Evidence map›Paper›PMID 19363134›Full record

Trial reportAmerican journal of physiology. Heart and circulatory physiology2009

Superoxide-mediated inactivation of nitric oxide and peroxynitrite formation by tobacco smoke in vascular endothelium: studies in cultured cells and smokers.

Gonzalo Peluffo, Pablo Calcerrada, Lucia Piacenza, Nelson Pizzano, Rafael Radi

Open access · greenAbstract readClinical Trial
In one paragraph

Trial report in American journal of physiology. Heart and circulatory physiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.0field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 99 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Review
  5. Review
  6. Review
  7. Article
  8. Review
  9. Association between tobacco smoking and alcohol consumption with arterial stiffness.Journal of clinical hypertension (Greenwich, Conn.) · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Effects of Smoking on Diabetic Nephropathy.Frontiers in clinical diabetes and healthcare · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Review
  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 1 institution in 1 country.

Gonzalo PeluffoDepartmento de Bioquímica, Facultad de Medicina, Universidad de la República, 11800 Montevideo, Uruguay.
Pablo Calcerrada
Lucia Piacenza
Nelson Pizzano
Rafael Radi
Universidad de la República · UY

Funding

Howard Hughes Medical Institute
6 · The paper itself

Abstract

Tobacco smoke is known to cause nitric oxide ((*)NO) inactivation and endothelial dysfunction. In this work we evaluated the interplay between (.)NO and superoxide (O(2)(*-)) radicals and the consequent impact on (*)NO bioavailability and nitroxidative stress in bovine aortic endothelial cells exposed to cigarette smoke extract (CSE) and in smokers. Bovine aortic endothelial cells in the presence of CSE triggered O(2)(*-) production as indicated by spin-trapping electron paramagnetic resonance experiments. O(2)(*-) was produced both extracellulary (3.4 vs. 1.0 nmol.h(-1)*mg(-1); CSE vs. control; cytochrome c(3+) reduction assay) and intracellularly (40% inhibition of cytosolic aconitase). CSE also led to the production of peroxynitrite as evaluated by dihydrorhodamine oxidation and protein tyrosine nitration on cells. O(2)(*-) and peroxynitrite formation were decreased by ascorbate and alpha-tocopherol. Additionally, CSE led to the oxidation of endothelial nitric oxide synthase increasing the monomeric inactive form of endothelial nitric oxide synthase. Smokers and age-matched healthy volunteers were supplemented orally with 500 mg ascorbate plus 400 IU all-rac-alpha-tocopherol every 12 h for 165 days. Smokers had endothelial dysfunction compared with control subjects (95% confidence interval: 2.5, 8.3 vs. 10.6, 14.2; P < 0.05) as assessed by flow-mediated dilation of the brachial artery, and plasma levels of protein 3-nitrotyrosine were 1.4-fold higher. The loss of flow-mediated dilation in smokers reverted after a long-term antioxidant supplementation (95% confidence interval: 13.9, 19.9; P < 0.05), reaching values comparable with the control population. Our data indicate that elements on tobacco smoke, most likely through redox cycling, divert (*)NO toward peroxynitrite by inducing O(2)(*-) production in vascular endothelial cells both in vitro and in vivo.

Indexed as

Adultalpha-TocopherolAnimalsAntioxidantsAortaAscorbic AcidBrachial ArteryCattleCells, CulturedEndothelial CellsFemaleHumansMaleNitric OxideNitric Oxide Synthase Type IIIOxidative Stressalpha-TocopherolAntioxidantsAscorbic AcidNitric OxideNitric Oxide Synthase Type IIINOS3 protein, humanPeroxynitrous AcidSuperoxides

Identifiers

PMID19363134
PMCPMC2716106
OpenAlexW2111504812

What Socratic 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 Socratic graph.