Evidence map›Paper›PMID 18496816›Full record

ArticleMolecular nutrition & food research2008

Analysis of Saccharomyces cerevisiae null allele strains identifies a larger role for DNA damage versus oxidative stress pathways in growth inhibition by selenium.

Eden Seitomer, Bharvi Balar, Dongming He, Paul R Copeland, Terri Goss Kinzy

Abstract read
In one paragraph

Article in Molecular nutrition & food research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

11 citing papers in PubMed, 29 citations in OpenAlex.

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  10. Review
  11. The glutaredoxin GLRX-21 functions to prevent selenium-induced oxidative stress in Caenorhabditis elegans.Toxicological sciences : an official journal of the Society of Toxicology · 2010
    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

5 authors at 1 institution in 1 country.

Eden SeitomerDepartment of Molecular Genetics, Microbiology and Immunology, UMDNJ Robert Wood Johnson Medical School, NJ 08854-5635, USA.
Bharvi Balar
Dongming He
Paul R Copeland
Terri Goss Kinzy
Rutgers, The State University of New Jersey · US

Funding

Development of selenomethionine resistant yeastR21GM074180 · NIGMS · UNIV OF MED/DENT NJ-R W JOHNSON MED SCH · PI KINZY, TERRI GOSS · 2006 to 2007
$421k
NIGMS NIH HHS GM074180NIGMS NIH HHS R21 GM074180
6 · The paper itself

Abstract

Selenium toxicity is a growing environmental concern due to widespread availability of high-dose selenium supplements and the development of high-selenium agricultural drainage basins. To begin to analyze the effects of selenium toxicity at the genetic level, we have systematically determined which genes are involved in responding to high environmental selenium using a collection of viable haploid null allele strains of Saccharomyces cerevisiae representing three major stress pathways: the RAD9-dependent DNA repair pathway, the RAD6/RAD18 DNA damage tolerance pathway, and the oxidative stress pathway. A total of 53 null allele strains were tested for growth defects in the presence of a range of sodium selenite and selenomethionine (SeMet) concentrations. Our results show that approximately 64-72% of the strains lacking RAD9-dependent DNA repair or RAD6/RAD18 DNA damage tolerance pathway genes show reduced growth in sodium selenite versus approximately 28-36% in SeMet. Interestingly both compounds reduced growth in approximately 21-25% of the strains lacking oxidative stress genes. These data suggest that both selenite and SeMet are likely inducing DNA damage by generating reactive species. The anticipated effects of loss of components of the oxidative stress pathway were not observed, likely due to apparent redundancies in these gene products that may keep the damaging effects in check.

Indexed as

DNA DamageCell DivisionDNA, FungalDNA RepairGene DeletionHumansOxidative StressRadiation ToleranceSaccharomyces cerevisiaeSeleniumSodium SeleniteSpecies SpecificityDNA, FungalSeleniumSodium Selenite

Identifiers

PMID18496816
PMCPMC2650619
OpenAlexW1997267097

What OpenQuestion holds

Textmetadata
LicenceTDM
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.