Evidence map›Paper›PMID 18839291›Full record

ReviewJournal of bioenergetics and biomembranes2008

The inhibition of mitochondrial cytochrome oxidase by the gases carbon monoxide, nitric oxide, hydrogen cyanide and hydrogen sulfide: chemical mechanism and physiological significance.

Chris E Cooper, Guy C Brown

Abstract readReview
PubMed Publisher
In one paragraph

Review in Journal of bioenergetics and biomembranes, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 284 papers.

0numbers the graph read from it
0cells of the map it votes in
284citing papers in PubMed
13.2field-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

284 citing papers in PubMed, 712 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. Intracellular Crosstalk of the Gasotransmitter Trio (NO, CO, HInternational journal of molecular sciences · 2026
    Review
  8. Review
  9. Article
  10. Article
  11. Review
  12. The Chronic Elevated Consumption ofInternational journal of molecular sciences · 2026
    Article
  13. Article
  14. Article
  15. Article
  16. Cysteine Signalling in Plant Pathogen Response.Plant, cell & environment · 2025
    Article
  17. The role of gasotransmitters in Parkinson's disease: Interplay of nitric oxide, carbon monoxide, and hydrogen sulfide.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  18. Article
  19. Cyanide overproduction impairs cellular bioenergetics in Down syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  20. Redirecting Intermediary Metabolism to Counteract Cyanide Poisoning.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Review

224 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

2 authors at 2 institutions in 1 country.

Chris E CooperDepartment of Biological Sciences, University of Essex, Colchester, UK. ccooper@essex.ac.uk
Guy C Brown
University of Cambridge · GBUniversity of Essex · GB

Funding

Biotechnology and Biological Sciences Research Council BB/D017858/1
6 · The paper itself

Abstract

The four gases, nitric oxide (NO), carbon monoxide (CO), hydrogen sulfide (H(2)S) and hydrogen cyanide (HCN) all readily inhibit oxygen consumption by mitochondrial cytochrome oxidase. This inhibition is responsible for much of their toxicity when they are applied externally to the body. However, recently these gases have all been implicated, to greater or lesser extents, in normal cellular signalling events. In this review we analyse the chemistry of this inhibition, comparing and contrasting mechanism and discussing physiological consequences. The inhibition by NO and CO is dependent on oxygen concentration, but that of HCN and H(2)S is not. NO and H(2)S are readily metabolised by oxidative processes within cytochrome oxidase. In these cases the enzyme may act as a physiological detoxifier of these gases. CO oxidation is much slower and unlikely to be as physiologically important. The evidence for normal physiological levels of these gases interacting with cytochrome oxidase is equivocal, in part because there is little robust data about their steady state concentrations. A reasonable case can be made for NO, and perhaps CO and H(2)S, inhibiting cytochrome oxidase in vivo, but endogenous levels of HCN seem unlikely to be high enough.

Indexed as

AnimalsCarbon MonoxideElectron Transport Complex IVEnzyme InhibitorsGasesHumansHydrogen CyanideHydrogen SulfideHypoxiaMitochondriaModels, BiologicalNitric OxideSignal TransductionCarbon MonoxideElectron Transport Complex IVEnzyme InhibitorsGasesHydrogen CyanideHydrogen SulfideNitric Oxide

Identifiers

PMID18839291
OpenAlexW2049220790

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.