ArticleToxicological sciences : an official journal of the Society of Toxicology2010
The glutaredoxin GLRX-21 functions to prevent selenium-induced oxidative stress in Caenorhabditis elegans.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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23 citing papers in PubMed, 54 citations in OpenAlex.
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- HIF-1 Has a Central Role inFrontiers in genetics · 2020Article
- The glutathione system and the related thiol network in Caenorhabditis elegans.Redox biology · 2019Review
- Treatment of Caenorhabditis elegans with Small Selenium Species Enhances Antioxidant Defense Systems.Molecular nutrition & food research · 2019Article
- Selenium species-dependent toxicity, bioavailability and metabolic transformations in Caenorhabditis elegans.Metallomics : integrated biometal science · 2018Article
- Antagonistic Growth Effects of Mercury and Selenium in Caenorhabditis elegans Are Chemical-Species-Dependent and Do Not Depend on Internal Hg/Se Ratios.Environmental science & technology · 2016Article
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- 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
- Article
- Deletion of thioredoxin reductase and effects of selenite and selenate toxicity in Caenorhabditis elegans.PloS one · 2013Article
- Protective efficacy of selenite against lead-induced neurotoxicity in Caenorhabditis elegans.PloS one · 2013Article
- Selenium induces cholinergic motor neuron degeneration in Caenorhabditis elegans.Neurotoxicology · 2012Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Selenium is an essential micronutrient that functions as an antioxidant. Yet, at higher concentrations, selenium is pro-oxidant and toxic. In extreme cases, exposures to excess selenium can lead to death or selenosis, a syndrome characterized by teeth, hair and nail loss, and nervous system alterations. Recent interest in selenium as an anti- tumorigenic agent has reemphasized the need to understand the mechanisms underlying the cellular consequences of increased selenium exposure. We show here, that in the nematode, Caenorhabditis elegans, selenium has a concentration range in which it functions as an antioxidant, but beyond this range it exhibits a dose- and time-dependent lethality. Oxidation-induced fluorescence emitted by the dye, carboxy-H(2)DCFDA, indicative of reactive oxygen species formation was significantly higher in animals after a brief exposure to 5mM sodium selenite. Longer-term exposures lead to a progressive selenium-induced motility impairment that could be partially prevented by coincident exposure to the cellular antioxidant-reduced glutathione. The C elegans glrx-21 gene belongs to the family of glutaredoxins (glutathione-dependent oxidoreductases) and the glrx-21(tm2921) allele is a null mutation that renders animals hypersensitive for the selenium-induced motility impairment, but not lethality. In addition, the lethality of animals with the tm2921 mutation exposed to selenium was unaffected by the addition of reduced glutathione, suggesting that GLRX-21 is required for glutathione to moderate this selenium-induced lethality. Our findings provide the first description of selenium-induced toxicity in C elegans and support its use as a model for elucidating the mechanisms of selenium toxicity.
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