Evidence map›Paper›PMID 18640266›Full record

ArticleFree radical biology & medicine2008

Decreased pulmonary extracellular superoxide dismutase during systemic inflammation.

Junji Ueda, Marlene E Starr, Hitoshi Takahashi, Jie Du, Ling Yi Chang, James D Crapo, B Mark Evers, Hiroshi Saito

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Divergent Sepsis Pathophysiology in Older Adults.Antioxidants & redox signaling · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  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

8 authors at 4 institutions in 1 country.

Junji UedaDepartment of Surgery, University of Texas Medical Branch, Galveston, TX 77555, USA.
Marlene E Starr
Hitoshi Takahashi
Jie Du
Ling Yi Chang
James D Crapo
B Mark Evers
Hiroshi Saito
The University of Texas Medical Branch at Galveston · USBaylor College of Medicine · USNational Jewish Health · USUniversity of Colorado Denver · US

Funding

Vulnerability to sepsis in old ageR01AG025908 · NIA · UNIVERSITY OF TEXAS MEDICAL BR GALVESTON · PI SAITO, HIROSHI · 2005 to 2009
$1.1M
NIA NIH HHS R01 AG025908NIA NIH HHS R01-AG025908
6 · The paper itself

Abstract

Oxidative damage is a major cause of lung injury during systemic inflammatory response syndrome. In this study, the expression of an antioxidant enzyme, extracellular superoxide dismutase (EC-SOD), and its protective role against pulmonary oxidative damage were investigated using mouse models of systemic inflammation. Intraperitoneal injection with bacterial endotoxin lipopolysaccharides (LPS; 20 mg/kg) caused oxidative damage in lungs as assessed by increased tyrosine nitration in proteins. LPS administration also resulted in a rapid and significant loss of more than 80% of pulmonary EC-SOD in a time- and dose-dependent manner, but other types of SODs, cytoplasmic CuZn-SOD and mitochondrial Mn-SOD, were not affected. EC-SOD protein is most abundant in lungs but also present at high levels in other tissues such as heart and white fat; however, the LPS-mediated decrease in this enzyme was most apparent in the lungs. Intravenous injection of mice with tumor necrosis factor alpha (10 microg per mouse) also caused a 60% decrease in EC-SOD in the lungs, suggesting that the EC-SOD down-regulation is mediated by this LPS-inducible inflammatory cytokine. A protective role for EC-SOD against LPS-mediated systemic inflammation was shown by an increased survival rate (75% vs 29% in 5 days) and decreased pulmonary oxidative damage in EC-SOD transgenic mice that overexpress the human EC-SOD gene. These results demonstrate that the inflammation-mediated EC-SOD down-regulation has a major pathophysiological impact during the systemic inflammatory response syndrome.

Indexed as

AnimalsBase SequenceBlotting, NorthernDNA PrimersDose-Response Relationship, DrugDown-RegulationExtracellular SpaceInflammationLipopolysaccharidesLungMiceMice, Inbred C57BLMice, TransgenicSuperoxide DismutaseTranscription, GeneticDNA PrimersLipopolysaccharidesSuperoxide Dismutase

Identifiers

PMID18640266
PMCPMC2953464
OpenAlexW2009248160

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.