Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease
Identifieur interne : 004026 ( Main/Exploration ); précédent : 004025; suivant : 004027Nigral glutathione deficiency is not specific for idiopathic Parkinson's disease
Auteurs : Paul S. Fitzmaurice [Canada] ; Lee Ang [Canada] ; Mark Guttman [Canada] ; Ali H. Rajput [Canada] ; Yoshiaki Furukawa [Canada] ; Stephen J. Kish [Canada]Source :
- Movement Disorders [ 0885-3185 ] ; 2003-09.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Analyse quantitative, Homme.
English descriptors
- KwdEn :
- Aged, Antioxidants (metabolism), Comparative study, Glutathione, Glutathione (deficiency), Human, Humans, Idiopathic, Locus niger, Multiple System Atrophy (metabolism), Multiple system atrophy, Oxidative Stress, Oxidative stress, Parkinson Disease (metabolism), Parkinson disease, Parkinson's disease, Pathogenesis, Quantitative analysis, Substantia Nigra (metabolism), Supranuclear Palsy, Progressive (metabolism), Supranuclear ophthalmoplegia, Uric Acid (metabolism), glutathione, multiple system atrophy, oxidative stress, progressive supranuclear palsy, substantia nigra.
- MESH :
- chemical , deficiency : Glutathione.
- chemical , metabolism : Antioxidants, Uric Acid.
- metabolism : Multiple System Atrophy, Parkinson Disease, Substantia Nigra, Supranuclear Palsy, Progressive.
- Aged, Humans, Oxidative Stress.
Abstract
The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [−30%], PSP [−21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [−20%]). GSH levels were normal in all examined normal and degenerating extra‐nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (−19 to −30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD. © 2003 Movement Disorder Society
Url:
DOI: 10.1002/mds.10486
Affiliations:
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Le document en format XML
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Rajput</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Division of Neurology, University of Saskatchewan, Saskatoon, Saskatchewan</wicri:regionArea><wicri:noRegion>Saskatchewan</wicri:noRegion></affiliation></author><author><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Movement Disorders Research Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author><author><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name><affiliation wicri:level="1"><country xml:lang="fr">Canada</country><wicri:regionArea>Human Neurochemical Pathology Laboratory, Centre for Addiction and Mental Health, Toronto, Ontario</wicri:regionArea><wicri:noRegion>Ontario</wicri:noRegion></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2003-09">2003-09</date><biblScope unit="vol">18</biblScope><biblScope unit="issue">9</biblScope><biblScope unit="page" from="969">969</biblScope><biblScope unit="page" to="976">976</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">57555A8D09E20110590BCE420F0B37968371034D</idno><idno type="DOI">10.1002/mds.10486</idno><idno type="ArticleID">MDS10486</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antioxidants (metabolism)</term><term>Comparative study</term><term>Glutathione</term><term>Glutathione (deficiency)</term><term>Human</term><term>Humans</term><term>Idiopathic</term><term>Locus niger</term><term>Multiple System Atrophy (metabolism)</term><term>Multiple system atrophy</term><term>Oxidative Stress</term><term>Oxidative stress</term><term>Parkinson Disease (metabolism)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Pathogenesis</term><term>Quantitative analysis</term><term>Substantia Nigra (metabolism)</term><term>Supranuclear Palsy, Progressive (metabolism)</term><term>Supranuclear ophthalmoplegia</term><term>Uric Acid (metabolism)</term><term>glutathione</term><term>multiple system atrophy</term><term>oxidative stress</term><term>progressive supranuclear palsy</term><term>substantia nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="deficiency" xml:lang="en"><term>Glutathione</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antioxidants</term><term>Uric Acid</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Multiple System Atrophy</term><term>Parkinson Disease</term><term>Substantia Nigra</term><term>Supranuclear Palsy, Progressive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Humans</term><term>Oxidative Stress</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Analyse quantitative</term><term>Atrophie multisystématisée</term><term>Etude comparative</term><term>Glutathion</term><term>Homme</term><term>Idiopathique</term><term>Locus niger</term><term>Ophtalmoplégie supranucléaire</term><term>Parkinson maladie</term><term>Pathogénie</term><term>Stress oxydatif</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Analyse quantitative</term><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The consistent findings of decreased levels of the major antioxidant glutathione in substantia nigra of patients with idiopathic Parkinson's disease (PD) has provided most of the basis for the oxidative stress hypothesis of the etiology of PD. To establish whether a nigral glutathione deficiency is unique to PD, as is generally assumed, or is present in other Parkinsonian conditions associated with nigral damage, we compared levels of reduced glutathione (GSH) in postmortem brain of patients with PD to those with progressive supranuclear palsy (PSP) and multiple system atrophy (MSA). As compared with the controls, nigral GSH levels were decreased in the PD and PSP patient groups (P < 0.05 for PD [−30%], PSP [−21%]), whereas a similar decrease in the MSA patient group did not reach statistical significance (P = 0.078, MSA [−20%]). GSH levels were normal in all examined normal and degenerating extra‐nigral brain areas in PSP and MSA. A trend for decreased levels of uric acid (antioxidant and product of purine catabolism) also was observed in nigra of all patient groups (−19 to −30%). These data suggest that glutathione depletion, possibly consequent to overutilisation in oxidative stress reactions, could play a causal role in nigral degeneration in all nigrostriatal dopamine deficiency disorders, and that antioxidant therapeutic approaches should not be restricted to PD. © 2003 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Canada</li></country></list><tree><country name="Canada"><noRegion><name sortKey="Fitzmaurice, Paul S" sort="Fitzmaurice, Paul S" uniqKey="Fitzmaurice P" first="Paul S." last="Fitzmaurice">Paul S. Fitzmaurice</name></noRegion><name sortKey="Ang, Lee" sort="Ang, Lee" uniqKey="Ang L" first="Lee" last="Ang">Lee Ang</name><name sortKey="Furukawa, Yoshiaki" sort="Furukawa, Yoshiaki" uniqKey="Furukawa Y" first="Yoshiaki" last="Furukawa">Yoshiaki Furukawa</name><name sortKey="Guttman, Mark" sort="Guttman, Mark" uniqKey="Guttman M" first="Mark" last="Guttman">Mark Guttman</name><name sortKey="Kish, Stephen J" sort="Kish, Stephen J" uniqKey="Kish S" first="Stephen J." last="Kish">Stephen J. Kish</name><name sortKey="Rajput, Ali H" sort="Rajput, Ali H" uniqKey="Rajput A" first="Ali H." last="Rajput">Ali H. Rajput</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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