Evidence map›Paper›PMID 18684987›Full record

ReviewAmerican journal of physiology. Cell physiology2008

Radical-free biology of oxidative stress.

Dean P Jones

Open access · greenAbstract readReview
In one paragraph

Review in American journal of physiology. Cell physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 524 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
524citing papers in PubMed, 2 pooled it
27.4field-weighted citation impact, top 1% 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

524 citing papers in PubMed, 2 syntheses or guidelines pooled it, 1,190 citations in OpenAlex.

  1. Pooled it
  2. A Review ofNutrients · 2019
    Pooled it
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Journal of microbiology and biotechnology · 2026
    Article
  10. Review
  11. Update: Is exercise-induced oxidative stress a friend or foe?Sports medicine and health science · 2026
    Review
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Cardiotoxicity induced by traditional chemotherapy: mechanisms and mitigation strategies.Apoptosis : an international journal on programmed cell death · 2026
    Review
  18. Review
  19. Article
  20. Review

464 more citing papers are in PubMed but not listed here.

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

1 author at 1 institution in 1 country.

Dean P JonesDivision of Pulmonary, Allergy and Critical Care Medicine, Clinical Biomarkers Laboratory, Department of Medicine, Emory University School of Medicine, Atlanta, Georgia 30322, USA. dpjones@emory.edu
Emory University · US

Funding

Thioredoxin-2 protection against mitochondrial oxidative toxicityR01ES009047 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 1998 to 2013
$3.9M
Nuclear and Cytoplasmic Redox in Oxidative StressR01ES011195 · NIEHS · EMORY UNIVERSITY · PI JONES, DEAN PAUL · 2001 to 2011
$3.3M
NIEHS NIH HHS ES-009047NIEHS NIH HHS ES-011195
6 · The paper itself

Abstract

Free radical-induced macromolecular damage has been studied extensively as a mechanism of oxidative stress, but large-scale intervention trials with free radical scavenging antioxidant supplements show little benefit in humans. The present review summarizes data supporting a complementary hypothesis for oxidative stress in disease that can occur without free radicals. This hypothesis, which is termed the "redox hypothesis," is that oxidative stress occurs as a consequence of disruption of thiol redox circuits, which normally function in cell signaling and physiological regulation. The redox states of thiol systems are sensitive to two-electron oxidants and controlled by the thioredoxins (Trx), glutathione (GSH), and cysteine (Cys). Trx and GSH systems are maintained under stable, but nonequilibrium conditions, due to a continuous oxidation of cell thiols at a rate of about 0.5% of the total thiol pool per minute. Redox-sensitive thiols are critical for signal transduction (e.g., H-Ras, PTP-1B), transcription factor binding to DNA (e.g., Nrf-2, nuclear factor-kappaB), receptor activation (e.g., alphaIIbbeta3 integrin in platelet activation), and other processes. Nonradical oxidants, including peroxides, aldehydes, quinones, and epoxides, are generated enzymatically from both endogenous and exogenous precursors and do not require free radicals as intermediates to oxidize or modify these thiols. Because of the nonequilibrium conditions in the thiol pathways, aberrant generation of nonradical oxidants at rates comparable to normal oxidation may be sufficient to disrupt function. Considerable opportunity exists to elucidate specific thiol control pathways and develop interventional strategies to restore normal redox control and protect against oxidative stress in aging and age-related disease.

Indexed as

Free RadicalsOxidantsOxidative StressFree RadicalsOxidants

Identifiers

PMID18684987
PMCPMC2575825
OpenAlexW2167424396

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.