ArticlePloS one2012
Sodium selenide toxicity is mediated by O2-dependent DNA breaks.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 64 citations in OpenAlex.
- Harnessing Methylselenol (CHAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Selenite Interacting with Thiols Catalytically Releases NO from GSNO, Cleaves Plasmid DNA and Reduces the Hypotensive Effect of GSNO in Rats.Biological trace element research · 2026Article
- The oxidative cost of losing low temperature viability protein 1 [Ltv1]: insights into cellular damage and homeostasis.FEMS yeast research · 2026Article
- Metabolic changes in Phycomyces blakesleeanus mycelia during selenite reduction and cellular localization of synthesized SeNPs.World journal of microbiology & biotechnology · 2025Article
- Products of Selenite/Thiols Interaction Have Reducing Properties, Cleave Plasmid DNA and Decrease Rat Blood Pressure and Tension of Rat Mesenteric Artery.Biological trace element research · 2025Article
- Assessing the Impacts of Different Levels of Nano-Selenium on Growth Performance, Serum Metabolites, and Gene Expression in Heat-Stressed Growing Quails.Veterinary sciences · 2024Article
- Review
- Pharmaceutical and Safety Profile Evaluation of Novel Selenocompounds with Noteworthy Anticancer Activity.Pharmaceutics · 2022Article
- A Systematic Survey of Characteristic Features of Yeast Cell Death Triggered by External Factors.Journal of fungi (Basel, Switzerland) · 2021Review
- Investigation of RNA metabolism through large-scale genetic interaction profiling in yeast.Nucleic acids research · 2021Article
- Utilization of redox modulating small molecules that selectively act as pro-oxidants in cancer cells to open a therapeutic window for improving cancer therapy.Redox biology · 2021Review
- Exposure to the Methylselenol Precursor Dimethyldiselenide Induces a Reductive Endoplasmic Reticulum Stress inInternational journal of molecular sciences · 2021Article
- Methylselenol Produced In Vivo from Methylseleninic Acid or Dimethyl Diselenide Induces Toxic Protein Aggregation inInternational journal of molecular sciences · 2021Article
- Therapeutic Potential of Selenium in Glioblastoma.Frontiers in neuroscience · 2021Review
- Review
- Metabolic Response of the YeastInternational journal of molecular sciences · 2020Article
- Understanding the Redox Biology of Selenium in the Search of Targeted Cancer Therapies.Antioxidants (Basel, Switzerland) · 2020Review
- Effect of selenium on growth and antioxidative system of yeast cells.Molecular biology reports · 2019Article
- Editor's Highlight: A Genome-wide Screening of Target Genes Against Silver Nanoparticles in Fission Yeast.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Exposure to selenomethionine causes selenocysteine misincorporation and protein aggregation in Saccharomyces cerevisiae.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hydrogen selenide is a recurrent metabolite of selenium compounds. However, few experiments studied the direct link between this toxic agent and cell death. To address this question, we first screened a systematic collection of Saccharomyces cerevisiae haploid knockout strains for sensitivity to sodium selenide, a donor for hydrogen selenide (H(2)Se/HSe(-/)Se(2-)). Among the genes whose deletion caused hypersensitivity, homologous recombination and DNA damage checkpoint genes were over-represented, suggesting that DNA double-strand breaks are a dominant cause of hydrogen selenide toxicity. Consistent with this hypothesis, treatment of S. cerevisiae cells with sodium selenide triggered G2/M checkpoint activation and induced in vivo chromosome fragmentation. In vitro, sodium selenide directly induced DNA phosphodiester-bond breaks via an O(2)-dependent reaction. The reaction was inhibited by mannitol, a hydroxyl radical quencher, but not by superoxide dismutase or catalase, strongly suggesting the involvement of hydroxyl radicals and ruling out participations of superoxide anions or hydrogen peroxide. The (•)OH signature could indeed be detected by electron spin resonance upon exposure of a solution of sodium selenide to O(2). Finally we showed that, in vivo, toxicity strictly depended on the presence of O(2). Therefore, by combining genome-wide and biochemical approaches, we demonstrated that, in yeast cells, hydrogen selenide induces toxic DNA breaks through an O(2)-dependent radical-based mechanism.
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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.