Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.
Identifieur interne : 004955 ( Ncbi/Checkpoint ); précédent : 004954; suivant : 004956Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.
Auteurs : B. Pardo [Espagne] ; M A Mena ; S. Fahn ; J. García De YébenesSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 1993.
English descriptors
- KwdEn :
- Ascorbic Acid (pharmacology), Brain (metabolism), Brain (pathology), Brain Neoplasms (metabolism), Brain Neoplasms (pathology), Catecholamines (metabolism), Cell Line, Drug Interactions, Female, Humans, Levodopa (toxicity), Male, Neuroblastoma (metabolism), Neuroblastoma (pathology), Parkinson Disease (drug therapy), Quinones (metabolism), Selegiline (pharmacology).
- 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 x 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 x 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.
DOI: 10.1002/mds.870080305
PubMed: 8341291
Affiliations:
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pubmed:8341291Le document en format XML
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<author><name sortKey="Pardo, B" sort="Pardo, B" uniqKey="Pardo B" first="B" last="Pardo">B. Pardo</name>
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<author><name sortKey="Mena, M A" sort="Mena, M A" uniqKey="Mena M" first="M A" last="Mena">M A Mena</name>
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<author><name sortKey="Fahn, S" sort="Fahn, S" uniqKey="Fahn S" first="S" last="Fahn">S. Fahn</name>
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<author><name sortKey="Garcia De Yebenes, J" sort="Garcia De Yebenes, J" uniqKey="Garcia De Yebenes J" first="J" last="García De Yébenes">J. García De Yébenes</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.</title>
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<affiliation wicri:level="3"><nlm:affiliation>Department of Research, Centro Ramón y Cajal, Madrid, Spain.</nlm:affiliation>
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<author><name sortKey="Mena, M A" sort="Mena, M A" uniqKey="Mena M" first="M A" last="Mena">M A Mena</name>
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<author><name sortKey="Fahn, S" sort="Fahn, S" uniqKey="Fahn S" first="S" last="Fahn">S. Fahn</name>
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<author><name sortKey="Garcia De Yebenes, J" sort="Garcia De Yebenes, J" uniqKey="Garcia De Yebenes J" first="J" last="García De Yébenes">J. García De Yébenes</name>
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<series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title>
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<term>Brain Neoplasms (metabolism)</term>
<term>Brain Neoplasms (pathology)</term>
<term>Catecholamines (metabolism)</term>
<term>Cell Line</term>
<term>Drug Interactions</term>
<term>Female</term>
<term>Humans</term>
<term>Levodopa (toxicity)</term>
<term>Male</term>
<term>Neuroblastoma (metabolism)</term>
<term>Neuroblastoma (pathology)</term>
<term>Parkinson Disease (drug therapy)</term>
<term>Quinones (metabolism)</term>
<term>Selegiline (pharmacology)</term>
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<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Catecholamines</term>
<term>Quinones</term>
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<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>
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<term>Brain Neoplasms</term>
<term>Neuroblastoma</term>
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<term>Brain Neoplasms</term>
<term>Neuroblastoma</term>
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<front><div type="abstract" xml:lang="en">Levodopa, at concentrations of 0.25 x 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 x 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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<name sortKey="Mena, M A" sort="Mena, M A" uniqKey="Mena M" first="M A" last="Mena">M A Mena</name>
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<country name="Espagne"><region name="Communauté de Madrid"><name sortKey="Pardo, B" sort="Pardo, B" uniqKey="Pardo B" first="B" last="Pardo">B. Pardo</name>
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