Document Detail


Selenium induces cholinergic motor neuron degeneration in Caenorhabditis elegans.
MedLine Citation:
PMID:  22560997     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Annette O Estevez; Catherine L Mueller; Kathleen L Morgan; Nathaniel J Szewczyk; Luke Teece; Antonio Miranda-Vizuete; Miguel Estevez
Related Documents :
435137 - Visual evoked responses in pernicious anemia.
23022747 - Correlated basal expression of immediate early gene egr1 and tyrosine hydroxylase in ze...
23144607 - Distinct neurogenomic states in basal ganglia subregions relate differently to singing ...
23623427 - Polybutylcyanoacrylate nanoparticle-mediated neurotrophin-3 gene delivery for different...
15638097 - Impaired neural conduction in crossed visual pathways in patients with ocular hypertens...
1614547 - Objective analysis of the topological organization of the primate cortical visual system.
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2012-04-25
Journal Detail:
Title:  Neurotoxicology     Volume:  33     ISSN:  1872-9711     ISO Abbreviation:  Neurotoxicology     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-10-12     Completed Date:  2013-03-21     Revised Date:  2013-05-13    
Medline Journal Info:
Nlm Unique ID:  7905589     Medline TA:  Neurotoxicology     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1021-32     Citation Subset:  IM    
Copyright Information:
Copyright © 2012 Elsevier Inc. All rights reserved.
Affiliation:
Department of Neurology, University of Arizona, Tucson, AZ 85724-5023, USA. aestevez@email.arizona.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Actins / metabolism
Adjuvants, Immunologic / pharmacology
Analysis of Variance
Animals
Animals, Genetically Modified
Antioxidants / toxicity*
Caenorhabditis elegans
Caenorhabditis elegans Proteins / genetics
Cell Count
Cholinergic Neurons / drug effects*
Dose-Response Relationship, Drug
Galactosides / metabolism
Glutathione / metabolism
Green Fluorescent Proteins / genetics
Levamisole / pharmacology
Motor Neurons* / drug effects,  metabolism,  pathology
Movement / drug effects
Muscle Proteins / metabolism
Muscles / drug effects,  metabolism,  pathology
Mutation / genetics
Nerve Degeneration / chemically induced*,  pathology*
Paralysis / chemically induced
Receptors, Cholinergic / genetics
Reproduction / drug effects,  genetics
Selenium / toxicity*
Signal Transduction / drug effects
Vesicular Acetylcholine Transport Proteins / genetics
Grant Support
ID/Acronym/Agency:
R01 AR054342/AR/NIAMS NIH HHS; R21 ES012305/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Actins; 0/Adjuvants, Immunologic; 0/Antioxidants; 0/Caenorhabditis elegans Proteins; 0/Galactosides; 0/Muscle Proteins; 0/Receptors, Cholinergic; 0/Vesicular Acetylcholine Transport Proteins; 0/beta-galactoside; 147336-22-9/Green Fluorescent Proteins; 14769-73-4/Levamisole; 70-18-8/Glutathione; 7782-49-2/Selenium
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


Previous Document:  Detecting chronic solvent encephalopathy in occupations at risk.
Next Document:  Impact of catechol-o-methyltransferase polymorphisms on risperidone treatment for schizophrenia and ...