Evidence map›Paper›PMID 26136689›Full record

ArticleFrontiers in physiology2015

The basic chemistry of exercise-induced DNA oxidation: oxidative damage, redox signaling, and their interplay.

James N Cobley, Nikos V Margaritelis, James P Morton, Graeme L Close, Michalis G Nikolaidis, John K Malone

Open access · goldAbstract read
In one paragraph

Article in Frontiers in physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 3 pooled it
2.0field-weighted citation impact, top 14% 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

20 citing papers in PubMed, 3 syntheses or guidelines pooled it, 43 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. Article
  5. Proteoforms as the true units of physiological function.European journal of applied physiology · 2026
    Review
  6. Review
  7. Ten "Cheat Codes" for Measuring Oxidative Stress in Humans.Antioxidants (Basel, Switzerland) · 2024
    Review
  8. Article
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  13. Article
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  19. Pathophysiology of bronchoconstriction: role of oxidatively damaged DNA repair.Current opinion in allergy and clinical immunology · 2016
    Review
  20. Review
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

6 authors at 3 institutions in 2 countries.

James N CobleyDivision of Sport and Exercise Sciences, Abertay University Dundee, UK.
Nikos V MargaritelisExercise Physiology and Biochemistry Laboratory, School of Physical Education and Sport Sciences at Serres, Aristotle University of Thessaloniki Serres, Greece.
James P MortonMuscle Metabolism Research Group, Research Institute for Sport and Exercise Science, Liverpool John Moores University Liverpool, UK.
Graeme L CloseMuscle Metabolism Research Group, Research Institute for Sport and Exercise Science, Liverpool John Moores University Liverpool, UK.
Michalis G NikolaidisExercise Physiology and Biochemistry Laboratory, School of Physical Education and Sport Sciences at Serres, Aristotle University of Thessaloniki Serres, Greece.
John K MaloneDivision of Sport and Exercise Sciences, Abertay University Dundee, UK.
Abertay University · GBAristotle University of Thessaloniki · GRLiverpool John Moores University · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acute exercise increases reactive oxygen and nitrogen species generation. This phenomenon is associated with two major outcomes: (1) redox signaling and (2) macromolecule damage. Mechanistic knowledge of how exercise-induced redox signaling and macromolecule damage are interlinked is limited. This review focuses on the interplay between exercise-induced redox signaling and DNA damage, using hydroxyl radical ((·)OH) and hydrogen peroxide (H2O2) as exemplars. It is postulated that the biological fate of H2O2 links the two processes and thus represents a bifurcation point between redox signaling and damage. Indeed, H2O2 can participate in two electron signaling reactions but its diffusion and chemical properties permit DNA oxidation following reaction with transition metals and (·)OH generation. It is also considered that the sensing of DNA oxidation by repair proteins constitutes a non-canonical redox signaling mechanism. Further layers of interaction are provided by the redox regulation of DNA repair proteins and their capacity to modulate intracellular H2O2 levels. Overall, exercise-induced redox signaling and DNA damage may be interlinked to a greater extent than was previously thought but this requires further investigation.

Indexed as

DNA damageexercisehydrogen peroxidehydroxyl radicalmitochondrial DNA damageredox signaling

Identifiers

PMID26136689
PMCPMC4469819
OpenAlexW1588923203

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.