Ascorbic acid protects against levodopa‐induced neurotoxicity on a catecholamine‐rich human neuroblastoma cell line
Identifieur interne : 005E18 ( Main/Exploration ); précédent : 005E17; suivant : 005E19Ascorbic acid protects against levodopa‐induced neurotoxicity on a catecholamine‐rich human neuroblastoma cell line
Auteurs : Beatriz Pardo [Espagne] ; María Angeles Mena [Espagne] ; Stanley Fahn [États-Unis] ; Justo García De Yébenes [Espagne]Source :
- Movement Disorders [ 0885-3185 ] ; 1993.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Homme.
English descriptors
- KwdEn :
- Antiparkinson agent, Ascorbic Acid (pharmacology), Ascorbic acid, Brain (metabolism), Brain (pathology), Brain Neoplasms (metabolism), Brain Neoplasms (pathology), Catecholamines (metabolism), Cell Line, Cell culture, Dopa, Drug Interactions, Female, Human, Humans, Levodopa, Levodopa (toxicity), Male, Neuroblastoma, Neuroblastoma (metabolism), Neuroblastoma (pathology), Neuroblastoma cell, Neurotoxicity, Parkinson Disease (drug therapy), Prevention, Quinones (metabolism), Selegiline (pharmacology), Toxicity, Tumor.
- MESH :
- chemical , metabolism : Catecholamines, Quinones.
- chemical , pharmacology : Ascorbic Acid, Selegiline.
- drug therapy : Parkinson Disease.
- metabolism : Brain, Brain Neoplasms, Neuroblastoma.
- pathology : Brain, Brain Neoplasms, Neuroblastoma.
- chemical , toxicity : Levodopa.
- Cell Line, Drug Interactions, Female, Humans, Male.
Abstract
Levodopa, at concentrations of 0.25 × 10−4 M or larger, is toxic for the human neuroblastoma cell NB69. Toxicity is associated with high levels of quinones, increased activity of complex II‐III, and lack of changes of complex I of the mitochondrial respiratory chain. Deprenyl, which does not alter the production of quinones, has a partial protective effect. Tocopherol, 23 or 115 × 10−6 M, lacks significant preventive effect on levodopa toxicity, but ascorbic acid, 10−3 M, prevents levodopa toxicity and quinone formation. Deprenyl, 10−4 M, provides additional protection in cultures treated with levodopa and ascorbic acid. Our results indicate that ascorbic acid and deprenyl prevent levodopa neurotoxicity by unrelated mechanisms. Both compounds should be considered as complementary drugs to test for slowing the progression of Parkinson's disease.
Url:
DOI: 10.1002/mds.870080305
Affiliations:
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Le document en format XML
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<author><name sortKey="Fahn, Stanley" sort="Fahn, Stanley" uniqKey="Fahn S" first="Stanley" last="Fahn">Stanley Fahn</name>
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<author><name sortKey="De Yebenes, Justo Garcia" sort="De Yebenes, Justo Garcia" uniqKey="De Yebenes J" first="Justo García" last="De Yébenes">Justo García De Yébenes</name>
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<title level="j" type="sub">Official Journal of the Movement Disorder Society</title>
<title level="j" type="abbrev">Mov. Disord.</title>
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<term>Ascorbic Acid (pharmacology)</term>
<term>Ascorbic acid</term>
<term>Brain (metabolism)</term>
<term>Brain (pathology)</term>
<term>Brain Neoplasms (metabolism)</term>
<term>Brain Neoplasms (pathology)</term>
<term>Catecholamines (metabolism)</term>
<term>Cell Line</term>
<term>Cell culture</term>
<term>Dopa</term>
<term>Drug Interactions</term>
<term>Female</term>
<term>Human</term>
<term>Humans</term>
<term>Levodopa</term>
<term>Levodopa (toxicity)</term>
<term>Male</term>
<term>Neuroblastoma</term>
<term>Neuroblastoma (metabolism)</term>
<term>Neuroblastoma (pathology)</term>
<term>Neuroblastoma cell</term>
<term>Neurotoxicity</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Prevention</term>
<term>Quinones (metabolism)</term>
<term>Selegiline (pharmacology)</term>
<term>Toxicity</term>
<term>Tumor</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catecholamines</term>
<term>Quinones</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Ascorbic Acid</term>
<term>Selegiline</term>
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<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Parkinson Disease</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Brain</term>
<term>Brain Neoplasms</term>
<term>Neuroblastoma</term>
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<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term>
<term>Brain Neoplasms</term>
<term>Neuroblastoma</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Levodopa</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Cell Line</term>
<term>Drug Interactions</term>
<term>Female</term>
<term>Humans</term>
<term>Male</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Antiparkinsonien</term>
<term>Ascorbique acide</term>
<term>Culture cellulaire</term>
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<term>Neuroblastome</term>
<term>Prévention</term>
<term>Toxicité</term>
<term>Tumeur</term>
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<front><div type="abstract" xml:lang="en">Levodopa, at concentrations of 0.25 × 10−4 M or larger, is toxic for the human neuroblastoma cell NB69. Toxicity is associated with high levels of quinones, increased activity of complex II‐III, and lack of changes of complex I of the mitochondrial respiratory chain. Deprenyl, which does not alter the production of quinones, has a partial protective effect. Tocopherol, 23 or 115 × 10−6 M, lacks significant preventive effect on levodopa toxicity, but ascorbic acid, 10−3 M, prevents levodopa toxicity and quinone formation. Deprenyl, 10−4 M, provides additional protection in cultures treated with levodopa and ascorbic acid. Our results indicate that ascorbic acid and deprenyl prevent levodopa neurotoxicity by unrelated mechanisms. Both compounds should be considered as complementary drugs to test for slowing the progression of Parkinson's disease.</div>
</front>
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<country name="États-Unis"><region name="État de New York"><name sortKey="Fahn, Stanley" sort="Fahn, Stanley" uniqKey="Fahn S" first="Stanley" last="Fahn">Stanley Fahn</name>
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