Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine
Identifieur interne : 001E17 ( Istex/Corpus ); précédent : 001E16; suivant : 001E18Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine
Auteurs : Michael Gassen ; Aviva Gross ; Moussa B. H. YoudimSource :
- Movement Disorders [ 0885-3185 ] ; 1998-03.
English descriptors
- KwdEn :
Abstract
A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.
Url:
DOI: 10.1002/mds.870130208
Links to Exploration step
ISTEX:3334495DAC3CB893E84E891E6EFB19164120FD3CLe document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title><author><name sortKey="Gassen, Michael" sort="Gassen, Michael" uniqKey="Gassen M" first="Michael" last="Gassen">Michael Gassen</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Gross, Aviva" sort="Gross, Aviva" uniqKey="Gross A" first="Aviva" last="Gross">Aviva Gross</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Youdim, Moussa B H" sort="Youdim, Moussa B H" uniqKey="Youdim M" first="Moussa B. H." last="Youdim">Moussa B. H. Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:3334495DAC3CB893E84E891E6EFB19164120FD3C</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/mds.870130208</idno><idno type="url">https://api.istex.fr/document/3334495DAC3CB893E84E891E6EFB19164120FD3C/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001E17</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title><author><name sortKey="Gassen, Michael" sort="Gassen, Michael" uniqKey="Gassen M" first="Michael" last="Gassen">Michael Gassen</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Gross, Aviva" sort="Gross, Aviva" uniqKey="Gross A" first="Aviva" last="Gross">Aviva Gross</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author><author><name sortKey="Youdim, Moussa B H" sort="Youdim, Moussa B H" uniqKey="Youdim M" first="Moussa B. H." last="Youdim">Moussa B. H. Youdim</name><affiliation><mods:affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. 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="1998-03">1998-03</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="242">242</biblScope><biblScope unit="page" to="248">248</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">3334495DAC3CB893E84E891E6EFB19164120FD3C</idno><idno type="DOI">10.1002/mds.870130208</idno><idno type="ArticleID">MDS870130208</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Antioxidants</term><term>Apomorphine</term><term>Free radicals</term><term>Iron chelation</term><term>Neuroprotection</term><term>PC12 cells</term><term>Parkinson's disease</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.</div></front></TEI><istex><corpusName>wiley</corpusName><author><json:item><name>Michael Gassen</name><affiliations><json:string>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</json:string></affiliations></json:item><json:item><name>Aviva Gross</name><affiliations><json:string>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</json:string></affiliations></json:item><json:item><name>Moussa B. H. Youdim</name><affiliations><json:string>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</json:string></affiliations></json:item></author><subject><json:item><lang><json:string>eng</json:string></lang><value>Apomorphine</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Parkinson's disease</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Free radicals</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Antioxidants</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Iron chelation</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>PC12 cells</value></json:item><json:item><lang><json:string>eng</json:string></lang><value>Neuroprotection</value></json:item></subject><language><json:string>eng</json:string></language><abstract>A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.</abstract><qualityIndicators><score>5.481</score><pdfVersion>1.3</pdfVersion><pdfPageSize>612 x 792 pts (letter)</pdfPageSize><refBibsNative>true</refBibsNative><abstractCharCount>1090</abstractCharCount><pdfWordCount>3537</pdfWordCount><pdfCharCount>22588</pdfCharCount><pdfPageCount>7</pdfPageCount><abstractWordCount>162</abstractWordCount></qualityIndicators><title>Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title><genre><json:string>Serial article</json:string></genre><host><volume>13</volume><pages><total>7</total><last>248</last><first>242</first></pages><issn><json:string>0885-3185</json:string></issn><issue>2</issue><subject><json:item><value>Article</value></json:item></subject><genre></genre><language><json:string>unknown</json:string></language><title>Movement Disorders</title><doi><json:string>10.1002/(ISSN)1531-8257</json:string></doi></host><publicationDate>1998</publicationDate><copyrightDate>1998</copyrightDate><doi><json:string>10.1002/mds.870130208</json:string></doi><id>3334495DAC3CB893E84E891E6EFB19164120FD3C</id><fulltext><json:item><original>true</original><mimetype>application/pdf</mimetype><extension>pdf</extension><uri>https://api.istex.fr/document/3334495DAC3CB893E84E891E6EFB19164120FD3C/fulltext/pdf</uri></json:item><json:item><original>false</original><mimetype>application/zip</mimetype><extension>zip</extension><uri>https://api.istex.fr/document/3334495DAC3CB893E84E891E6EFB19164120FD3C/fulltext/zip</uri></json:item><istex:fulltextTEI uri="https://api.istex.fr/document/3334495DAC3CB893E84E891E6EFB19164120FD3C/fulltext/tei"><teiHeader type="text"><fileDesc><titleStmt><title level="a" type="main" xml:lang="en">Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title></titleStmt><publicationStmt><authority>ISTEX</authority><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><availability><p>Wiley Subscription Services, Inc., A Wiley Company</p></availability><date>1998</date></publicationStmt><sourceDesc><biblStruct type="inbook"><analytic><title level="a" type="main" xml:lang="en">Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title><author><persName><forename type="first">Michael</forename><surname>Gassen</surname></persName><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation></author><author><persName><forename type="first">Aviva</forename><surname>Gross</surname></persName><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation></author><author><persName><forename type="first">Moussa B. H.</forename><surname>Youdim</surname></persName><note type="correspondence"><p>Correspondence: Department of Pharmacology, Faculty of Medicine, Technion, P.O. Box 9649, Haifa 31096, Israel</p></note><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation></author></analytic><monogr><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="pISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><idno type="DOI">10.1002/(ISSN)1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-03"></date><biblScope unit="vol">13</biblScope><biblScope unit="issue">2</biblScope><biblScope unit="page" from="242">242</biblScope><biblScope unit="page" to="248">248</biblScope></imprint></monogr><idno type="istex">3334495DAC3CB893E84E891E6EFB19164120FD3C</idno><idno type="DOI">10.1002/mds.870130208</idno><idno type="ArticleID">MDS870130208</idno></biblStruct></sourceDesc></fileDesc><profileDesc><creation><date>1998</date></creation><langUsage><language ident="en">en</language></langUsage><abstract xml:lang="en"><p>A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.</p></abstract><textClass xml:lang="en"><keywords scheme="keyword"><list><head>Keywords</head><item><term>Apomorphine</term></item><item><term>Parkinson's disease</term></item><item><term>Free radicals</term></item><item><term>Antioxidants</term></item><item><term>Iron chelation</term></item><item><term>PC12 cells</term></item><item><term>Neuroprotection</term></item></list></keywords></textClass><textClass><keywords scheme="Journal Subject"><list><head>Article category</head><item><term>Article</term></item></list></keywords></textClass></profileDesc><revisionDesc><change when="1997-04-28">Received</change><change when="1997-08-05">Registration</change><change when="1998-03">Published</change></revisionDesc></teiHeader></istex:fulltextTEI><json:item><original>false</original><mimetype>text/plain</mimetype><extension>txt</extension><uri>https://api.istex.fr/document/3334495DAC3CB893E84E891E6EFB19164120FD3C/fulltext/txt</uri></json:item></fulltext><metadata><istex:metadataXml wicri:clean="Wiley, elements deleted: body"><istex:xmlDeclaration>version="1.0" encoding="UTF-8" standalone="yes"</istex:xmlDeclaration><istex:document><component version="2.0" type="serialArticle" xml:lang="en"><header><publicationMeta level="product"><publisherInfo><publisherName>Wiley Subscription Services, Inc., A Wiley Company</publisherName><publisherLoc>Hoboken</publisherLoc></publisherInfo><doi registered="yes">10.1002/(ISSN)1531-8257</doi><issn type="print">0885-3185</issn><issn type="electronic">1531-8257</issn><idGroup><id type="product" value="MDS"></id></idGroup><titleGroup><title type="main" xml:lang="en" sort="MOVEMENT DISORDERS">Movement Disorders</title><title type="tocForm">Movement Disorders</title><title type="subtitle">Official Journal of the Movement Disorder Society</title><title type="short">Mov. Disord.</title></titleGroup></publicationMeta><publicationMeta level="part" position="20"><doi origin="wiley" registered="yes">10.1002/mds.v13:2</doi><numberingGroup><numbering type="journalVolume" number="13">13</numbering><numbering type="journalIssue">2</numbering></numberingGroup><coverDate startDate="1998-03">March 1998</coverDate></publicationMeta><publicationMeta level="unit" type="article" position="8" status="forIssue"><doi origin="wiley" registered="yes">10.1002/mds.870130208</doi><idGroup><id type="unit" value="MDS870130208"></id></idGroup><countGroup><count type="pageTotal" number="7"></count></countGroup><titleGroup><title type="articleCategory">Article</title><title type="tocHeading1">Articles</title></titleGroup><copyright ownership="thirdParty">Copyright © 1998 Movement Disorder Society</copyright><eventGroup><event type="manuscriptReceived" date="1997-04-28"></event><event type="manuscriptRevised" date="1997-08-01"></event><event type="manuscriptAccepted" date="1997-08-05"></event><event type="firstOnline" date="2004-11-04"></event><event type="publishedOnlineFinalForm" date="2004-11-04"></event><event type="xmlConverted" agent="Converter:JWSART34_TO_WML3G version:2.3.2 mode:FullText source:HeaderRef result:HeaderRef" date="2010-03-09"></event><event type="xmlConverted" agent="Converter:WILEY_ML3G_TO_WILEY_ML3GV2 version:3.8.8" date="2014-02-02"></event><event type="xmlConverted" agent="Converter:WML3G_To_WML3G version:4.1.7 mode:FullText,remove_FC" date="2014-10-31"></event></eventGroup><numberingGroup><numbering type="pageFirst">242</numbering><numbering type="pageLast">248</numbering></numberingGroup><correspondenceTo>Department of Pharmacology, Faculty of Medicine, Technion, P.O. Box 9649, Haifa 31096, Israel</correspondenceTo><linkGroup><link type="toTypesetVersion" href="file:MDS.MDS870130208.pdf"></link></linkGroup></publicationMeta><contentMeta><countGroup><count type="figureTotal" number="7"></count><count type="tableTotal" number="0"></count><count type="referenceTotal" number="27"></count></countGroup><titleGroup><title type="main" xml:lang="en">Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H<sub>2</sub>O<sub>2</sub> and 6‐hydroxydopamine</title><title type="short" xml:lang="en">APOMORPHINE PROTECTS PC12 CELLS FROM H<sub>2</sub>O<sub>2</sub> AND 6‐HYDROXYDOPAMINE</title></titleGroup><creators><creator xml:id="au1" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Michael</givenNames><familyName>Gassen</familyName></personName></creator><creator xml:id="au2" creatorRole="author" affiliationRef="#af1"><personName><givenNames>Aviva</givenNames><familyName>Gross</familyName></personName></creator><creator xml:id="au3" creatorRole="author" affiliationRef="#af1" corresponding="yes"><personName><givenNames>Moussa B. H.</givenNames><familyName>Youdim</familyName></personName></creator></creators><affiliationGroup><affiliation xml:id="af1" countryCode="IL" type="organization"><unparsedAffiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</unparsedAffiliation></affiliation></affiliationGroup><keywordGroup xml:lang="en" type="author"><keyword xml:id="kwd1">Apomorphine</keyword><keyword xml:id="kwd2">Parkinson's disease</keyword><keyword xml:id="kwd3">Free radicals</keyword><keyword xml:id="kwd4">Antioxidants</keyword><keyword xml:id="kwd5">Iron chelation</keyword><keyword xml:id="kwd6">PC12 cells</keyword><keyword xml:id="kwd7">Neuroprotection</keyword></keywordGroup><abstractGroup><abstract type="main" xml:lang="en"><title type="main">Abstract</title><p>A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D<sub>1</sub>/D<sub>2</sub>‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H<sub>2</sub>O<sub>2</sub> (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H<sub>2</sub>O<sub>2</sub> toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off <sc>L</sc>‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.</p></abstract></abstractGroup></contentMeta></header></component></istex:document></istex:metadataXml><!--Version 0.6 générée le 3-12-2015--><mods version="3.6"><titleInfo lang="en"><title>Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine</title></titleInfo><titleInfo type="abbreviated" lang="en"><title>APOMORPHINE PROTECTS PC12 CELLS FROM H2O2 AND 6‐HYDROXYDOPAMINE</title></titleInfo><titleInfo type="alternative" contentType="CDATA" lang="en"><title>Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H</title></titleInfo><name type="personal"><namePart type="given">Michael</namePart><namePart type="family">Gassen</namePart><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Aviva</namePart><namePart type="family">Gross</namePart><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Moussa B. H.</namePart><namePart type="family">Youdim</namePart><affiliation>Department of Pharmacology, Eve Topf and National Parkinson's Foundation Centers for Neurodegenerative Disease, Bruce Rappaport Family Research Institute, Faculty of Medicine, Technion, Haifa, Israel</affiliation><description>Correspondence: Department of Pharmacology, Faculty of Medicine, Technion, P.O. Box 9649, Haifa 31096, Israel</description><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre authority="originalCategForm">article</genre><originInfo><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><place><placeTerm type="text">Hoboken</placeTerm></place><dateIssued encoding="w3cdtf">1998-03</dateIssued><dateCaptured encoding="w3cdtf">1997-04-28</dateCaptured><dateValid encoding="w3cdtf">1997-08-05</dateValid><copyrightDate encoding="w3cdtf">1998</copyrightDate></originInfo><language><languageTerm type="code" authority="rfc3066">en</languageTerm><languageTerm type="code" authority="iso639-2b">eng</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType><extent unit="figures">7</extent><extent unit="references">27</extent></physicalDescription><abstract lang="en">A significant body of evidence has been provided to support the hypothesis that oxidant stress may be responsible for the degeneration of dopaminergic neurons in the substantia nigra pars compacta in Parkinson's disease. Apomorphine, a dopamine D1/D2‐receptor agonist in the clinical therapy of Parkinson's disease, has been found to be a potent antioxidant and to prevent free radical reaction in rat brain mitochondrial fraction. In this article we show that 1–10 μM of apomorphine protects rat pheochromocytoma (PC12) cells from the toxic effects of H2O2 (0.6 mM) and the neurotoxin 6‐hydroxydopamine (150 μM). These effects were not exhibited by ascorbic acid, desferal, lisuride, or bromocriptine. Although pergolide exhibited some protection of PC12 cells against H2O2 toxicity, it was not as potent as apomorphine. In light of the present findings and the clinical reports that parkinsonian patients on long‐term apomorphine stabilize clinically and can be weaned off L‐dopa, one may assume that apomorphine can exert a neuroprotective activity via its potent antioxidant properties.</abstract><subject lang="en"><genre>Keywords</genre><topic>Apomorphine</topic><topic>Parkinson's disease</topic><topic>Free radicals</topic><topic>Antioxidants</topic><topic>Iron chelation</topic><topic>PC12 cells</topic><topic>Neuroprotection</topic></subject><relatedItem type="host"><titleInfo><title>Movement Disorders</title><subTitle>Official Journal of the Movement Disorder Society</subTitle></titleInfo><titleInfo type="abbreviated"><title>Mov. Disord.</title></titleInfo><subject><genre>article category</genre><topic>Article</topic></subject><identifier type="ISSN">0885-3185</identifier><identifier type="eISSN">1531-8257</identifier><identifier type="DOI">10.1002/(ISSN)1531-8257</identifier><identifier type="PublisherID">MDS</identifier><part><date>1998</date><detail type="volume"><caption>vol.</caption><number>13</number></detail><detail type="issue"><caption>no.</caption><number>2</number></detail><extent unit="pages"><start>242</start><end>248</end><total>7</total></extent></part></relatedItem><identifier type="istex">3334495DAC3CB893E84E891E6EFB19164120FD3C</identifier><identifier type="DOI">10.1002/mds.870130208</identifier><identifier type="ArticleID">MDS870130208</identifier><accessCondition type="use and reproduction" contentType="copyright">Copyright © 1998 Movement Disorder Society</accessCondition><recordInfo><recordOrigin>Wiley Subscription Services, Inc., A Wiley Company</recordOrigin><recordContentSource>WILEY</recordContentSource></recordInfo></mods></metadata><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Santé/explor/MovDisordV3/Data/Istex/Corpus
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 001E17 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Istex/Corpus/biblio.hfd -nk 001E17 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Santé
|area= MovDisordV3
|flux= Istex
|étape= Corpus
|type= RBID
|clé= ISTEX:3334495DAC3CB893E84E891E6EFB19164120FD3C
|texte= Apomorphine enantiomers protect cultured pheochromocytoma (PC12) cells from oxidative stress induced by H2O2 and 6‐hydroxydopamine
}}
| This area was generated with Dilib version V0.6.23. |  |