Evidence map›Paper›PMID 30844486›Full record

ArticleBiochimica et biophysica acta. General subjects2019

Long chain lipid hydroperoxides increase the glutathione redox potential through glutathione peroxidase 4.

Elizabeth M Corteselli, Eugene Gibbs-Flournoy, Steven O Simmons, Philip Bromberg, Avram Gold, James M Samet

Open access · greenAbstract read
In one paragraph

Article in Biochimica et biophysica acta. General subjects, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.2field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
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  8. Review
  9. Individual and Joint Effect ofAntioxidants (Basel, Switzerland) · 2022
    Article
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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

6 authors at 3 institutions in 1 country.

Elizabeth M CorteselliDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
Eugene Gibbs-FlournoyOak Ridge Institute for Science and Education, Oak Ridge, TN, USA.
Steven O SimmonsNational Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.
Philip BrombergCenter for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina, Chapel Hill, NC, USA.
Avram GoldDepartment of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.
James M SametEnvironmental Public Health Division, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill, NC, USA. Electronic address: samet.james@epa.gov.
Environmental Protection Agency · USUniversity of North Carolina at Chapel Hill · USOak Ridge Associated Universities · US

Funding

UNC-CH CENTER FOR ENVIRONMENTAL HEALTH &SUSCEPTIBILITYP30ES010126 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI Stephanie Engel · 2001 to 2026
$36.3M
Polyunsaturated Fatty Acids as Determinants of Redox Changes and Inflammatory Responses in Human Airway Epithelial Cells Exposed to OzoneF31ES029020 · NIEHS · UNIV OF NORTH CAROLINA CHAPEL HILL · PI CORTESELLI, ELIZABETH MARIE · 2018 to 2019
$82k
Intramural EPA EPA999999NIEHS NIH HHS F31 ES029020NIEHS NIH HHS P30 ES010126
6 · The paper itself

Abstract

backgroundPeroxidation of PUFAs by a variety of endogenous and xenobiotic electrophiles is a recognized pathophysiological process that can lead to adverse health effects. Although secondary products generated from peroxidized PUFAs have been relatively well studied, the role of primary lipid hydroperoxides in mediating early intracellular oxidative events is not well understood.

methodsLive cell imaging was used to monitor changes in glutathione (GSH) oxidation in HAEC expressing the fluorogenic sensor roGFP during exposure to 9-hydroperoxy-10E,12Z-octadecadienoic acid (9-HpODE), a biologically important long chain lipid hydroperoxide, and its secondary product 9-hydroxy-10E,12Z-octadecadienoic acid (9-HODE). The role of hydrogen peroxide (H

resultsExposure to 9-HpODE caused a dose-dependent increase in GSH oxidation in HAEC that was independent of intracellular or extracellular H

conclusionsLong chain lipid hydroperoxides can directly alter cytosolic E SIGNIFICANCE: These results reveal a previously unrecognized consequence of lipid peroxidation, which may provide insight into disease states involving lipid peroxidation in their pathogenesis.

Indexed as

Cells, CulturedDose-Response Relationship, DrugGlutathioneGlutathione PeroxidaseHumansHydrogen PeroxideLinoleic AcidsLinoleic Acids, ConjugatedOxidation-ReductionPhospholipid Hydroperoxide Glutathione Peroxidase9-hydroperoxy-11,12-octadecadienoic acid9-hydroxy-10,12-octadecadienoic acidGlutathioneGlutathione PeroxidaseHydrogen PeroxideLinoleic AcidsLinoleic Acids, ConjugatedPhospholipid Hydroperoxide Glutathione PeroxidaseGlutathioneGlutathione peroxidase 4HydroperoxideLipid peroxidation

Identifiers

PMID30844486
PMCPMC6823641
OpenAlexW2919712725

What OpenQuestion holds

Textmetadata
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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.