Evidence map›Paper›PMID 22811713›Full record

ArticleInternational journal of cell biology2012

The Chemical Interplay between Nitric Oxide and Mitochondrial Cytochrome c Oxidase: Reactions, Effectors and Pathophysiology.

Paolo Sarti, Elena Forte, Alessandro Giuffrè, Daniela Mastronicola, Maria Chiara Magnifico, Marzia Arese

Open access · goldAbstract read
In one paragraph

Article in International journal of cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

  1. UBE2C-TRIM21-driven NOS2 degradation stabilizes Tregs and suppresses pyroptotic signaling in thyrocytes in Hashimoto's thyroiditis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Article
  3. Review
  4. Review
  5. Review
  6. Article
  7. Photobiomodulation and nitric oxide signaling.Nitric oxide : biology and chemistry · 2023
    Review
  8. Review
  9. Dual near-infrared II laser modulates the cellular redox state of T cells and augments the efficacy of cancer immunotherapy.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  10. Near-infrared II photobiomodulation augments nitric oxide bioavailability via phosphorylation of endothelial nitric oxide synthase.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2022
    Article
  11. Biological Mechanisms ofAntioxidants (Basel, Switzerland) · 2021
    Review
  12. Bacterial Oxidases of the CytochromeAntioxidants & redox signaling · 2021
    Review
  13. Article
  14. Plant Nitric Oxide Signaling under Drought Stress.Plants (Basel, Switzerland) · 2021
    Review
  15. Nitric Oxide Does Not Inhibit but Is Metabolized by the CytochromeInternational journal of molecular sciences · 2020
    Article
  16. Review
  17. Article
  18. Review
  19. AMPK, Mitochondrial Function, and Cardiovascular Disease.International journal of molecular sciences · 2020
    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 1 country.

Paolo SartiDepartment of Biochemical Sciences and Istituto Pasteur-Fondazione Cenci Bolognetti, Sapienza University of Rome, Piazzale Aldo Moro 5, 00185 Rome, Italy.
Elena Forte
Alessandro Giuffrè
Daniela Mastronicola
Maria Chiara Magnifico
Marzia Arese
Sapienza University of Rome · ITInstitute of Molecular Biology and Pathology · ITIstituto Pasteur · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Nitric oxide (NO) reacts with Complex I and cytochrome c oxidase (CcOX, Complex IV), inducing detrimental or cytoprotective effects. Two alternative reaction pathways (PWs) have been described whereby NO reacts with CcOX, producing either a relatively labile nitrite-bound derivative (CcOX-NO(2) (-), PW1) or a more stable nitrosyl-derivative (CcOX-NO, PW2). The two derivatives are both inhibited, displaying different persistency and O(2) competitiveness. In the mitochondrion, during turnover with O(2), one pathway prevails over the other one depending on NO, cytochrome c(2+) and O(2) concentration. High cytochrome c(2+), and low O(2) proved to be crucial in favoring CcOX nitrosylation, whereas under-standard cell-culture conditions formation of the nitrite derivative prevails. All together, these findings suggest that NO can modulate physiologically the mitochondrial respiratory/OXPHOS efficiency, eventually being converted to nitrite by CcOX, without cell detrimental effects. It is worthy to point out that nitrite, far from being a simple oxidation byproduct, represents a source of NO particularly important in view of the NO cell homeostasis, the NO production depends on the NO synthases whose activity is controlled by different stimuli/effectors; relevant to its bioavailability, NO is also produced by recycling cell/body nitrite. Bioenergetic parameters, such as mitochondrial ΔΨ, lactate, and ATP production, have been assayed in several cell lines, in the presence of endogenous or exogenous NO and the evidence collected suggests a crucial interplay between CcOX and NO with important energetic implications.

Identifiers

PMID22811713
PMCPMC3395247
OpenAlexW2166291947

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.