Evidence map›Paper›PMID 19376220›Full record

ArticleFree radical biology & medicine2009

Oxidative stress-induced changes in pyridine nucleotides and chemoattractant 5-lipoxygenase products in aging neutrophils.

François D Graham, Karl-Rudolf Erlemann, Sylvie Gravel, Joshua Rokach, William S Powell

Open access · greenAbstract read
In one paragraph

Article in Free radical biology & medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 37 citations in OpenAlex.

  1. Trial
  2. Review
  3. Article
  4. Gram-Negative BacteriaFrontiers in pharmacology · 2021
    Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Uroporphyria in the Cyp1a2-/- mouse.Blood cells, molecules & diseases · 2011
    Article
  15. Article
  16. 5-Oxo-ETE and the OXE receptor.Prostaglandins & other lipid mediators · 2009
    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

5 authors at 3 institutions in 2 countries.

François D GrahamMeakins-Christie Laboratories, McGill University, Montreal, QC, Canada.
Karl-Rudolf Erlemann
Sylvie Gravel
Joshua Rokach
William S Powell
Christie (Canada) · CAFlorida Institute of Technology · USMcGill University · CA

Funding

Biochemical Pathways of 12-HETE and 12-KETE MetabolismR01HL081873 · NHLBI · FLORIDA INSTITUTE OF TECHNOLOGY · PI ROKACH, JOSHUA · 2005 to 2010
$2.1M
NHLBI NIH HHS HL81873NHLBI NIH HHS R01 HL081873
6 · The paper itself

Abstract

Neutrophils spontaneously undergo apoptosis, which is associated with increased oxidative stress. We found that there is a dramatic shift in the formation of 5-lipoxygenase products during this process. Freshly isolated neutrophils rapidly convert leukotriene B(4) (LTB(4)) and 5-hydroxy-6,8,11,14-eicosatetraenoic acid (5-HETE) to their biologically inactive omega-oxidation products. However, omega-oxidation is impaired in neutrophils cultured for 24 h, when only 25% of the cells are nonapoptotic, resulting in the persistence of LTB(4) and a dramatic shift in 5-HETE metabolism to the potent granulocyte chemoattractant 5-oxo-6,8,11,14-eicosatetraenoic acid (5-oxo-ETE). The reduced omega-oxidation activity seems to be due to a reduction in LTB(4) 20-hydroxylase activity, whereas the increased 5-oxo-ETE formation is caused by a dramatic increase in the 5-hydroxyeicosanoid dehydrogenase cofactor NADP(+). NAD(+), but not NADPH, also increased, as did the GSSG/GSH ratio, indicative of oxidative stress. The changes in 5-HETE metabolism and pyridine nucleotides were inhibited by antiapoptotic agents (GM-CSF, forskolin) and antioxidants (diphenylene iodonium, catalase, deferoxamine), suggesting the involvement of H(2)O(2) and possibly other reactive oxygen species. These results suggest that in severe inflammation, aging neutrophils that have evaded rapid uptake by macrophages may produce increased amounts of the chemoattractants 5-oxo-ETE and LTB(4), resulting in delayed resolution or exacerbation of the inflammatory process.

Indexed as

Alcohol OxidoreductasesAntioxidantsApoptosisArachidonate 5-LipoxygenaseArachidonic AcidsBiomimeticsCells, CulturedCellular SenescenceChemotactic FactorsColforsinCytochrome P-450 Enzyme SystemCytochrome P450 Family 4HumansHydroxyeicosatetraenoic AcidsLeukotriene B4NADP5-hydroxy-6,8,11,14-eicosatetraenoic acid5-hydroxyeicosanoid dehydrogenase5-oxo-6,8,11,14-eicosatetraenoic acidAlcohol OxidoreductasesAntioxidantsArachidonate 5-LipoxygenaseArachidonic AcidsChemotactic FactorsColforsinCytochrome P-450 Enzyme SystemCytochrome P450 Family 4Hydroxyeicosatetraenoic AcidsLeukotriene B4leukotriene B4 20-hydroxylaseNADPpyridinePyridinesSuperoxide Dismutase

Identifiers

PMID19376220
PMCPMC2891157
OpenAlexW2000982325

What OpenQuestion holds

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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.