ArticlePloS one2014
Exposure to mitochondrial genotoxins and dopaminergic neurodegeneration in Caenorhabditis elegans.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 85 citations in OpenAlex.
- Dietary mycotoxin toxicity inAdvances in neurotoxicology · 2026Article
- LRRK2-mediated mitochondrial dysfunction in Parkinson's disease.The Biochemical journal · 2025Review
- Studying the mechanisms of neurodegeneration:Frontiers in cellular neuroscience · 2025Review
- PET Imaging with [Antioxidants (Basel, Switzerland) · 2024Article
- Extracellular vesicles from the microalga Tetraselmis chuii are biocompatible and exhibit unique bone tropism along with antioxidant and anti-inflammatory properties.Communications biology · 2024Article
- Comprehensive characterization of mitochondrial bioenergetics at different larval stages reveals novel insights about the developmental metabolism ofbioRxiv : the preprint server for biology · 2024Article
- Dendrite morphogenesis in Caenorhabditis elegans.Genetics · 2024Review
- Morphological hallmarks of dopaminergic neurodegeneration are associated with altered neuron function in Caenorhabditis elegans.Neurotoxicology · 2024Article
- Article
- Towards improved screening of toxins for Parkinson's risk.NPJ Parkinson's disease · 2023Review
- Mitochondria in the Spotlight:Cells · 2023Review
- Aflatoxin BInternational journal of molecular sciences · 2023Article
- Applications of a powerful model organism Caenorhabditis elegans to study the neurotoxicity induced by heavy metals and pesticides.Physiological research · 2023Article
- Neurotoxicology of metals and metallic nanoparticles inAdvances in neurotoxicology · 2023Article
- Article
- The intertwining between lead and ethanol in the model organismFrontiers in toxicology · 2022Review
- Mild pentachlorophenol-mediated uncoupling of mitochondria depletes ATP but does not cause an oxidized redox state or dopaminergic neurodegeneration inCurrent research in toxicology · 2022Article
- Mitochondrial DNA Mutagenesis: Feature of and Biomarker for Environmental Exposures and Aging.Current environmental health reports · 2021Review
- Neuroimmune disruptions from naturally occurring levels of mycotoxins.Environmental science and pollution research international · 2021Review
- Trauma-induced regulation of VHP-1 modulates the cellular response to mechanical stress.Nature communications · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Neurodegeneration has been correlated with mitochondrial DNA (mtDNA) damage and exposure to environmental toxins, but causation is unclear. We investigated the ability of several known environmental genotoxins and neurotoxins to cause mtDNA damage, mtDNA depletion, and neurodegeneration in Caenorhabditis elegans. We found that paraquat, cadmium chloride and aflatoxin B1 caused more mitochondrial than nuclear DNA damage, and paraquat and aflatoxin B1 also caused dopaminergic neurodegeneration. 6-hydroxydopamine (6-OHDA) caused similar levels of mitochondrial and nuclear DNA damage. To further test whether the neurodegeneration could be attributed to the observed mtDNA damage, C. elegans were exposed to repeated low-dose ultraviolet C radiation (UVC) that resulted in persistent mtDNA damage; this exposure also resulted in dopaminergic neurodegeneration. Damage to GABAergic neurons and pharyngeal muscle cells was not detected. We also found that fasting at the first larval stage was protective in dopaminergic neurons against 6-OHDA-induced neurodegeneration. Finally, we found that dopaminergic neurons in C. elegans are capable of regeneration after laser surgery. Our findings are consistent with a causal role for mitochondrial DNA damage in neurodegeneration, but also support non mtDNA-mediated mechanisms.
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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.