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


Journal

Biochimica et biophysica acta. General subjects
ISSN: 1872-8006
Titre abrégé: Biochim Biophys Acta Gen Subj
Pays: Netherlands
ID NLM: 101731726

Informations de publication

Date de publication:
05 2019
Historique:
received: 04 09 2018
revised: 08 02 2019
accepted: 03 03 2019
pubmed: 8 3 2019
medline: 4 12 2019
entrez: 8 3 2019
Statut: ppublish

Résumé

Peroxidation 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. Live 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 Exposure to 9-HpODE caused a dose-dependent increase in GSH oxidation in HAEC that was independent of intracellular or extracellular H Long chain lipid hydroperoxides can directly alter cytosolic E These results reveal a previously unrecognized consequence of lipid peroxidation, which may provide insight into disease states involving lipid peroxidation in their pathogenesis.

Sections du résumé

BACKGROUND
Peroxidation 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.
METHODS
Live 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
RESULTS
Exposure to 9-HpODE caused a dose-dependent increase in GSH oxidation in HAEC that was independent of intracellular or extracellular H
CONCLUSIONS
Long 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.

Identifiants

pubmed: 30844486
pii: S0304-4165(19)30052-2
doi: 10.1016/j.bbagen.2019.03.002
pmc: PMC6823641
mid: NIHMS1526290
pii:
doi:

Substances chimiques

Linoleic Acids 0
Linoleic Acids, Conjugated 0
9-hydroxy-10,12-octadecadienoic acid 15514-85-9
9-hydroperoxy-11,12-octadecadienoic acid 63121-49-3
Hydrogen Peroxide BBX060AN9V
Phospholipid Hydroperoxide Glutathione Peroxidase EC 1.11.1.12
Glutathione Peroxidase EC 1.11.1.9
Glutathione GAN16C9B8O

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, N.I.H., Intramural Research Support, U.S. Gov't, Non-P.H.S.

Langues

eng

Sous-ensembles de citation

IM

Pagination

950-959

Subventions

Organisme : Intramural EPA
ID : EPA999999
Pays : United States
Organisme : NIEHS NIH HHS
ID : F31 ES029020
Pays : United States
Organisme : NIEHS NIH HHS
ID : P30 ES010126
Pays : United States

Informations de copyright

Copyright © 2019 Elsevier B.V. All rights reserved.

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Auteurs

Elizabeth M Corteselli (EM)

Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.

Eugene Gibbs-Flournoy (E)

Oak Ridge Institute for Science and Education, Oak Ridge, TN, USA.

Steven O Simmons (SO)

National Center for Computational Toxicology, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA.

Philip Bromberg (P)

Center for Environmental Medicine, Asthma, and Lung Biology, University of North Carolina, Chapel Hill, NC, USA.

Avram Gold (A)

Department of Environmental Sciences and Engineering, Gillings School of Global Public Health, University of North Carolina, Chapel Hill, NC, USA.

James M Samet (JM)

Environmental 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.

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Classifications MeSH