GlutaredoxinV1, Main, Exploration, bibRecord, 000B22

Glutathione disulfide induces neural cell death via a 12-lipoxygenase pathway.

Identifieur interne : 000B22 ( Main/Exploration ); précédent : 000B21; suivant : 000B23

Glutathione disulfide induces neural cell death via a 12-lipoxygenase pathway.

Auteurs : H-A Park [États-Unis] ; S. Khanna ; C. Rink ; S. Gnyawali ; S. Roy ; C K Sen

Source :

Cell death and differentiation [ 1476-5403 ] ; 2009.

RBID : pubmed:19373248

Descripteurs français

KwdFr :
- Animaux (MeSH), Arachidonate 12-lipoxygenase (génétique), Arachidonate 12-lipoxygenase (métabolisme), Carmustine (pharmacologie), Disulfure de glutathion (pharmacologie), Disulfure de glutathion (toxicité), Inhibiteurs de la lipoxygénase (MeSH), Lignée cellulaire (MeSH), Microinjections (MeSH), Mort cellulaire (effets des médicaments et des substances chimiques), Potentiel de membrane mitochondriale (MeSH), Souris (MeSH), Souris knockout (MeSH), Transduction du signal (MeSH).
MESH :
- effets des médicaments et des substances chimiques : Mort cellulaire.
- génétique : Arachidonate 12-lipoxygenase.
- métabolisme : Arachidonate 12-lipoxygenase.
- pharmacologie : Carmustine, Disulfure de glutathion.
- toxicité : Disulfure de glutathion.
- Animaux, Inhibiteurs de la lipoxygénase, Lignée cellulaire, Microinjections, Potentiel de membrane mitochondriale, Souris, Souris knockout, Transduction du signal.

English descriptors

KwdEn :
- Animals (MeSH), Arachidonate 12-Lipoxygenase (genetics), Arachidonate 12-Lipoxygenase (metabolism), Carmustine (pharmacology), Cell Death (drug effects), Cell Line (MeSH), Glutathione Disulfide (pharmacology), Glutathione Disulfide (toxicity), Lipoxygenase Inhibitors (MeSH), Membrane Potential, Mitochondrial (MeSH), Mice (MeSH), Mice, Knockout (MeSH), Microinjections (MeSH), Signal Transduction (MeSH).
MESH :
- chemical , genetics : Arachidonate 12-Lipoxygenase.
- chemical , metabolism : Arachidonate 12-Lipoxygenase.
- chemical , pharmacology : Carmustine, Glutathione Disulfide.
- drug effects : Cell Death.
- chemical , toxicity : Glutathione Disulfide.
- Animals, Cell Line, Lipoxygenase Inhibitors, Membrane Potential, Mitochondrial, Mice, Mice, Knockout, Microinjections, Signal Transduction.

Abstract

Oxidized glutathione (GSSG) is commonly viewed as a byproduct of GSH metabolism. The pathophysiological significance of GSSG per se remains poorly understood. Adopting a microinjection approach to isolate GSSG elevation within the cell, this work identifies that GSSG can trigger neural HT4 cell death via a 12-lipoxygenase (12-Lox)-dependent mechanism. In vivo, stereotaxic injection of GSSG into the brain caused lesion in wild-type mice but less so in 12-Lox knockout mice. Microinjection of graded amounts identified 0.5 mM as the lethal [GSSG]i in resting cells. Interestingly, this threshold was shifted to the left by 20-fold (0.025 mM) in GSH-deficient cells. This is important because tissue GSH lowering is commonly noted in the context of several diseases as well as in aging. Inhibition of GSSG reductase by BCNU is known to result in GSSG accumulation and caused cell death in a 12-Lox-sensitive manner. GSSG S-glutathionylated purified 12-Lox as well as in a model of glutamate-induced HT4 cell death in vitro where V5-tagged 12-Lox was expressed in cells. Countering glutamate-induced 12-Lox S-glutathionylation by glutaredoxin-1 overexpression protected against cell death. Strategies directed at improving or arresting cellular GSSG clearance may be effective in minimizing oxidative stress-related tissue injury or potentiating the killing of tumor cells, respectively.

DOI: 10.1038/cdd.2009.37
PubMed: 19373248
PubMed Central: PMC2990696

Affiliations:

Links toward previous steps (curation, corpus...)

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Le document en format XML

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<term>Arachidonate 12-Lipoxygenase (metabolism)</term>
<term>Carmustine (pharmacology)</term>
<term>Cell Death (drug effects)</term>
<term>Cell Line (MeSH)</term>
<term>Glutathione Disulfide (pharmacology)</term>
<term>Glutathione Disulfide (toxicity)</term>
<term>Lipoxygenase Inhibitors (MeSH)</term>
<term>Membrane Potential, Mitochondrial (MeSH)</term>
<term>Mice (MeSH)</term>
<term>Mice, Knockout (MeSH)</term>
<term>Microinjections (MeSH)</term>
<term>Signal Transduction (MeSH)</term>
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<term>Arachidonate 12-lipoxygenase (métabolisme)</term>
<term>Carmustine (pharmacologie)</term>
<term>Disulfure de glutathion (pharmacologie)</term>
<term>Disulfure de glutathion (toxicité)</term>
<term>Inhibiteurs de la lipoxygénase (MeSH)</term>
<term>Lignée cellulaire (MeSH)</term>
<term>Microinjections (MeSH)</term>
<term>Mort cellulaire (effets des médicaments et des substances chimiques)</term>
<term>Potentiel de membrane mitochondriale (MeSH)</term>
<term>Souris (MeSH)</term>
<term>Souris knockout (MeSH)</term>
<term>Transduction du signal (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Arachidonate 12-Lipoxygenase</term>
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<term>Glutathione Disulfide</term>
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<keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Cell Death</term>
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<keywords scheme="MESH" qualifier="effets des médicaments et des substances chimiques" xml:lang="fr"><term>Mort cellulaire</term>
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<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>Arachidonate 12-lipoxygenase</term>
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<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Carmustine</term>
<term>Disulfure de glutathion</term>
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<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Glutathione Disulfide</term>
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<keywords scheme="MESH" qualifier="toxicité" xml:lang="fr"><term>Disulfure de glutathion</term>
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<term>Cell Line</term>
<term>Lipoxygenase Inhibitors</term>
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<term>Mice</term>
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<term>Microinjections</term>
<term>Potentiel de membrane mitochondriale</term>
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<front><div type="abstract" xml:lang="en">Oxidized glutathione (GSSG) is commonly viewed as a byproduct of GSH metabolism. The pathophysiological significance of GSSG per se remains poorly understood. Adopting a microinjection approach to isolate GSSG elevation within the cell, this work identifies that GSSG can trigger neural HT4 cell death via a 12-lipoxygenase (12-Lox)-dependent mechanism. In vivo, stereotaxic injection of GSSG into the brain caused lesion in wild-type mice but less so in 12-Lox knockout mice. Microinjection of graded amounts identified 0.5 mM as the lethal [GSSG]i in resting cells. Interestingly, this threshold was shifted to the left by 20-fold (0.025 mM) in GSH-deficient cells. This is important because tissue GSH lowering is commonly noted in the context of several diseases as well as in aging. Inhibition of GSSG reductase by BCNU is known to result in GSSG accumulation and caused cell death in a 12-Lox-sensitive manner. GSSG S-glutathionylated purified 12-Lox as well as in a model of glutamate-induced HT4 cell death in vitro where V5-tagged 12-Lox was expressed in cells. Countering glutamate-induced 12-Lox S-glutathionylation by glutaredoxin-1 overexpression protected against cell death. Strategies directed at improving or arresting cellular GSSG clearance may be effective in minimizing oxidative stress-related tissue injury or potentiating the killing of tumor cells, respectively.</div>
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Glutathione disulfide induces neural cell death via a 12-lipoxygenase pathway.

Glutathione disulfide induces neural cell death via a 12-lipoxygenase pathway.

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