ArticleEnvironmental toxicology and pharmacology2018
Chronic exposure to a glyphosate-containing pesticide leads to mitochondrial dysfunction and increased reactive oxygen species production in Caenorhabditis elegans.
Article in Environmental toxicology and pharmacology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
33 citing papers in PubMed, 96 citations in OpenAlex.
- Protective effects of rosmarinic acid against carbaryl-exposed toxicity in honey bees (Apis mellifera): histopathological and molecular docking evidence.Veterinary research communications · 2026Article
- Impact of glyphosate and its mixture with 2,4-D and dicamba on gut biochemical function, intestinal barrier integrity and microbiome composition in adult rats with prenatal commencement of exposure.Archives of toxicology · 2026Article
- Effects of Glyphosate and RoundupInternational journal of molecular sciences · 2026Article
- Pesticides Drive Liver Diseases Through Non-Apoptotic Regulated Cell Death Pathways.Diseases (Basel, Switzerland) · 2026Review
- Mitochondrial Gene Expression as a Novel Biomarker for Detecting and Discriminating Neurotoxic Pesticide Exposure inInsects · 2026Article
- Article
- Mitochondria in the Spotlight:Cells · 2023Review
- Applications of a powerful model organism Caenorhabditis elegans to study the neurotoxicity induced by heavy metals and pesticides.Physiological research · 2023Article
- High-quality genome ofiScience · 2023Article
- Protection of Mitochondrial Potential and Activity by Oxyprenylated Phenylpropanoids.Antioxidants (Basel, Switzerland) · 2023Article
- Biological effects of sub-lethal doses of glyphosate and AMPA on cardiac myoblasts.Frontiers in physiology · 2023Article
- IAA Plays an Important Role in Alkaline Stress Tolerance by Modulating Root Development and ROS Detoxifying Systems in Rice Plants.International journal of molecular sciences · 2022Article
- Fluorescence determination of glyphosate based on a DNA-templated copper nanoparticle biosensor.Mikrochimica acta · 2022Article
- Physiological and oxidative stress responses ofRSC advances · 2022Article
- Comparative Toxicogenomics of Glyphosate and Roundup Herbicides by Mammalian Stem Cell-Based Genotoxicity Assays and Molecular Profiling in Sprague-Dawley Rats.Toxicological sciences : an official journal of the Society of Toxicology · 2022Article
- The effects of low-toxic herbicide Roundup and glyphosate on mitochondria.EXCLI journal · 2022Review
- Glyphosate and its formulations Roundup Bioflow and RangerPro alter bacterial and fungal community composition in the rat caecum microbiome.Frontiers in microbiology · 2022Article
- Low-toxic herbicides Roundup and Atrazine disturb free radical processes in Daphnia in environmentally relevant concentrations.EXCLI journal · 2022Article
- A Common Feature of Pesticides: Oxidative Stress-The Role of Oxidative Stress in Pesticide-Induced Toxicity.Oxidative medicine and cellular longevity · 2022Review
- Effects of Pesticides on Longevity and Bioenergetics in Invertebrates-The Impact of Polyphenolic Metabolites.International journal of molecular sciences · 2021Article
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.