Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells : Suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine
Identifieur interne : 003328 ( Main/Exploration ); précédent : 003327; suivant : 003329Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells : Suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine
Auteurs : W. Maruyama [Japon] ; A. A. Boulton [Canada] ; B. A. Davis [Canada] ; P. Dostert [France] ; M. Naoi [Japon]Source :
- Journal of neural transmission [ 0300-9564 ] ; 2001.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Endogenous N-methyl(R)salsolinol, which caused parkinsonism in rats by injection in the striatum, was found to induce apoptosis in dopaminergic neuroblastoma SH-SY5Y cells. After 12-h incubation with 500 μM N-methyl(R)salsolinol, almost all the cells died with apoptosis and necrotic cell death was negligible. N-Methyl(R)salsolinol was much more potent to induce apoptosis than the (S)-enantiomer. The mechanism of apoptosis was studied in relation to changes in mitochondrial membrane potential, ΔΨm, using a fluorescent indicator, JC-1. Red fluorescence of J-aggregates representing hyperpolarized ΔΨm was found to decrease significantly within 60min after incubation with N-methyl(R)salsolinol, but not by the (S)-enantiomer at the same concentration. It suggests that mitochondria may recognize the stereo-chemical structure of N-methyl(R) salsolinol. Aliphatic propargylamines, (R)-N-(2-heptyl)-N-methylpropargyl-amine and (R)-N-(2-heptyl)propargylamine, were found to prevent ΔΨm loss and subsequent apoptosis induced by N-methyl(R)salsolinol. These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines.
Affiliations:
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Maruyama</name><affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Laboratory of Biochemistry and Metabolism, Department of Basic Gerontology, National Institute for Longevity Sciences</s1><s2>Obu, Aichi</s2><s3>JPN</s3><sZ>1 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Obu, Aichi</wicri:noRegion></affiliation></author><author><name sortKey="Boulton, A A" sort="Boulton, A A" uniqKey="Boulton A" first="A. A." last="Boulton">A. A. Boulton</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Neuropsychiatry Research Unit, Department of Psychiatry, University of Saskatchewan</s1><s2>Saskatoon, Saskatchewan</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Saskatoon, Saskatchewan</wicri:noRegion></affiliation></author><author><name sortKey="Davis, B A" sort="Davis, B A" uniqKey="Davis B" first="B. A." last="Davis">B. A. Davis</name><affiliation wicri:level="1"><inist:fA14 i1="02"><s1>Neuropsychiatry Research Unit, Department of Psychiatry, University of Saskatchewan</s1><s2>Saskatoon, Saskatchewan</s2><s3>CAN</s3><sZ>2 aut.</sZ><sZ>3 aut.</sZ></inist:fA14><country>Canada</country><wicri:noRegion>Saskatoon, Saskatchewan</wicri:noRegion></affiliation></author><author><name sortKey="Dostert, P" sort="Dostert, P" uniqKey="Dostert P" first="P." last="Dostert">P. Dostert</name><affiliation wicri:level="3"><inist:fA14 i1="03"><s1>Biotrial</s1><s2>Rennes</s2><s3>FRA</s3><sZ>4 aut.</sZ></inist:fA14><country>France</country><placeName><region type="region">Région Bretagne</region><region type="old region">Région Bretagne</region><settlement type="city">Rennes</settlement></placeName></affiliation></author><author><name sortKey="Naoi, M" sort="Naoi, M" uniqKey="Naoi M" first="M." last="Naoi">M. Naoi</name><affiliation wicri:level="1"><inist:fA14 i1="04"><s1>Department of Brain Sciences, Institute of Applied Biochemistry, Yagi Memorial Park</s1><s2>Mitake, Gifu</s2><s3>JPN</s3><sZ>5 aut.</sZ></inist:fA14><country>Japon</country><wicri:noRegion>Mitake, Gifu</wicri:noRegion></affiliation></author></analytic><series><title level="j" type="main">Journal of neural transmission</title><title level="j" type="abbreviated">J. neural transm.</title><idno type="ISSN">0300-9564</idno><imprint><date when="2001">2001</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Journal of neural transmission</title><title level="j" type="abbreviated">J. neural transm.</title><idno type="ISSN">0300-9564</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Apoptosis</term><term>Dopaminergic neuron</term><term>Enantiomer</term><term>Membrane potential</term><term>Mitochondria</term><term>Neurotoxin</term><term>Parkinson disease</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Neurotoxine</term><term>Enantiomère</term><term>Neurone dopaminergique</term><term>Apoptose</term><term>Potentiel membrane</term><term>Mitochondrie</term><term>Parkinson maladie</term><term>Salsolinol(N-méthyl)</term><term>Lignée SHSY5Y</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Endogenous N-methyl(R)salsolinol, which caused parkinsonism in rats by injection in the striatum, was found to induce apoptosis in dopaminergic neuroblastoma SH-SY5Y cells. After 12-h incubation with 500 μM N-methyl(R)salsolinol, almost all the cells died with apoptosis and necrotic cell death was negligible. N-Methyl(R)salsolinol was much more potent to induce apoptosis than the (S)-enantiomer. The mechanism of apoptosis was studied in relation to changes in mitochondrial membrane potential, ΔΨm, using a fluorescent indicator, JC-1. Red fluorescence of J-aggregates representing hyperpolarized ΔΨm was found to decrease significantly within 60min after incubation with N-methyl(R)salsolinol, but not by the (S)-enantiomer at the same concentration. It suggests that mitochondria may recognize the stereo-chemical structure of N-methyl(R) salsolinol. Aliphatic propargylamines, (R)-N-(2-heptyl)-N-methylpropargyl-amine and (R)-N-(2-heptyl)propargylamine, were found to prevent ΔΨm loss and subsequent apoptosis induced by N-methyl(R)salsolinol. These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines.</div></front></TEI><affiliations><list><country><li>Canada</li><li>France</li><li>Japon</li></country><region><li>Région Bretagne</li></region><settlement><li>Rennes</li></settlement></list><tree><country name="Japon"><noRegion><name sortKey="Maruyama, W" sort="Maruyama, W" uniqKey="Maruyama W" first="W." last="Maruyama">W. Maruyama</name></noRegion><name sortKey="Naoi, M" sort="Naoi, M" uniqKey="Naoi M" first="M." last="Naoi">M. Naoi</name></country><country name="Canada"><noRegion><name sortKey="Boulton, A A" sort="Boulton, A A" uniqKey="Boulton A" first="A. A." last="Boulton">A. A. Boulton</name></noRegion><name sortKey="Davis, B A" sort="Davis, B A" uniqKey="Davis B" first="B. A." last="Davis">B. A. Davis</name></country><country name="France"><region name="Région Bretagne"><name sortKey="Dostert, P" sort="Dostert, P" uniqKey="Dostert P" first="P." last="Dostert">P. Dostert</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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