Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death
Identifieur interne : 002746 ( Istex/Corpus ); précédent : 002745; suivant : 002747Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death
Auteurs : Jaswinder S. Bains ; Christopher A. ShawSource :
- Brain Research Reviews [ 0165-0173 ] ; 1997.
Abstract
Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. In context to the above, we provide a GSH-depletion model of neurodegenerative disorders, suggest experimental verifications of this model, and propose potential therapeutic approaches for preventing or halting these diseases.
Url:
DOI: 10.1016/S0165-0173(97)00045-3
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Shaw</name><affiliation><mods:affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:C620F3FA61A696E7FCBB69BFD52E265BA5C3B615</idno><date when="1997" year="1997">1997</date><idno type="doi">10.1016/S0165-0173(97)00045-3</idno><idno type="url">https://api-v5.istex.fr/document/C620F3FA61A696E7FCBB69BFD52E265BA5C3B615/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">002746</idno><idno type="wicri:explorRef" wicri:stream="Istex" wicri:step="Corpus" wicri:corpus="ISTEX">002746</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death</title><author><name sortKey="Bains, Jaswinder S" sort="Bains, Jaswinder S" uniqKey="Bains J" first="Jaswinder S" last="Bains">Jaswinder S. Bains</name><affiliation><mods:affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</mods:affiliation></affiliation></author><author><name sortKey="Shaw, Christopher A" sort="Shaw, Christopher A" uniqKey="Shaw C" first="Christopher A" last="Shaw">Christopher A. Shaw</name><affiliation><mods:affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Brain Research Reviews</title><title level="j" type="abbrev">BRESR</title><idno type="ISSN">0165-0173</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997">1997</date><biblScope unit="volume">25</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="335">335</biblScope><biblScope unit="page" to="358">358</biblScope></imprint><idno type="ISSN">0165-0173</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0165-0173</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. In context to the above, we provide a GSH-depletion model of neurodegenerative disorders, suggest experimental verifications of this model, and propose potential therapeutic approaches for preventing or halting these diseases.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Jaswinder S Bains</name><affiliations><json:string>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</json:string></affiliations></json:item><json:item><name>Christopher A Shaw</name><affiliations><json:string>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Aging</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>ALS</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Alzheimer</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Glutathione</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neurotransmitter</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Oxidative stress</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson</value></json:item></subject><language><json:string>eng</json:string></language><originalGenre><json:string>Review article</json:string></originalGenre><abstract>Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. 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In (c) binding data is quantified by densitometry from five control and five ALS patients. Data from individual subjects are shown as filled circles (nCi/mg). Film calibration was made using Amersham [14C]-microscales. [35S] GSH binding was increased significantly in both dorsal and ventral horns from ALS subjects compared with controls. Calibration bar equals 2 mm. Abbreviations: dh=dorsal horn, vh=ventral horn, sg=substantia gelatinosa, Con=control, ALS=amyotrophic lateral sclerosis. For details of methods, see Lanius et al. [151].</note><note type="content">Fig. 3: Proposed GSH-depletion model for neurodegenerative disorders.</note><note type="content">Table 1: Potential causal factors leading to oxidative stress in various neurodegenerative disorders</note></notesStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a">Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death</title><author xml:id="author-0000"><persName><forename type="first">Jaswinder S</forename><surname>Bains</surname></persName><affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</affiliation></author><author xml:id="author-0001"><persName><forename type="first">Christopher A</forename><surname>Shaw</surname></persName><affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</affiliation></author><idno type="istex">C620F3FA61A696E7FCBB69BFD52E265BA5C3B615</idno><idno type="DOI">10.1016/S0165-0173(97)00045-3</idno><idno type="PII">S0165-0173(97)00045-3</idno></analytic><monogr><title level="j">Brain Research Reviews</title><title level="j" type="abbrev">BRESR</title><idno type="pISSN">0165-0173</idno><idno type="PII">S0165-0173(00)X0014-8</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1997"></date><biblScope unit="volume">25</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="335">335</biblScope><biblScope unit="page" to="358">358</biblScope></imprint></monogr></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1997</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. In context to the above, we provide a GSH-depletion model of neurodegenerative disorders, suggest experimental verifications of this model, and propose potential therapeutic approaches for preventing or halting these diseases.</p></abstract><textClass><keywords scheme="keyword"><list><head>Keywords</head><item><term>Aging</term></item><item><term>ALS</term></item><item><term>Alzheimer</term></item><item><term>Glutathione</term></item><item><term>Neurotransmitter</term></item><item><term>Oxidative stress</term></item><item><term>Parkinson</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><extension>txt</extension><original>false</original><mimetype>text/plain</mimetype><uri>https://api-v5.istex.fr/document/C620F3FA61A696E7FCBB69BFD52E265BA5C3B615/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: ce:floats; body; tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"><istex:entity SYSTEM="gr1" NDATA="IMAGE" name="gr1"></istex:entity><istex:entity SYSTEM="gr2" NDATA="IMAGE" name="gr2"></istex:entity><istex:entity SYSTEM="gr3" NDATA="IMAGE" name="gr3"></istex:entity></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="rev"><item-info><jid>BRESR</jid><aid>93011</aid><ce:pii>S0165-0173(97)00045-3</ce:pii><ce:doi>10.1016/S0165-0173(97)00045-3</ce:doi><ce:copyright year="1997" type="full-transfer">Elsevier Science B.V.</ce:copyright></item-info><head><ce:dochead><ce:textfn>Full-length review</ce:textfn></ce:dochead><ce:title>Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death</ce:title><ce:author-group><ce:author><ce:given-name>Jaswinder S</ce:given-name><ce:surname>Bains</ce:surname><ce:cross-ref refid="CORR1">*</ce:cross-ref></ce:author><ce:author><ce:given-name>Christopher A</ce:given-name><ce:surname>Shaw</ce:surname></ce:author><ce:affiliation><ce:textfn>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</ce:textfn></ce:affiliation><ce:correspondence id="CORR1"><ce:label>*</ce:label><ce:text>Corresponding author. Fax: +1 (604) 822-2316; E-mail: jbains@unixg.ubc.ca</ce:text></ce:correspondence></ce:author-group><ce:date-accepted day="9" month="10" year="1997"></ce:date-accepted><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. In context to the above, we provide a GSH-depletion model of neurodegenerative disorders, suggest experimental verifications of this model, and propose potential therapeutic approaches for preventing or halting these diseases.</ce:simple-para></ce:abstract-sec></ce:abstract><ce:keywords class="keyword"><ce:section-title>Keywords</ce:section-title><ce:keyword><ce:text>Aging</ce:text></ce:keyword><ce:keyword><ce:text>ALS</ce:text></ce:keyword><ce:keyword><ce:text>Alzheimer</ce:text></ce:keyword><ce:keyword><ce:text>Glutathione</ce:text></ce:keyword><ce:keyword><ce:text>Neurotransmitter</ce:text></ce:keyword><ce:keyword><ce:text>Oxidative stress</ce:text></ce:keyword><ce:keyword><ce:text>Parkinson</ce:text></ce:keyword></ce:keywords></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Neurodegenerative disorders in humans: the role of glutathione in oxidative stress-mediated neuronal death</title></titleInfo><name type="personal"><namePart type="given">Jaswinder S</namePart><namePart type="family">Bains</namePart><affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</affiliation><description>Corresponding author. Fax: +1 (604) 822-2316; E-mail: jbains@unixg.ubc.ca</description><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Christopher A</namePart><namePart type="family">Shaw</namePart><affiliation>Departments of Ophthalmology, Physiology and Neuroscience, c/o Department of Anatomy, The University of British Columbia, #226-2177 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="review-article" displayLabel="Review article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1997</dateIssued><copyrightDate encoding="w3cdtf">1997</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Oxidative stress has been implicated in both normal aging and in various neurodegenerative disorders and may be a common mechanism underlying various forms of cell death including necrosis, apoptosis, and excitotoxicity. In this review, we develop the hypothesis that oxidative stress-mediated neuronal loss may be initiated by a decline in the antioxidant molecule glutathione (GSH). GSH plays multiple roles in the nervous system including free radical scavenger, redox modulator of ionotropic receptor activity, and possible neurotransmitter. GSH depletion can enhance oxidative stress and may also increase the levels of excitotoxic molecules; both types of action can initiate cell death in distinct neuronal populations. Evidence for a role of oxidative stress and diminished GSH status is presented for Lou Gehrig's disease (ALS), Parkinson's disease, and Alzheimer's disease. Potential links to the Guamanian variant of these diseases (ALS–PD complex) are discussed. In context to the above, we provide a GSH-depletion model of neurodegenerative disorders, suggest experimental verifications of this model, and propose potential therapeutic approaches for preventing or halting these diseases.</abstract><note type="content">Section title: Full-length review</note><note type="content">Fig. 1: Oxidation–reduction pathway: relationship of reduced GSH to oxidized (GSSG) glutathione.</note><note type="content">Fig. 2: [35]S GSH binding in cervical spinal cord sections from control (a) and ALS (b). In (c) binding data is quantified by densitometry from five control and five ALS patients. Data from individual subjects are shown as filled circles (nCi/mg). Film calibration was made using Amersham [14C]-microscales. [35S] GSH binding was increased significantly in both dorsal and ventral horns from ALS subjects compared with controls. Calibration bar equals 2 mm. Abbreviations: dh=dorsal horn, vh=ventral horn, sg=substantia gelatinosa, Con=control, ALS=amyotrophic lateral sclerosis. For details of methods, see Lanius et al. [151].</note><note type="content">Fig. 3: Proposed GSH-depletion model for neurodegenerative disorders.</note><note type="content">Table 1: Potential causal factors leading to oxidative stress in various neurodegenerative disorders</note><subject><genre>Keywords</genre><topic>Aging</topic><topic>ALS</topic><topic>Alzheimer</topic><topic>Glutathione</topic><topic>Neurotransmitter</topic><topic>Oxidative stress</topic><topic>Parkinson</topic></subject><relatedItem type="host"><titleInfo><title>Brain Research Reviews</title></titleInfo><titleInfo type="abbreviated"><title>BRESR</title></titleInfo><genre type="journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">199712</dateIssued></originInfo><identifier type="ISSN">0165-0173</identifier><identifier type="PII">S0165-0173(00)X0014-8</identifier><part><date>199712</date><detail type="volume"><number>25</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue pages"><start>255</start><end>408</end></extent><extent unit="pages"><start>335</start><end>358</end></extent></part></relatedItem><identifier type="istex">C620F3FA61A696E7FCBB69BFD52E265BA5C3B615</identifier><identifier type="DOI">10.1016/S0165-0173(97)00045-3</identifier><identifier type="PII">S0165-0173(97)00045-3</identifier><accessCondition type="use and reproduction" contentType="copyright">©1997 Elsevier Science B.V.</accessCondition><recordInfo><recordContentSource>ELSEVIER</recordContentSource><recordOrigin>Elsevier Science B.V., ©1997</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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