2017.11.005
[Indexed for MEDLINE]
Free PMC Article

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