Evidence map›Paper›PMID 19902015›Full record

ArticleJournal of clinical biochemistry and nutrition2009

Sources of extracellular, oxidatively-modified DNA lesions: implications for their measurement in urine.

Marcus S Cooke, Paul T Henderson, Mark D Evans

Open access · bronzeAbstract read
In one paragraph

Article in Journal of clinical biochemistry and nutrition, 2009. 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
3.2field-weighted citation impact, top 7% 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, 49 citations in OpenAlex.

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  4. Short-duration hyperoxia causes genotoxicity in mouse lungs: protection by volatile anesthetic isoflurane.American journal of physiology. Lung cellular and molecular physiology · 2019
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  19. A novel method for efficient collection of normal mesothelial cells in vivo.Journal of clinical biochemistry and nutrition · 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

3 authors at 2 institutions in 2 countries.

Marcus S CookeRadiation and Oxidative Stress Section, Department of Cancer Studies and Molecular Medicine, Robert Kilpatrick Clinical Sciences Bilding, University of Leicester, LE2 7LX, UK.
Paul T Henderson
Mark D Evans
University of Leicester · GBUniversity of California Davis Medical Center · US

Funding

Staff InvestigatorsP30CA093373 · NCI · UNIVERSITY OF CALIFORNIA DAVIS · PI Gina M Dayton · 2002 to 2026
$84.9M
VITAMIN C (ASCORBATE) METABOLISM IN DROSPHILA MELANOGASTERP41RR013461 · NCRR · UNIVERSITY OF CALIF-LAWRNC LVRMR NAT LAB · PI HASKELL, MARJORIE J · 1999 to 2011
$20.8M
NCI NIH HHS P30 CA093373NCRR NIH HHS P41 RR013461
6 · The paper itself

Abstract

There is a robust mechanistic basis for the role of oxidation damage to DNA in the aetiology of various major diseases (cardiovascular, neurodegenerative, cancer). Robust, validated biomarkers are needed to measure oxidative damage in the context of molecular epidemiology, to clarify risks associated with oxidative stress, to improve our understanding of its role in health and disease and to test intervention strategies to ameliorate it. Of the urinary biomarkers for DNA oxidation, 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) is the most studied. However, there are a number of factors which hamper our complete understanding of what meausrement of this lesion in urine actually represents. DNA repair is thought to be a major contributor to urinary 8-oxodG levels, although the precise pathway(s) has not been proven, plus possible contribution from cell turnover and diet are possible confounders. Most recently, evidence has arisen which suggests that nucleotide salvage of 8-oxodG and 8-oxoGua can contribute substantially to 8-oxoG levels in DNA and RNA, at least in rapidly dividing cells. This new observation may add an further confounder to the conclusion that 8-oxoGua or 8-oxodG, and its nucleobase equivalent 8-oxoguanine, concentrations in urine are simply a consequence of DNA repair. Further studies are required to define the relative contributions of metabolism, disease and diet to oxidised nucleic acids and their metabolites in urine in order to develop urinalyis as a better tool for understanding human disease.

Indexed as

cell deathDNA damageDNA repairoxidative stressurine

Identifiers

PMID19902015
PMCPMC2771246
OpenAlexW2246970578

What OpenQuestion holds

Textmetadata
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.