Cysteinyl-glycine reduction as marker for levodopa-induced oxidative stress in Parkinson's disease patients.
Identifieur interne : 001333 ( PubMed/Corpus ); précédent : 001332; suivant : 001334Cysteinyl-glycine reduction as marker for levodopa-induced oxidative stress in Parkinson's disease patients.
Auteurs : Thomas Müller ; Siegfried MuhlackSource :
- Movement disorders : official journal of the Movement Disorder Society [ 1531-8257 ] ; 2011.
English descriptors
- KwdEn :
- Analysis of Variance, Antiparkinson Agents (blood), Antiparkinson Agents (pharmacology), Antiparkinson Agents (therapeutic use), Carbidopa (blood), Carbidopa (pharmacology), Carbidopa (therapeutic use), Dipeptides (blood), Female, Humans, Levodopa (blood), Levodopa (pharmacology), Levodopa (therapeutic use), Male, Oxidative Stress (drug effects), Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Tyrosine (analogs & derivatives), Tyrosine (blood).
- MESH :
- chemical , analogs & derivatives : Tyrosine.
- chemical , blood : Antiparkinson Agents, Carbidopa, Dipeptides, Levodopa, Tyrosine.
- chemical , pharmacology : Antiparkinson Agents, Carbidopa, Levodopa.
- chemical , therapeutic use : Antiparkinson Agents, Carbidopa, Levodopa.
- drug effects : Oxidative Stress.
- drug therapy : Parkinson Disease.
- physiopathology : Parkinson Disease.
- Analysis of Variance, Female, Humans, Male.
Abstract
Oxidative stress is influenced by the thiol homeostasis, which determines the redox milieu. One of its components is Cysteinyl-glycine (Cys-Gly) generation, as its metabolic precursor is the free radicals scavenging glutathione. Levodopa is under suspicion to promote oxidative stress via the turnover of its metabolite dopamine in abundant mitochondria. Objective was to investigate the impact of levodopa on Cys-Gly plasma metabolism. Fifteen patients with Parkinson's disease orally took one 200-mg levodopa/50-mg carbidopa (CD) containing tablet. Levodopa, its derivative 3-O-methyldopa (3-OMD), and free Cys-Gly were measured at baseline, 60 and 120 min following levodopa/CD administration. Cys-gly concentrations decreased, levodopa and 3-OMD levels increased. Inverse relationships appeared between computed differences of Cys-gly and 3-OMD bioavailability. We conclude that Cys-Gly decline is related to levodopa metabolism to 3-OMD. Cys-Gly decay may result from the alternative transformation of glutathione to its oxidized form glutathione dissulfide as consequence of free radical scavenging.
DOI: 10.1002/mds.23384
PubMed: 21462263
Links to Exploration step
pubmed:21462263Le document en format XML
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One of its components is Cysteinyl-glycine (Cys-Gly) generation, as its metabolic precursor is the free radicals scavenging glutathione. Levodopa is under suspicion to promote oxidative stress via the turnover of its metabolite dopamine in abundant mitochondria. Objective was to investigate the impact of levodopa on Cys-Gly plasma metabolism. Fifteen patients with Parkinson's disease orally took one 200-mg levodopa/50-mg carbidopa (CD) containing tablet. Levodopa, its derivative 3-O-methyldopa (3-OMD), and free Cys-Gly were measured at baseline, 60 and 120 min following levodopa/CD administration. Cys-gly concentrations decreased, levodopa and 3-OMD levels increased. Inverse relationships appeared between computed differences of Cys-gly and 3-OMD bioavailability. We conclude that Cys-Gly decline is related to levodopa metabolism to 3-OMD. Cys-Gly decay may result from the alternative transformation of glutathione to its oxidized form glutathione dissulfide as consequence of free radical scavenging.</div></front></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">21462263</PMID><DateCreated><Year>2011</Year><Month>04</Month><Day>04</Day></DateCreated><DateCompleted><Year>2011</Year><Month>07</Month><Day>29</Day></DateCompleted><DateRevised><Year>2013</Year><Month>11</Month><Day>21</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1531-8257</ISSN><JournalIssue CitedMedium="Internet"><Volume>26</Volume><Issue>3</Issue><PubDate><Year>2011</Year><Month>Feb</Month><Day>15</Day></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Cysteinyl-glycine reduction as marker for levodopa-induced oxidative stress in Parkinson's disease patients.</ArticleTitle><Pagination><MedlinePgn>543-6</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1002/mds.23384</ELocationID><Abstract><AbstractText>Oxidative stress is influenced by the thiol homeostasis, which determines the redox milieu. One of its components is Cysteinyl-glycine (Cys-Gly) generation, as its metabolic precursor is the free radicals scavenging glutathione. Levodopa is under suspicion to promote oxidative stress via the turnover of its metabolite dopamine in abundant mitochondria. Objective was to investigate the impact of levodopa on Cys-Gly plasma metabolism. Fifteen patients with Parkinson's disease orally took one 200-mg levodopa/50-mg carbidopa (CD) containing tablet. Levodopa, its derivative 3-O-methyldopa (3-OMD), and free Cys-Gly were measured at baseline, 60 and 120 min following levodopa/CD administration. Cys-gly concentrations decreased, levodopa and 3-OMD levels increased. Inverse relationships appeared between computed differences of Cys-gly and 3-OMD bioavailability. We conclude that Cys-Gly decline is related to levodopa metabolism to 3-OMD. Cys-Gly decay may result from the alternative transformation of glutathione to its oxidized form glutathione dissulfide as consequence of free radical scavenging.</AbstractText><CopyrightInformation>Copyright © 2010 Movement Disorder Society.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Müller</LastName><ForeName>Thomas</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Department of Neurology, St. Joseph Hospital Berlin-Weissensee, Berlin, Germany. th.mueller@alexius.de</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Muhlack</LastName><ForeName>Siegfried</ForeName><Initials>S</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</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="D004151">Dipeptides</NameOfSubstance></Chemical><Chemical><RegistryNumber>384644SZ9T</RegistryNumber><NameOfSubstance UI="C028505">cysteinylglycine</NameOfSubstance></Chemical><Chemical><RegistryNumber>42HK56048U</RegistryNumber><NameOfSubstance UI="D014443">Tyrosine</NameOfSubstance></Chemical><Chemical><RegistryNumber>46627O600J</RegistryNumber><NameOfSubstance UI="D007980">Levodopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>MNX7R8C5VO</RegistryNumber><NameOfSubstance UI="D002230">Carbidopa</NameOfSubstance></Chemical><Chemical><RegistryNumber>V3O7J20DWN</RegistryNumber><NameOfSubstance UI="C008404">3-methoxytyrosine</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000704">Analysis of Variance</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D000978">Antiparkinson Agents</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002230">Carbidopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004151">Dipeptides</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000097">blood</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D005260">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D006801">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D007980">Levodopa</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName><QualifierName MajorTopicYN="N" UI="Q000627">therapeutic use</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D018384">Oxidative Stress</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000187">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000503">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D014443">Tyrosine</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000031">analogs & derivatives</QualifierName><QualifierName MajorTopicYN="N" UI="Q000097">blood</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="entrez"><Year>2011</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2011</Year><Month>4</Month><Day>5</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2011</Year><Month>7</Month><Day>30</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="doi">10.1002/mds.23384</ArticleId><ArticleId IdType="pubmed">21462263</ArticleId></ArticleIdList></PubmedData></pubmed></record>Pour manipuler ce document sous Unix (Dilib)
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