Evidence map›Paper›PMID 20869434›Full record

ArticleFree radical biology & medicine2010

Mitochondrial peroxiredoxins are critical for the maintenance of redox state and the survival of adult Drosophila.

Svetlana N Radyuk, Igor Rebrin, Vladimir I Klichko, Barbara H Sohal, Katarzyna Michalak, Judith Benes, Rajindar S Sohal, William C Orr

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
1.4field-weighted citation impact, top 21% 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

30 citing papers in PubMed, 50 citations in OpenAlex.

  1. Heat stress drives opposing redox shifts in temperate versus tropicalbioRxiv : the preprint server for biology · 2026
    Article
  2. Article
  3. Article
  4. Review
  5. Article
  6. Redox regulation in lifespan determination.The Journal of biological chemistry · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Article
  11. Hyperoxidation of Peroxiredoxins and Effects on Physiology ofAntioxidants (Basel, Switzerland) · 2021
    Article
  12. Article
  13. Redox signalling and ageing: insights from Drosophila.Biochemical Society transactions · 2020
    Review
  14. Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Svetlana N RadyukDepartment of Biological Sciences, Southern Methodist University, Dallas, TX 75275, USA.
Igor Rebrin
Vladimir I Klichko
Barbara H Sohal
Katarzyna Michalak
Judith Benes
Rajindar S Sohal
William C Orr
Southern Methodist University · USUniversity of Southern California · US

Funding

GLUTATHIONE, OXIDATIVE STRESS, AND AGINGR01AG015122 · NIA · SOUTHERN METHODIST UNIVERSITY · PI ORR, WILLIAM C. · 1998 to 2010
$3.0M
NIA NIH HHS R01 AG015122NIA NIH HHS R01 AG15122
6 · The paper itself

Abstract

Drosophila mitochondria contain two peroxidases, peroxiredoxin 3 (dPrx3) and peroxiredoxin 5 (dPrx5), which together constitute the sole known intramitochondrial mechanism for the catalytic removal of hydrogen and organic peroxides. dPrx3 exists exclusively within mitochondria, whereas dPrx5 is also present in some other intracellular compartments. Levels of these two peroxiredoxins were genetically manipulated, singly and together, in D. melanogaster, for the purpose of understanding their respective functions. Underexpression of dPrx3 by 90-95% had no discernable effect on life span under normal or oxidative stress conditions; the dPrx5 null flies were previously reported to exhibit a 10% shortening of mean life span and an increase in sensitivity to oxidative stress. Flies underexpressing both dPrx3 and dPrx5 showed an 80% decrease in life span, a severe disruption in thiol homeostasis, and a massive induction of apoptosis in the muscle and digestive system tissues. The early mortality in flies underexpressing both peroxiredoxins was partially offset by overexpression of thioredoxin reductase but not mitochondrion-targeted catalase. These results suggest that mitochondrial peroxiredoxins confer specific protection for thioredoxin/glutathione systems, play a critical role in the maintenance of global thiol homeostasis, and prevent the age-associated apoptosis and premature death.

Indexed as

AnimalsApoptosisCatalaseDown-RegulationDrosophila melanogasterDrosophila ProteinsGlutathioneGlutathione DisulfideMitochondrial ProteinsOxidation-ReductionOxidative StressPeroxiredoxinsSulfhydryl CompoundsThioredoxin-Disulfide ReductaseCatalaseDrosophila ProteinsGlutathioneGlutathione DisulfideMitochondrial ProteinsPeroxiredoxinsSulfhydryl CompoundsThioredoxin-Disulfide Reductase

Identifiers

PMID20869434
PMCPMC3005798
OpenAlexW2039208764

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.