Apparent antioxidant effect of l-deprenyl on hydroxyl radical formation and nigral injury elicited by MPP+ in vivo
Identifieur interne : 002563 ( Main/Exploration ); précédent : 002562; suivant : 002564Apparent antioxidant effect of l-deprenyl on hydroxyl radical formation and nigral injury elicited by MPP+ in vivo
Auteurs : Ruey-Meei Wu [Taïwan, États-Unis] ; Chuang C. Chiueh [États-Unis] ; Agu Pert [États-Unis] ; Dennis L. Murphy [États-Unis]Source :
- European Journal of Pharmacology [ 0014-2999 ] ; 1993.
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Abstract
Using a modified microdialysis procedure, we confirmed that intrastriatal administration of 1-methyl-4-phenylpyridinium ion (MPP+) induced a sustained overflow of dopamine accompanied by increased formation of hydroxyl free radicals (.OH) as reflected by salicylate hydroxylation. Pretreatment with l-deprenyl (selegiline 60 pmol, intrastriatal perfusion) significantly decreased the.OH formation elicited by MPP+ (75 nmol). There was a small decrease of dopamine efflux and an insignificant change of the ratio of 3,4-dihydroxyphenylacetic acid (DOPAC)/dopamine following l-deprenyl pretreatment. These in vivo findings support prior in vitro data that an unique antioxidant property of l-deprenyl may be independent of its inhibition of type B monoamine oxidase. In addition, intranigral co-administration of l-deprenyl (4.2 nmol) with MPP+ (4.2 nmol) completely protected nigral neurons from probable oxidative injuries induced by MPP+ (4.2 nmol), as reflected by a near 50% loss of striatal dopamine ipsilateral to the side of infusion of drug into the substantia nigra. This apparent neuroprotective effect of l-deprenyl on midbrain nigral neurons was also confirmed by histological findings. The present in vivo data clearly demonstrate that l-deprenyl can protect nigral neurons against dopamien neurotoxicity produced by MPP+, as suggested by an earlier in vitro study. Thus, l-deprenyl can preserve the function of MPP+-damaged nigral neurons perhaps by its apparent antioxidant property in addition to its blockade of the bioactivation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to toxic pyridinium metabolites by type B monoamine oxidase.
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DOI: 10.1016/0014-2999(93)90181-G
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Murphy</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:0DF226AB4794DC3FC2895FFC5BAC4DB161EC20E3</idno><date when="1993" year="1993">1993</date><idno type="doi">10.1016/0014-2999(93)90181-G</idno><idno type="url">https://api.istex.fr/document/0DF226AB4794DC3FC2895FFC5BAC4DB161EC20E3/fulltext/pdf</idno><idno type="wicri:Area/Main/Corpus">001923</idno><idno type="wicri:Area/Main/Curation">001675</idno><idno type="wicri:Area/Main/Exploration">002563</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Apparent antioxidant effect of l-deprenyl on hydroxyl radical formation and nigral injury elicited by MPP+ in vivo</title><author><name sortKey="Wu, Ruey Meei" sort="Wu, Ruey Meei" uniqKey="Wu R" first="Ruey-Meei" last="Wu">Ruey-Meei Wu</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, National Taiwan University Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Clinical Science and National Institute of Mental Health, National Institutes of Health, Building 10, Room 3D-41 Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Chiueh, Chuang C" sort="Chiueh, Chuang C" uniqKey="Chiueh C" first="Chuang C." last="Chiueh">Chuang C. Chiueh</name><affiliation><wicri:noCountry code="no comma">Corresponding author. Tel. (1)-301-496-9820; fax (1)-301-402-0188.</wicri:noCountry></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Laboratory of Clinical Science and National Institute of Mental Health, National Institutes of Health, Building 10, Room 3D-41 Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Pert, Agu" sort="Pert, Agu" uniqKey="Pert A" first="Agu" last="Pert">Agu Pert</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Biological Psychiatry Branch, National Institute of Mental Health, National Institutes of Health, Building 10, Room 3D-41, Bethesda, MD 20892</wicri:regionArea><placeName><region type="state">Maryland</region></placeName></affiliation></author><author><name sortKey="Murphy, Dennis L" sort="Murphy, Dennis L" uniqKey="Murphy D" first="Dennis L." last="Murphy">Dennis L. 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Pretreatment with l-deprenyl (selegiline 60 pmol, intrastriatal perfusion) significantly decreased the.OH formation elicited by MPP+ (75 nmol). There was a small decrease of dopamine efflux and an insignificant change of the ratio of 3,4-dihydroxyphenylacetic acid (DOPAC)/dopamine following l-deprenyl pretreatment. These in vivo findings support prior in vitro data that an unique antioxidant property of l-deprenyl may be independent of its inhibition of type B monoamine oxidase. In addition, intranigral co-administration of l-deprenyl (4.2 nmol) with MPP+ (4.2 nmol) completely protected nigral neurons from probable oxidative injuries induced by MPP+ (4.2 nmol), as reflected by a near 50% loss of striatal dopamine ipsilateral to the side of infusion of drug into the substantia nigra. This apparent neuroprotective effect of l-deprenyl on midbrain nigral neurons was also confirmed by histological findings. The present in vivo data clearly demonstrate that l-deprenyl can protect nigral neurons against dopamien neurotoxicity produced by MPP+, as suggested by an earlier in vitro study. Thus, l-deprenyl can preserve the function of MPP+-damaged nigral neurons perhaps by its apparent antioxidant property in addition to its blockade of the bioactivation of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) to toxic pyridinium metabolites by type B monoamine oxidase.</div></front></TEI><affiliations><list><country><li>Taïwan</li><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="Taïwan"><noRegion><name sortKey="Wu, Ruey Meei" sort="Wu, Ruey Meei" uniqKey="Wu R" first="Ruey-Meei" last="Wu">Ruey-Meei Wu</name></noRegion></country><country name="États-Unis"><region name="Maryland"><name sortKey="Wu, Ruey Meei" sort="Wu, Ruey Meei" uniqKey="Wu R" first="Ruey-Meei" last="Wu">Ruey-Meei Wu</name></region><name sortKey="Chiueh, Chuang C" sort="Chiueh, Chuang C" uniqKey="Chiueh C" first="Chuang C." last="Chiueh">Chuang C. Chiueh</name><name sortKey="Murphy, Dennis L" sort="Murphy, Dennis L" uniqKey="Murphy D" first="Dennis L." last="Murphy">Dennis L. Murphy</name><name sortKey="Pert, Agu" sort="Pert, Agu" uniqKey="Pert A" first="Agu" last="Pert">Agu Pert</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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