Evidence map›Paper›PMID 23935510›Full record

ArticlePLoS genetics2013

Oxidative stress and replication-independent DNA breakage induced by arsenic in Saccharomyces cerevisiae.

Ireneusz Litwin, Tomasz Bocer, Dorota Dziadkowiec, Robert Wysocki

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
0.9field-weighted citation impact, top 26% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

19 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
  2. Review
  3. Update of the risk assessment of inorganic arsenic in food.EFSA journal. European Food Safety Authority · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Molecular insight of arsenic-induced carcinogenesis and its prevention.Naunyn-Schmiedeberg's archives of pharmacology · 2017
    Review
  15. Article
  16. Article
  17. Review
  18. Article
  19. A Comet Assay for DNA Damage and Repair After Exposure to Carbon-Ion Beams or X-rays inDose-response : a publication of International Hormesis Society
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Ireneusz LitwinInstitute of Experimental Biology, University of Wroclaw, Wroclaw, Poland.
Tomasz Bocer
Dorota Dziadkowiec
Robert Wysocki
University of Wrocław · PLRzeszów University · PL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Arsenic is a well-established human carcinogen of poorly understood mechanism of genotoxicity. It is generally accepted that arsenic acts indirectly by generating oxidative DNA damage that can be converted to replication-dependent DNA double-strand breaks (DSBs), as well as by interfering with DNA repair pathways and DNA methylation. Here we show that in budding yeast arsenic also causes replication and transcription-independent DSBs in all phases of the cell cycle, suggesting a direct genotoxic mode of arsenic action. This is accompanied by DNA damage checkpoint activation resulting in cell cycle delays in S and G2/M phases in wild type cells. In G1 phase, arsenic activates DNA damage response only in the absence of the Yku70-Yku80 complex which normally binds to DNA ends and inhibits resection of DSBs. This strongly indicates that DSBs are produced by arsenic in G1 but DNA ends are protected by Yku70-Yku80 and thus invisible for the checkpoint response. Arsenic-induced DSBs are processed by homologous recombination (HR), as shown by Rfa1 and Rad52 nuclear foci formation and requirement of HR proteins for cell survival during arsenic exposure. We show further that arsenic greatly sensitizes yeast to phleomycin as simultaneous treatment results in profound accumulation of DSBs. Importantly, we observed a similar response in fission yeast Schizosaccharomyces pombe, suggesting that the mechanisms of As(III) genotoxicity may be conserved in other organisms.

Indexed as

Oxidative StressArsenicCell Cycle CheckpointsDNA-Binding ProteinsDNA Breaks, Double-StrandedDNA MethylationDNA RepairDNA ReplicationEvolution, MolecularHomologous RecombinationHumansRad52 DNA Repair and Recombination ProteinReplication Protein ASaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSchizosaccharomycesArsenicDNA-Binding ProteinsRad52 DNA Repair and Recombination ProteinRAD52 protein, S cerevisiaeReplication Protein ARFA1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsYKU70 protein, S cerevisiaeYKU80 protein, S cerevisiae

Identifiers

PMID23935510
PMCPMC3723488
OpenAlexW2073271772

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.