Evidence map›Paper›PMID 23583329›Full record

ArticleFree radical biology & medicine2013

Sites of superoxide and hydrogen peroxide production during fatty acid oxidation in rat skeletal muscle mitochondria.

Irina V Perevoshchikova, Casey L Quinlan, Adam L Orr, Akos A Gerencser, Martin D Brand

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.

0numbers the graph read from it
0cells of the map it votes in
59citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

59 citing papers in PubMed, 118 citations in OpenAlex.

  1. Review
  2. Rethinking Human Energy Metabolism.Current issues in molecular biology · 2026
    Review
  3. Review
  4. Review
  5. Review
  6. Review
  7. Review
  8. Article
  9. Review
  10. Article
  11. Article
  12. Review
  13. Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Review
  19. Article
  20. Redox Regulation of Lipid Mobilization in Adipose Tissues.Antioxidants (Basel, Switzerland) · 2021
    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

5 authors at 1 institution in 1 country.

Irina V PerevoshchikovaBuck Institute for Research on Aging, Novato, CA 94945, USA. Electronic address: irper@buckinstitute.org.
Casey L QuinlanBuck Institute for Research on Aging, Novato, CA 94945, USA.
Adam L OrrBuck Institute for Research on Aging, Novato, CA 94945, USA.
Akos A GerencserBuck Institute for Research on Aging, Novato, CA 94945, USA.
Martin D BrandBuck Institute for Research on Aging, Novato, CA 94945, USA.
Buck Institute for Research on Aging · US

Funding

Mitochondrial sites of reactive oxygen species generation in cells.R01AG033542 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI BRAND, MARTIN D · 2009 to 2010
$970k
Research Training and Education in GeroscienceTL1AG032116 · NIA · BUCK INSTITUTE FOR RESEARCH ON AGING · PI GREENBERG, DAVID ALAN · 2007 to 2011
$530k
NIA NIH HHS R01 AG033542NIA NIH HHS R01AG033542NIA NIH HHS TL1 AG032116NIA NIH HHS TL1AG032116
6 · The paper itself

Abstract

H2O2 production by skeletal muscle mitochondria oxidizing palmitoylcarnitine was examined under two conditions: the absence of respiratory chain inhibitors and the presence of myxothiazol to inhibit complex III. Without inhibitors, respiration and H2O2 production were low unless carnitine or malate was added to limit acetyl-CoA accumulation. With palmitoylcarnitine alone, H2O2 production was dominated by complex II (44% from site IIF in the forward reaction); the remainder was mostly from complex I (34%, superoxide from site IF). With added carnitine, H2O2 production was about equally shared between complexes I, II, and III. With added malate, it was 75% from complex III (superoxide from site IIIQo) and 25% from site IF. Thus complex II (site IIF in the forward reaction) is a major source of H2O2 production during oxidation of palmitoylcarnitine ± carnitine. Under the second condition (myxothiazol present to keep ubiquinone reduced), the rates of H2O2 production were highest in the presence of palmitoylcarnitine ± carnitine and were dominated by complex II (site IIF in the reverse reaction). About half the rest was from site IF, but a significant portion, ∼40pmol H2O2·min(-1)·mg protein(-1), was not from complex I, II, or III and was attributed to the proteins of β-oxidation (electron-transferring flavoprotein (ETF) and ETF-ubiquinone oxidoreductase). The maximum rate from the ETF system was ∼200pmol H2O2·min(-1)·mg protein(-1) under conditions of compromised antioxidant defense and reduced ubiquinone pool. Thus complex II and the ETF system both contribute to H2O2 productionduring fatty acid oxidation under appropriate conditions.

Indexed as

AnimalsElectron Transport Complex IIFatty AcidsFemaleHydrogen PeroxideMitochondria, MuscleMuscle, SkeletalOxidation-ReductionOxygen ConsumptionPalmitoylcarnitineRatsRats, WistarSuperoxidesElectron Transport Complex IIFatty AcidsHydrogen PeroxidePalmitoylcarnitineSuperoxidesComplex IComplex IIComplex IIIElectron-transferring flavoproteinElectron transferring flavoprotein–ubiquinone oxidoreductaseETFETFQORFree radicalsPalmitatePalmitoylcarnitineROSSuccinate dehydrogenase

Identifiers

PMID23583329
PMCPMC3871980
OpenAlexW2080474405

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.