Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease
Identifieur interne : 000816 ( Main/Corpus ); précédent : 000815; suivant : 000817Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease
Auteurs : C. Mytilineou ; P. Werner ; S. Molinari ; A. Di Rocco ; G. Cohen ; D. YahrSource :
- Journal of Neural Transmission - Parkinson's Disease and Dementia Section [ 0936-3076 ] ; 1994-10-01.
Abstract
Summary: Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.
Url:
DOI: 10.1007/BF02260943
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Molinari</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Di Rocco, A" sort="Di Rocco, A" uniqKey="Di Rocco A" first="A." last="Di Rocco">A. Di Rocco</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Cohen, G" sort="Cohen, G" uniqKey="Cohen G" first="G." last="Cohen">G. Cohen</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. 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Cohen</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</mods:affiliation></affiliation><affiliation><mods:affiliation>Department Fishberg Center for Neurobiology, Mount Sinai School of Medicine, New York, NY, U.S.A.</mods:affiliation></affiliation></author><author><name sortKey="Yahr, D" sort="Yahr, D" uniqKey="Yahr D" first="D." last="Yahr">D. Yahr</name><affiliation><mods:affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title><title level="j" type="abbrev">J Neural Transm Gen Sect</title><idno type="ISSN">0936-3076</idno><idno type="eISSN">1435-1463</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>Vienna</pubPlace><date type="published" when="1994-10-01">1994-10-01</date><biblScope unit="volume">8</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="223">223</biblScope><biblScope unit="page" to="228">228</biblScope></imprint><idno type="ISSN">0936-3076</idno></series><idno type="istex">5CCD8084F66803233DB350DE7721F9280BE048DC</idno><idno type="DOI">10.1007/BF02260943</idno><idno type="ArticleID">Art7</idno><idno type="ArticleID">BF02260943</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0936-3076</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Summary: Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.</div></front></TEI><istex><corpusName>springer</corpusName><author><json:item><name>C. Mytilineou Ph.D.</name><affiliations><json:string>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</json:string></affiliations></json:item><json:item><name>P. 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These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. 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Y., U.S.A.</affiliation><affiliation>Department Fishberg Center for Neurobiology, Mount Sinai School of Medicine, New York, NY, U.S.A.</affiliation></author><author><persName><forename type="first">M.</forename><surname>Yahr</surname></persName><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. 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We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.</p></abstract><textClass><keywords scheme="Journal Subject"><list><head>Medicine & Public Health</head><item><term>Pharmacology/Toxicology</term></item><item><term>Psychiatry</term></item><item><term>Neurology</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1993-12-23">Created</change><change when="1994-10-01">Published</change><change xml:id="refBibs-istex" who="#ISTEX-API" when="2016-3-2">References added</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/5CCD8084F66803233DB350DE7721F9280BE048DC/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Springer, Publisher found" wicri:toSee="no header"><istex:xmlDeclaration>version="1.0" encoding="UTF-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//Springer-Verlag//DTD A++ V2.4//EN" URI="http://devel.springer.de/A++/V2.4/DTD/A++V2.4.dtd" name="istex:docType"></istex:docType><istex:document><Publisher><PublisherInfo><PublisherName>Springer-Verlag</PublisherName><PublisherLocation>Vienna</PublisherLocation></PublisherInfo><Journal><JournalInfo JournalProductType="ArchiveJournal" NumberingStyle="Unnumbered"><JournalID>722</JournalID><JournalPrintISSN>0936-3076</JournalPrintISSN><JournalElectronicISSN>1435-1463</JournalElectronicISSN><JournalTitle>Journal of Neural Transmission - 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Y.</State><Country>U.S.A.</Country></OrgAddress></Affiliation></AuthorGroup><Abstract ID="Abs1" Language="En"><Heading>Summary</Heading><Para>Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-<Superscript>14</Superscript>C]pyruvate and [1,4-<Superscript>14</Superscript>C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.</Para></Abstract><KeywordGroup Language="En"><Heading>Keywords</Heading><Keyword>Parkinson's disease</Keyword><Keyword>fibroblasts</Keyword><Keyword>mitochondria</Keyword><Keyword>pyruvate oxidation</Keyword><Keyword>respiration</Keyword></KeywordGroup></ArticleHeader><NoBody></NoBody></Article></Issue></Volume></Journal></Publisher></istex:document></istex:metadataXml><mods version="3.6"><titleInfo lang="en"><title>Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Impaired oxidative decarboxylation of pyruvate in fibroblasts from patients with Parkinson's disease</title></titleInfo><name type="personal"><namePart type="given">C.</namePart><namePart type="family">Mytilineou</namePart><namePart type="termsOfAddress">Ph.D.</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">P.</namePart><namePart type="family">Werner</namePart><affiliation>Department Biochemistry, Mount Sinai School of Medicine, New York, NY, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">S.</namePart><namePart type="family">Molinari</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">A.</namePart><namePart type="family">Di Rocco</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">G.</namePart><namePart type="family">Cohen</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</affiliation><affiliation>Department Fishberg Center for Neurobiology, Mount Sinai School of Medicine, New York, NY, U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">M.</namePart><namePart type="given">D.</namePart><namePart type="family">Yahr</namePart><affiliation>Department of Neurology, Mount Sinai School of Medicine, Box 1137, 10029, New York, N. Y., U.S.A.</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="brief communication" displayLabel="BriefCommunication"></genre><originInfo><publisher>Springer-Verlag</publisher><place><placeTerm type="text">Vienna</placeTerm></place><dateCreated encoding="w3cdtf">1993-12-23</dateCreated><dateIssued encoding="w3cdtf">1994-10-01</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">Summary: Whether or not a reported deficiency in brain mitochondrial complex I activity in Parkinson's disease represents a defect encompassing other organs or tissues has been a source of some controversy. We have examined mitochondrial respiration in fibroblasts from patients with Parkinson's disease by measuring the oxidative decarboxylation of [2-14C]pyruvate and [1,4-14C]succinate. We report that oxidation of pyruvate but not succinate was significantly reduced in fibroblasts from Parkinson patients when compared to healthy controls. These observations support the view that a widespread deficit in mitochondrial respiration exists in Parkinson's disease. Fibroblast cultures, moreover, are a source of affected proliferating cells, which can be used for in vitro studies of the nature of the respiratory defect and for testing of pharmacological interventions to correct the deficiency.</abstract><note>Short Communication</note><relatedItem type="host"><titleInfo><title>Journal of Neural Transmission - Parkinson's Disease and Dementia Section</title></titleInfo><titleInfo type="abbreviated"><title>J Neural Transm Gen Sect</title></titleInfo><genre type="Journal" displayLabel="Archive Journal"></genre><originInfo><dateIssued encoding="w3cdtf">1994-10-01</dateIssued><copyrightDate encoding="w3cdtf">1994</copyrightDate></originInfo><subject><genre>Medicine & Public Health</genre><topic>Pharmacology/Toxicology</topic><topic>Psychiatry</topic><topic>Neurology</topic></subject><identifier type="ISSN">0936-3076</identifier><identifier type="eISSN">1435-1463</identifier><identifier type="JournalID">722</identifier><identifier type="IssueArticleCount">8</identifier><identifier type="VolumeIssueCount">3</identifier><part><date>1994</date><detail type="volume"><number>8</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="pages"><start>223</start><end>228</end></extent></part><recordInfo><recordOrigin>Springer-Verlag, 1994</recordOrigin></recordInfo></relatedItem><identifier type="istex">5CCD8084F66803233DB350DE7721F9280BE048DC</identifier><identifier type="DOI">10.1007/BF02260943</identifier><identifier type="ArticleID">Art7</identifier><identifier type="ArticleID">BF02260943</identifier><accessCondition type="use and reproduction" contentType="copyright">Springer-Verlag</accessCondition><recordInfo><recordContentSource>SPRINGER</recordContentSource><recordOrigin>Springer-Verlag, 1994</recordOrigin></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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