ArticleNeurotoxicology2012
Selenium induces cholinergic motor neuron degeneration in Caenorhabditis elegans.
Article in Neurotoxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 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.
The trial behind it
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Who cites it
29 citing papers in PubMed, 77 citations in OpenAlex.
- Canine Idiopathic Epilepsy as a Natural Animal Model for Human Epilepsy: A Scoping Review Highlighting Metabolic Perspectives Beyond the Brain.Nutrients · 2026Article
- Selenium-EnrichedAntioxidants (Basel, Switzerland) · 2024Article
- Oxidative Stress in Amyotrophic Lateral Sclerosis: Synergy of Genetic and Environmental Factors.International journal of molecular sciences · 2022Review
- A perspective on persistent toxicants in veterans and amyotrophic lateral sclerosis: identifying exposures determining higher ALS risk.Journal of neurology · 2022Review
- Prenatal exposure to a mixture of elements and neurobehavioral outcomes in mid-childhood: Results from Project Viva.Environmental research · 2021Article
- Role of environmental pollutants in Alzheimer's disease: a review.Environmental science and pollution research international · 2020Review
- Effect of environmental toxicants on neuronal functions.Environmental science and pollution research international · 2020Review
- Deep learning-enabled analysis reveals distinct neuronal phenotypes induced by aging and cold-shock.BMC biology · 2020Article
- HIF-1 Has a Central Role inFrontiers in genetics · 2020Article
- LPS-induced sickness behavior is not affected by selenium but is switched off by psychogenic stress in rats.Veterinary research communications · 2019Article
- The glutathione system and the related thiol network in Caenorhabditis elegans.Redox biology · 2019Review
- Selenium species-dependent toxicity, bioavailability and metabolic transformations in Caenorhabditis elegans.Metallomics : integrated biometal science · 2018Article
- Toxicity evaluation of Wanzhou watershed of Yangtze Three Gorges Reservior in the flood season in Caenorhabditis elegans.Scientific reports · 2018Article
- Stem Cells as Potential Targets of Polyphenols in Multiple Sclerosis and Alzheimer's Disease.BioMed research international · 2018Review
- Degenerin channel activation causes caspase-mediated protein degradation and mitochondrial dysfunction in adult C. elegans muscle.Journal of cachexia, sarcopenia and muscle · 2016Article
- Selenium in the Therapy of Neurological Diseases. Where is it Going?Current neuropharmacology · 2016Review
- Role of environmental contaminants in the etiology of Alzheimer's disease: a review.Current Alzheimer research · 2015Review
- Assessment of selenium toxicity on the life cycle of Caenorhabditis elegans.Ecotoxicology (London, England) · 2014Article
- The neurodegenerative effects of selenium are inhibited by FOXO and PINK1/PTEN regulation of insulin/insulin-like growth factor signaling in Caenorhabditis elegans.Neurotoxicology · 2014Article
- Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases.Antioxidants & redox signaling · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 4 institutions in 3 countries.
Funding
Abstract
Selenium is an essential micronutrient required for cellular antioxidant systems, yet at higher doses it induces oxidative stress. Additionally, in vertebrates environmental exposures to toxic levels of selenium can cause paralysis and death. Here we show that selenium-induced oxidative stress leads to decreased cholinergic signaling and degeneration of cholinergic neurons required for movement and egg-laying in Caenorhabditis elegans. Exposure to high levels of selenium leads to proteolysis of a soluble muscle protein through mechanisms suppressible by two pharmacological agents, levamisole and aldicarb which enhance cholinergic signaling in muscle. In addition, animals with reduction-of-function mutations in genes encoding post-synaptic levamisole-sensitive acetylcholine receptor subunits or the vesicular acetylcholine transporter developed impaired forward movement faster during selenium-exposure than normal animals, again confirming that selenium reduces cholinergic signaling. Finally, the antioxidant reduced glutathione, inhibits selenium-induced reductions in egg-laying through a cellular protective mechanism dependent on the C. elegans glutaredoxin, GLRX-21. These studies provide evidence that the environmental toxicant selenium induces neurodegeneration of cholinergic neurons through depletion of glutathione, a mechanism linked to the neuropathology of Alzheimer's disease, amyotrophic lateral sclerosis, and Parkinson's disease.
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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.