Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.
Identifieur interne : 004955 ( Ncbi/Merge ); 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
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Fahn</name></author><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></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1993">1993</date><idno type="RBID">pubmed:8341291</idno><idno type="pmid">8341291</idno><idno type="doi">10.1002/mds.870080305</idno><idno type="wicri:Area/PubMed/Corpus">004C19</idno><idno type="wicri:Area/PubMed/Curation">004C19</idno><idno type="wicri:Area/PubMed/Checkpoint">004C85</idno><idno type="wicri:Area/Ncbi/Merge">004955</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.</title><author><name sortKey="Pardo, B" sort="Pardo, B" uniqKey="Pardo B" first="B" last="Pardo">B. Pardo</name><affiliation wicri:level="3"><nlm:affiliation>Department of Research, Centro Ramón y Cajal, Madrid, Spain.</nlm:affiliation><country xml:lang="fr">Espagne</country><wicri:regionArea>Department of Research, Centro Ramón y Cajal, Madrid</wicri:regionArea><placeName><settlement type="city">Madrid</settlement><region nuts="2" type="region">Communauté de Madrid</region></placeName></affiliation></author><author><name sortKey="Mena, M A" sort="Mena, M A" uniqKey="Mena M" first="M A" last="Mena">M A Mena</name></author><author><name sortKey="Fahn, S" sort="Fahn, S" uniqKey="Fahn S" first="S" last="Fahn">S. Fahn</name></author><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></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="1993" type="published">1993</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Ascorbic Acid (pharmacology)</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>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></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></keywords><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></keywords><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></keywords></textClass></profileDesc></teiHeader><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></TEI><pubmed><MedlineCitation Owner="NLM" Status="MEDLINE"><PMID Version="1">8341291</PMID><DateCreated><Year>1993</Year><Month>09</Month><Day>02</Day></DateCreated><DateCompleted><Year>1993</Year><Month>09</Month><Day>02</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>8</Volume><Issue>3</Issue><PubDate><Year>1993</Year><Month>Jul</Month></PubDate></JournalIssue><Title>Movement disorders : official journal of the Movement Disorder Society</Title><ISOAbbreviation>Mov. Disord.</ISOAbbreviation></Journal><ArticleTitle>Ascorbic acid protects against levodopa-induced neurotoxicity on a catecholamine-rich human neuroblastoma cell line.</ArticleTitle><Pagination><MedlinePgn>278-84</MedlinePgn></Pagination><Abstract><AbstractText>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.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Pardo</LastName><ForeName>B</ForeName><Initials>B</Initials><AffiliationInfo><Affiliation>Department of Research, Centro Ramón y Cajal, Madrid, Spain.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Mena</LastName><ForeName>M A</ForeName><Initials>MA</Initials></Author><Author ValidYN="Y"><LastName>Fahn</LastName><ForeName>S</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>García de Yébenes</LastName><ForeName>J</ForeName><Initials>J</Initials></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</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="D002395">Catecholamines</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D011809">Quinones</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>PQ6CK8PD0R</RegistryNumber><NameOfSubstance UI="D001205">Ascorbic Acid</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001205">Ascorbic Acid</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000494">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001921">Brain</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D001932">Brain Neoplasms</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002395">Catecholamines</DescriptorName><QualifierName MajorTopicYN="Y" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D002460">Cell Line</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D004347">Drug Interactions</DescriptorName></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="Y" UI="Q000633">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D008297">Male</DescriptorName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D009447">Neuroblastoma</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName><QualifierName MajorTopicYN="Y" UI="Q000473">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D010300">Parkinson Disease</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000188">drug therapy</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D011809">Quinones</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000378">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName MajorTopicYN="N" UI="D012642">Selegiline</DescriptorName><QualifierName MajorTopicYN="N" UI="Q000494">pharmacology</QualifierName></MeshHeading></MeshHeadingList></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="pubmed"><Year>1993</Year><Month>7</Month><Day>1</Day></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>1</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>1993</Year><Month>7</Month><Day>1</Day><Hour>0</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">8341291</ArticleId><ArticleId IdType="doi">10.1002/mds.870080305</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>Espagne</li></country><region><li>Communauté de Madrid</li></region><settlement><li>Madrid</li></settlement></list><tree><noCountry><name sortKey="Fahn, S" sort="Fahn, S" uniqKey="Fahn S" first="S" last="Fahn">S. Fahn</name><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><name sortKey="Mena, M A" sort="Mena, M A" uniqKey="Mena M" first="M A" last="Mena">M A Mena</name></noCountry><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></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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