ArticleToxicological sciences : an official journal of the Society of Toxicology2020
Drp-1-Dependent Mitochondrial Fragmentation Contributes to Cobalt Chloride-Induced Toxicity in Caenorhabditis elegans.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 22 citations in OpenAlex.
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- Pervasive food contaminant ochratoxin-A induces energy crisis: Mitochondrial dysfunction in human primary proximal tubule cells.Toxicology reports · 2025Article
- Evaluation of toxicological mechanisms of ochratoxin-A in human primary proximal tubule epithelial cells.bioRxiv : the preprint server for biology · 2025Article
- Nonapoptotic role of EGL-1 in exopher production and neuronal health inProceedings of the National Academy of Sciences of the United States of America · 2025Article
- ZA-II-05, a novel NMDA-receptor antagonist reverses vanadium-induced neurotoxicity in Caenorhabditis elegans (C. elegans).BMC neuroscience · 2024Article
- Evaluation of neurotoxicity and the role of oxidative stress of cobalt nanoparticles, titanium dioxide nanoparticles, and multiwall carbon nanotubes in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- ADAR-mediated regulation of PQM-1 expression in neurons impacts gene expression throughout C. elegans and regulates survival from hypoxia.PLoS biology · 2023Article
- Neurotoxicology of metals and metallic nanoparticles inAdvances in neurotoxicology · 2023Article
- Neurotoxicity Evaluation of Nanomaterials Using C. elegans: Survival, Locomotion Behaviors, and Oxidative Stress.Current protocols · 2022Article
- Dietary Supplements and Natural Products: An Update on Their Clinical Effectiveness and Molecular Mechanisms of Action During Accelerated Biological Aging.Frontiers in genetics · 2022Review
- Intercellular transfer of mitochondria via tunneling nanotubes protects against cobalt nanoparticle-induced neurotoxicity and mitochondrial damage.Nanotoxicology · 2021Article
- Evaluations of Environmental Pollutant-Induced Mitochondrial Toxicity Using Caenorhabditis elegans as a Model System.Methods in molecular biology (Clifton, N.J.) · 2021Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Excess cobalt may lead to metallosis, characterized by sensorineural hearing loss, visual, and cognitive impairment, and peripheral neuropathy. In the present study, we sought to address the molecular mechanisms of cobalt-induced neurotoxicity, using Caenorhabditis elegans as an experimental model. Exposure to cobalt chloride for 2 h significantly decreased the survival rate and lifespan in nematodes. Cobalt chloride exposure led to increased oxidative stress and upregulation of glutathione S-transferase 4. Consistently, its upstream regulator skn-1, a mammalian homolog of the nuclear factor erythroid 2-related factor 2, was activated. Among the mRNAs examined by quantitative real-time polymerase chain reactions, apoptotic activator egl-1, proapoptotic gene ced-9, autophagic (bec-1 and lgg-1), and mitochondrial fission regulator drp-1 were significantly upregulated upon cobalt exposure, concomitant with mitochondrial fragmentation, as determined by confocal microscopy. Moreover, drp-1 inhibition suppressed the cobalt chloride-induced reactive oxygen species generation, growth defects, and reduced mitochondrial fragmentation. Our novel findings suggest that the acute toxicity of cobalt is mediated by mitochondrial fragmentation and drp-1 upregulation.
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