No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.
Identifieur interne : 004946 ( PubMed/Checkpoint ); précédent : 004945; suivant : 004947No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.
Auteurs : J E Ahlskog [États-Unis] ; R J Uitti ; P A Low ; G M Tyce ; K K Nickander ; R C Petersen ; E. KokmenSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1995.
English descriptors
- KwdEn :
- Aged, Alzheimer Disease (blood), Alzheimer Disease (drug therapy), Alzheimer Disease (metabolism), Antiparkinson Agents (administration & dosage), Antiparkinson Agents (therapeutic use), Brain (metabolism), Carbidopa (administration & dosage), Carbidopa (therapeutic use), Diabetes Mellitus (blood), Diabetes Mellitus (metabolism), Ergolines (administration & dosage), Ergolines (therapeutic use), Female, Free Radicals, Humans, Levodopa (administration & dosage), Levodopa (therapeutic use), Lipid Peroxidation, Male, Malondialdehyde (blood), Malondialdehyde (metabolism), Oxidative Stress, Parkinson Disease (blood), Parkinson Disease (drug therapy), Parkinson Disease (metabolism), Selegiline (administration & dosage), Selegiline (therapeutic use), Vitamin E (administration & dosage), Vitamin E (therapeutic use).
- MESH :
- chemical , administration & dosage : Antiparkinson Agents, Carbidopa, Ergolines, Levodopa, Selegiline, Vitamin E.
- blood : Alzheimer Disease, Diabetes Mellitus, Malondialdehyde, Parkinson Disease.
- drug therapy : Alzheimer Disease, Parkinson Disease.
- metabolism : Alzheimer Disease, Brain, Diabetes Mellitus, Malondialdehyde, Parkinson Disease.
- chemical , therapeutic use : Antiparkinson Agents, Carbidopa, Ergolines, Levodopa, Selegiline, Vitamin E.
- Aged, Female, Free Radicals, Humans, Lipid Peroxidation, Male, Oxidative Stress.
Abstract
Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.
DOI: 10.1002/mds.870100507
PubMed: 8552107
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.</title><author><name sortKey="Ahlskog, J E" sort="Ahlskog, J E" uniqKey="Ahlskog J" first="J E" last="Ahlskog">J E Ahlskog</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mayo Clinic Rochester, Minnesota 55905, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic Rochester, Minnesota 55905</wicri:regionArea><wicri:noRegion>Minnesota 55905</wicri:noRegion></affiliation></author><author><name sortKey="Uitti, R J" sort="Uitti, R J" uniqKey="Uitti R" first="R J" last="Uitti">R J Uitti</name></author><author><name sortKey="Low, P A" sort="Low, P A" uniqKey="Low P" first="P A" last="Low">P A Low</name></author><author><name sortKey="Tyce, G M" sort="Tyce, G M" uniqKey="Tyce G" first="G M" last="Tyce">G M Tyce</name></author><author><name sortKey="Nickander, K K" sort="Nickander, K K" uniqKey="Nickander K" first="K K" last="Nickander">K K Nickander</name></author><author><name sortKey="Petersen, R C" sort="Petersen, R C" uniqKey="Petersen R" first="R C" last="Petersen">R C Petersen</name></author><author><name sortKey="Kokmen, E" sort="Kokmen, E" uniqKey="Kokmen E" first="E" last="Kokmen">E. Kokmen</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1995">1995</date><idno type="RBID">pubmed:8552107</idno><idno type="pmid">8552107</idno><idno type="doi">10.1002/mds.870100507</idno><idno type="wicri:Area/PubMed/Corpus">004938</idno><idno type="wicri:Area/PubMed/Curation">004938</idno><idno type="wicri:Area/PubMed/Checkpoint">004946</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.</title><author><name sortKey="Ahlskog, J E" sort="Ahlskog, J E" uniqKey="Ahlskog J" first="J E" last="Ahlskog">J E Ahlskog</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Mayo Clinic Rochester, Minnesota 55905, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology, Mayo Clinic Rochester, Minnesota 55905</wicri:regionArea><wicri:noRegion>Minnesota 55905</wicri:noRegion></affiliation></author><author><name sortKey="Uitti, R J" sort="Uitti, R J" uniqKey="Uitti R" first="R J" last="Uitti">R J Uitti</name></author><author><name sortKey="Low, P A" sort="Low, P A" uniqKey="Low P" first="P A" last="Low">P A Low</name></author><author><name sortKey="Tyce, G M" sort="Tyce, G M" uniqKey="Tyce G" first="G M" last="Tyce">G M Tyce</name></author><author><name sortKey="Nickander, K K" sort="Nickander, K K" uniqKey="Nickander K" first="K K" last="Nickander">K K Nickander</name></author><author><name sortKey="Petersen, R C" sort="Petersen, R C" uniqKey="Petersen R" first="R C" last="Petersen">R C Petersen</name></author><author><name sortKey="Kokmen, E" sort="Kokmen, E" uniqKey="Kokmen E" first="E" last="Kokmen">E. Kokmen</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="1995" type="published">1995</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Alzheimer Disease (blood)</term><term>Alzheimer Disease (drug therapy)</term><term>Alzheimer Disease (metabolism)</term><term>Antiparkinson Agents (administration & dosage)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Brain (metabolism)</term><term>Carbidopa (administration & dosage)</term><term>Carbidopa (therapeutic use)</term><term>Diabetes Mellitus (blood)</term><term>Diabetes Mellitus (metabolism)</term><term>Ergolines (administration & dosage)</term><term>Ergolines (therapeutic use)</term><term>Female</term><term>Free Radicals</term><term>Humans</term><term>Levodopa (administration & dosage)</term><term>Levodopa (therapeutic use)</term><term>Lipid Peroxidation</term><term>Male</term><term>Malondialdehyde (blood)</term><term>Malondialdehyde (metabolism)</term><term>Oxidative Stress</term><term>Parkinson Disease (blood)</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (metabolism)</term><term>Selegiline (administration & dosage)</term><term>Selegiline (therapeutic use)</term><term>Vitamin E (administration & dosage)</term><term>Vitamin E (therapeutic use)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Antiparkinson Agents</term><term>Carbidopa</term><term>Ergolines</term><term>Levodopa</term><term>Selegiline</term><term>Vitamin E</term></keywords><keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Alzheimer Disease</term><term>Diabetes Mellitus</term><term>Malondialdehyde</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Alzheimer Disease</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Alzheimer Disease</term><term>Brain</term><term>Diabetes Mellitus</term><term>Malondialdehyde</term><term>Parkinson Disease</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Carbidopa</term><term>Ergolines</term><term>Levodopa</term><term>Selegiline</term><term>Vitamin E</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Female</term><term>Free Radicals</term><term>Humans</term><term>Lipid Peroxidation</term><term>Male</term><term>Oxidative Stress</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8552107</PMID><DateCreated><Year>1996</Year><Month>02</Month><Day>20</Day></DateCreated><DateCompleted><Year>1996</Year><Month>02</Month><Day>20</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>10</Volume><Issue>5</Issue><PubDate><Year>1995</Year><Month>Sep</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>No evidence for systemic oxidant stress in Parkinson's or Alzheimer's disease.</ArticleTitle><Pagination><MedlinePgn>566-73</MedlinePgn></Pagination><Abstract><AbstractText>Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. Serum concentrations of two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Ahlskog</LastName><ForeName>J E</ForeName><Initials>JE</Initials><AffiliationInfo><Affiliation>Department of Neurology, Mayo Clinic Rochester, Minnesota 55905, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Uitti</LastName><ForeName>R J</ForeName><Initials>RJ</Initials></Author><Author ValidYN="Y"><LastName>Low</LastName><ForeName>P A</ForeName><Initials>PA</Initials></Author><Author ValidYN="Y"><LastName>Tyce</LastName><ForeName>G M</ForeName><Initials>GM</Initials></Author><Author ValidYN="Y"><LastName>Nickander</LastName><ForeName>K K</ForeName><Initials>KK</Initials></Author><Author ValidYN="Y"><LastName>Petersen</LastName><ForeName>R C</ForeName><Initials>RC</Initials></Author><Author ValidYN="Y"><LastName>Kokmen</LastName><ForeName>E</ForeName><Initials>E</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>GM 41797</GrantID><Acronym>GM</Acronym><Agency>NIGMS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS 22352</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>NS 30534</GrantID><Acronym>NS</Acronym><Agency>NINDS NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D003160">Comparative Study</PublicationType><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013487">Research Support, U.S. Gov't, P.H.S.</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>0</RegistryNumber><NameOfSubstance UI="D004873">Ergolines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>1406-18-4</RegistryNumber><NameOfSubstance UI="D014810">Vitamin E</NameOfSubstance></Chemical><Chemical><RegistryNumber>14611-51-9</RegistryNumber><NameOfSubstance UI="D012642">Selegiline</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>4Y8F71G49Q</RegistryNumber><NameOfSubstance 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UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002230">Carbidopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D003920">Diabetes Mellitus</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004873">Ergolines</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005609">Free Radicals</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="D015227">Lipid Peroxidation</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008315">Malondialdehyde</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="Y" UI="D018384">Oxidative Stress</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012642">Selegiline</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014810">Vitamin E</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000008">administration & dosage</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1995</Year><Month>9</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1995</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1995</Year><Month>9</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8552107</ArticleId><ArticleId IdType="doi">10.1002/mds.870100507</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>États-Unis</li></country></list><tree><noCountry><name sortKey="Kokmen, E" sort="Kokmen, E" uniqKey="Kokmen E" first="E" last="Kokmen">E. Kokmen</name><name sortKey="Low, P A" sort="Low, P A" uniqKey="Low P" first="P A" last="Low">P A Low</name><name sortKey="Nickander, K K" sort="Nickander, K K" uniqKey="Nickander K" first="K K" last="Nickander">K K Nickander</name><name sortKey="Petersen, R C" sort="Petersen, R C" uniqKey="Petersen R" first="R C" last="Petersen">R C Petersen</name><name sortKey="Tyce, G M" sort="Tyce, G M" uniqKey="Tyce G" first="G M" last="Tyce">G M Tyce</name><name sortKey="Uitti, R J" sort="Uitti, R J" uniqKey="Uitti R" first="R J" last="Uitti">R J Uitti</name></noCountry><country name="États-Unis"><noRegion><name sortKey="Ahlskog, J E" sort="Ahlskog, J E" uniqKey="Ahlskog J" first="J E" last="Ahlskog">J E Ahlskog</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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