Evidence map›Paper›PMID 24068103›Full record

ArticleNaunyn-Schmiedeberg's archives of pharmacology2014

Hydrogen sulfide protects endothelial nitric oxide function under conditions of acute oxidative stress in vitro.

Mohammad R Al-Magableh, Barbara K Kemp-Harper, Hooi H Ng, Alyson A Miller, Joanne L Hart

Abstract read
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In one paragraph

Article in Naunyn-Schmiedeberg's archives of pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

26 citing papers in PubMed, 59 citations in OpenAlex.

  1. Review
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  3. Review
  4. Article
  5. The Pathophysiology of HBiomolecules · 2022
    Review
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  7. Review
  8. Article
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  10. Article
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  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Hydrogen Sulfide and Cellular Redox Homeostasis.Oxidative medicine and cellular longevity · 2016
    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

5 authors at 3 institutions in 1 country.

Mohammad R Al-MagablehDepartment of Pharmacology, Monash University, Clayton, Victoria, 3800, Australia.
Barbara K Kemp-Harper
Hooi H Ng
Alyson A Miller
Joanne L Hart
Australian Regenerative Medicine Institute · AURMIT University · AUMonash University · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of this study was to examine the ability of H2S, released from NaHS to protect vascular endothelial function under conditions of acute oxidative stress by scavenging superoxide anions (O2(-)) and suppressing vascular superoxide anion production. O2(-) was generated in Krebs' solution by reacting hypoxanthine with xanthine oxidase (Hx-XO) or with the O2(-) generator pyrogallol to model acute oxidative stress in vitro. O2(-) generation was measured by lucigenin-enhanced chemiluminescence. Functional responses in mouse aortic rings were assessed using a small vessel myograph. NaHS scavenged O2(-) in a concentration-dependent manner. Isolated aortic rings exposed to either Hx-XO or pyrogallol displayed significantly attenuated maximum vasorelaxation responses to the endothelium-dependent vasodilator acetylcholine, and significantly reduced NO bioavailability, which was completely reversed if vessels were pre-incubated with NaHS (100 μM). NADPH-stimulated aortic O2(-) production was significantly attenuated by the NADPH oxidase inhibitor diphenyl iodonium. Prior treatment of vessels with NaHS (100 nM-100 μM; 30 min) inhibited NADPH-stimulated aortic O2(-) production in a concentration-dependent manner. This effect persisted when NaHS was washed out prior to measuring NADPH-stimulated O2(-) production. These data show for the first time that NaHS directly scavenges O2(-) and suppresses vascular NADPH oxidase-derived O2(-) production in vitro. Furthermore, these properties protect endothelial function and NO bioavailability in an in vitro model of acute oxidative stress. These results suggest that H2S can elicit vasoprotection by both scavenging O2(-) and by reducing vascular NADPH oxidase-derived O2(-) production.

Indexed as

AnimalsAortaDose-Response Relationship, DrugEndothelium, VascularHydrogen SulfideMaleMiceMice, Inbred C57BLNitric Oxide Synthase Type IIIOrgan Culture TechniquesOxidative StressVasodilationHydrogen SulfideNitric Oxide Synthase Type IIINos3 protein, mouse

Identifiers

PMID24068103
OpenAlexW1970735189

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.