Mitochondrial respiratory chain function in multiple system atrophy.
Identifieur interne : 004D15 ( Ncbi/Merge ); précédent : 004D14; suivant : 004D16Mitochondrial respiratory chain function in multiple system atrophy.
Auteurs : M. Gu [Royaume-Uni] ; M T Gash ; J M Cooper ; G K Wenning ; S E Daniel ; N P Quinn ; C D Marsden ; A H SchapiraSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1997.
English descriptors
- KwdEn :
- Aged, Antiparkinson Agents (administration & dosage), Antiparkinson Agents (therapeutic use), Atrophy (pathology), Blood Platelets, Brain (enzymology), Brain (pathology), Citrate (si)-Synthase (metabolism), Culture Techniques, Electron Transport, Humans, Levodopa (administration & dosage), Levodopa (therapeutic use), Middle Aged, Mitochondria (enzymology), Mitochondria (pathology), Nerve Degeneration, Parkinson Disease (diagnosis), Parkinson Disease (drug therapy), Substantia Nigra.
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Levodopa.
- chemical , metabolism : Citrate (si)-Synthase.
- chemical , therapeutic use : Antiparkinson Agents, Levodopa.
- diagnosis : Parkinson Disease.
- drug therapy : Parkinson Disease.
- enzymology : Brain, Mitochondria.
- pathology : Atrophy, Brain, Mitochondria.
- Aged, Blood Platelets, Culture Techniques, Electron Transport, Humans, Middle Aged, Nerve Degeneration, Substantia Nigra.
Abstract
Multiple system atrophy (MSA) is a clinico-pathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5-10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L-DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L-DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.
DOI: 10.1002/mds.870120323
PubMed: 9159739
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Mitochondrial respiratory chain function in multiple system atrophy.</title><author><name sortKey="Gu, M" sort="Gu, M" uniqKey="Gu M" first="M" last="Gu">M. Gu</name><affiliation wicri:level="2"><nlm:affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation></author><author><name sortKey="Gash, M T" sort="Gash, M T" uniqKey="Gash M" first="M T" last="Gash">M T Gash</name></author><author><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J M" last="Cooper">J M Cooper</name></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G K" last="Wenning">G K Wenning</name></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</name></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N P" last="Quinn">N P Quinn</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author><author><name sortKey="Schapira, A H" sort="Schapira, A H" uniqKey="Schapira A" first="A H" last="Schapira">A H Schapira</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1997">1997</date><idno type="RBID">pubmed:9159739</idno><idno type="pmid">9159739</idno><idno type="doi">10.1002/mds.870120323</idno><idno type="wicri:Area/PubMed/Corpus">004667</idno><idno type="wicri:Area/PubMed/Curation">004667</idno><idno type="wicri:Area/PubMed/Checkpoint">004624</idno><idno type="wicri:Area/Ncbi/Merge">004D15</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Mitochondrial respiratory chain function in multiple system atrophy.</title><author><name sortKey="Gu, M" sort="Gu, M" uniqKey="Gu M" first="M" last="Gu">M. Gu</name><affiliation wicri:level="2"><nlm:affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England.</nlm:affiliation><country>Royaume-Uni</country><placeName><region type="country">Angleterre</region></placeName><wicri:cityArea>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London</wicri:cityArea></affiliation></author><author><name sortKey="Gash, M T" sort="Gash, M T" uniqKey="Gash M" first="M T" last="Gash">M T Gash</name></author><author><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J M" last="Cooper">J M Cooper</name></author><author><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G K" last="Wenning">G K Wenning</name></author><author><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</name></author><author><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N P" last="Quinn">N P Quinn</name></author><author><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name></author><author><name sortKey="Schapira, A H" sort="Schapira, A H" uniqKey="Schapira A" first="A H" last="Schapira">A H Schapira</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1997" type="published">1997</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Atrophy (pathology)</term><term>Blood Platelets</term><term>Brain (enzymology)</term><term>Brain (pathology)</term><term>Citrate (si)-Synthase (metabolism)</term><term>Culture Techniques</term><term>Electron Transport</term><term>Humans</term><term>Levodopa (administration & dosage)</term><term>Levodopa (therapeutic use)</term><term>Middle Aged</term><term>Mitochondria (enzymology)</term><term>Mitochondria (pathology)</term><term>Nerve Degeneration</term><term>Parkinson Disease (diagnosis)</term><term>Parkinson Disease (drug therapy)</term><term>Substantia Nigra</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Citrate (si)-Synthase</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="enzymology" xml:lang="en"><term>Brain</term><term>Mitochondria</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Atrophy</term><term>Brain</term><term>Mitochondria</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Blood Platelets</term><term>Culture Techniques</term><term>Electron Transport</term><term>Humans</term><term>Middle Aged</term><term>Nerve Degeneration</term><term>Substantia Nigra</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Multiple system atrophy (MSA) is a clinico-pathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5-10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L-DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L-DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">9159739</PMID><DateCreated><Year>1997</Year><Month>07</Month><Day>28</Day></DateCreated><DateCompleted><Year>1997</Year><Month>07</Month><Day>28</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0885-3185</ISSN><JournalIssue CitedMedium="Print"><Volume>12</Volume><Issue>3</Issue><PubDate><Year>1997</Year><Month>May</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Mitochondrial respiratory chain function in multiple system atrophy.</ArticleTitle><Pagination><MedlinePgn>418-22</MedlinePgn></Pagination><Abstract><AbstractText>Multiple system atrophy (MSA) is a clinico-pathological entity distinct from idiopathic Parkinson's disease (PD) that is responsible for 5-10% of cases of parkinsonism. Degeneration of nigral neurones is a feature of both diseases. A specific deficiency of mitochondrial complex I activity has been found in PD substantia nigra. We have analysed mitochondrial function in substantia nigra and platelets from MSA patients to identify any respiratory chain defect in this disorder and to determine its tissue specificity. As our MSA patients had been on L-DOPA, we also sought to establish whether this treatment could cause the complex I defect as seen in PD. We found no significant difference in respiratory chain activity corrected for mitochondrial mass between control and MSA patients in either of the tissues studied. These results provide a biochemical dimension to the differences between MSA and idiopathic PD. In addition, the fact that L-DOPA failed to induce a complex I defect in MSA substantia nigra suggests that this treatment is unlikely to cause the complex I deficiency in PD, without additional factors that may operate in PD.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Gu</LastName><ForeName>M</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Department of Clinical Neurosciences, Royal Free Hospital School of Medicine, London, England.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gash</LastName><ForeName>M T</ForeName><Initials>MT</Initials></Author><Author ValidYN="Y"><LastName>Cooper</LastName><ForeName>J M</ForeName><Initials>JM</Initials></Author><Author ValidYN="Y"><LastName>Wenning</LastName><ForeName>G K</ForeName><Initials>GK</Initials></Author><Author ValidYN="Y"><LastName>Daniel</LastName><ForeName>S E</ForeName><Initials>SE</Initials></Author><Author ValidYN="Y"><LastName>Quinn</LastName><ForeName>N P</ForeName><Initials>NP</Initials></Author><Author ValidYN="Y"><LastName>Marsden</LastName><ForeName>C D</ForeName><Initials>CD</Initials></Author><Author ValidYN="Y"><LastName>Schapira</LastName><ForeName>A H</ForeName><Initials>AH</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>UNITED STATES</Country><MedlineTA>Mov Disord</MedlineTA><NlmUniqueID>8610688</NlmUniqueID><ISSNLinking>0885-3185</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D000978">Antiparkinson Agents</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 2.3.3.1</RegistryNumber><NameOfSubstance UI="D002950">Citrate (si)-Synthase</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000368">Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001284">Atrophy</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001792">Blood Platelets</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000201">enzymology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002950">Citrate (si)-Synthase</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D046508">Culture Techniques</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D004579">Electron Transport</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008875">Middle Aged</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008928">Mitochondria</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000201">enzymology</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009410">Nerve Degeneration</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000175">diagnosis</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D013378">Substantia Nigra</DescriptorName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1997</Year><Month>5</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1997</Year><Month>5</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">9159739</ArticleId><ArticleId IdType="doi">10.1002/mds.870120323</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li></region></list><tree><noCountry><name sortKey="Cooper, J M" sort="Cooper, J M" uniqKey="Cooper J" first="J M" last="Cooper">J M Cooper</name><name sortKey="Daniel, S E" sort="Daniel, S E" uniqKey="Daniel S" first="S E" last="Daniel">S E Daniel</name><name sortKey="Gash, M T" sort="Gash, M T" uniqKey="Gash M" first="M T" last="Gash">M T Gash</name><name sortKey="Marsden, C D" sort="Marsden, C D" uniqKey="Marsden C" first="C D" last="Marsden">C D Marsden</name><name sortKey="Quinn, N P" sort="Quinn, N P" uniqKey="Quinn N" first="N P" last="Quinn">N P Quinn</name><name sortKey="Schapira, A H" sort="Schapira, A H" uniqKey="Schapira A" first="A H" last="Schapira">A H Schapira</name><name sortKey="Wenning, G K" sort="Wenning, G K" uniqKey="Wenning G" first="G K" last="Wenning">G K Wenning</name></noCountry><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Gu, M" sort="Gu, M" uniqKey="Gu M" first="M" last="Gu">M. 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