Cysteinyl‐glycine reduction as marker for levodopa‐induced oxidative stress in Parkinson's disease patients
Identifieur interne : 001723 ( Main/Exploration ); précédent : 001722; suivant : 001724Cysteinyl‐glycine reduction as marker for levodopa‐induced oxidative stress in Parkinson's disease patients
Auteurs : Thomas Müller [Allemagne] ; Siegfried Muhlack [Allemagne]Source :
- Movement Disorders [ 0885-3185 ] ; 2011-02-15.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
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, Glycine, Human, Humans, Levodopa, Levodopa (blood), Levodopa (pharmacology), Levodopa (therapeutic use), Male, Nervous system diseases, Oxidative Stress (drug effects), Oxidative stress, Parkinson Disease (drug therapy), Parkinson Disease (physiopathology), Parkinson disease, Parkinson's disease, Tyrosine (analogs & derivatives), Tyrosine (blood), cysteinyl‐glycine, oxidative stress.
- 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. © 2011 Movement Disorder Society
Url:
DOI: 10.1002/mds.23384
Affiliations:
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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="2011-02-15">2011-02-15</date><biblScope unit="vol">26</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="543">543</biblScope><biblScope unit="page" to="546">546</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">A20639D34C0132483F05D6B9AE227F86DBDF0AFB</idno><idno type="DOI">10.1002/mds.23384</idno><idno type="ArticleID">MDS23384</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Analysis of Variance</term><term>Antiparkinson Agents (blood)</term><term>Antiparkinson Agents (pharmacology)</term><term>Antiparkinson Agents (therapeutic use)</term><term>Carbidopa (blood)</term><term>Carbidopa (pharmacology)</term><term>Carbidopa (therapeutic use)</term><term>Dipeptides (blood)</term><term>Female</term><term>Glycine</term><term>Human</term><term>Humans</term><term>Levodopa</term><term>Levodopa (blood)</term><term>Levodopa (pharmacology)</term><term>Levodopa (therapeutic use)</term><term>Male</term><term>Nervous system diseases</term><term>Oxidative Stress (drug effects)</term><term>Oxidative stress</term><term>Parkinson Disease (drug therapy)</term><term>Parkinson Disease (physiopathology)</term><term>Parkinson disease</term><term>Parkinson's disease</term><term>Tyrosine (analogs & derivatives)</term><term>Tyrosine (blood)</term><term>cysteinyl‐glycine</term><term>oxidative stress</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Tyrosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antiparkinson Agents</term><term>Carbidopa</term><term>Dipeptides</term><term>Levodopa</term><term>Tyrosine</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Antiparkinson Agents</term><term>Carbidopa</term><term>Levodopa</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antiparkinson Agents</term><term>Carbidopa</term><term>Levodopa</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Parkinson Disease</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Analysis of Variance</term><term>Female</term><term>Humans</term><term>Male</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Glycine</term><term>Homme</term><term>Lévodopa</term><term>Maladie de Parkinson</term><term>Pathologie du système nerveux</term><term>Stress oxydatif</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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. © 2011 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Berlin</li></region><settlement><li>Berlin</li></settlement></list><tree><country name="Allemagne"><region name="Berlin"><name sortKey="Muller, Thomas" sort="Muller, Thomas" uniqKey="Muller T" first="Thomas" last="Müller">Thomas Müller</name></region><name sortKey="Muhlack, Siegfried" sort="Muhlack, Siegfried" uniqKey="Muhlack S" first="Siegfried" last="Muhlack">Siegfried Muhlack</name><name sortKey="Muller, Thomas" sort="Muller, Thomas" uniqKey="Muller T" first="Thomas" last="Müller">Thomas Müller</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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