A review of the pharmacology of selegiline
Identifieur interne : 002725 ( Main/Exploration ); précédent : 002724; suivant : 002726A review of the pharmacology of selegiline
Auteurs : E. H. Heinonen [Finlande] ; R. Lammintausta [Finlande]Source :
- Acta Neurologica Scandinavica [ 0001-6314 ] ; 1991-10.
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Abstract
Selegiline (1‐deprenyl) is an irreversible inhibitor of monoamine oxidase (MAO) type B. Because in the human brain, dopamine is metabolised mainly by MAO‐B, selegiline increases dopamine content in the central nervous system. Besides the inhibition of MAO‐B, selegiline also inhibits the uptake of dopamine and noradrenaline into presynaptic nerve and increases the turnover of dopamine. Thanks to these properties, selegiline significantly potentiates the pharmacological effects of levodopa. These favourable characteristics have been applied in the treatment of Parkinson's disease using selegiline both with levodopa and alone. Unlike earlier MAO‐inhibitors, selegiline does not potentiate the hypertensive effects of tyramine. This is due to the selectivity to MAO‐B, leaving intestinal MAO‐A intact, and also due to the fact that selegiline inhibits the uptake of tyramine into neurons. Selegiline can prevent the parkinsonism caused by MPTP in animals; similar findings have been reported with other toxins like 6‐OHDA and DSP‐4, that destroys noradrenergic nuclei. Furthermore, selegiline reduces oxidative stress caused by degradation of dopamine and increases free radical elimination by enhancing superoxide dismutase and catalase activity. These findings may be important when considering the possible neuroprotective effects of selegiline. Besides the basic pharmacology also the interactions and pharmacokinetics of selegiline are reviewed in this article.
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DOI: 10.1111/j.1600-0404.1991.tb05020.x
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Heinonen</name><affiliation wicri:level="3"><country xml:lang="fr">Finlande</country><wicri:regionArea>Orion Corporation Farmos, Research and Development, Turku</wicri:regionArea><placeName><settlement type="city">Turku</settlement><region type="région" nuts="2">Finlande occidentale</region></placeName></affiliation></author><author><name sortKey="Lammintausta, R" sort="Lammintausta, R" uniqKey="Lammintausta R" first="R." last="Lammintausta">R. Lammintausta</name><affiliation wicri:level="3"><country xml:lang="fr">Finlande</country><wicri:regionArea>Orion Corporation Farmos, Research and Development, Turku</wicri:regionArea><placeName><settlement type="city">Turku</settlement><region type="région" nuts="2">Finlande occidentale</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Acta Neurologica Scandinavica</title><idno type="ISSN">0001-6314</idno><idno type="eISSN">1600-0404</idno><imprint><publisher>Blackwell Publishing Ltd</publisher><pubPlace>Oxford, UK</pubPlace><date type="published" when="1991-10">1991-10</date><biblScope unit="volume">84</biblScope><biblScope unit="issue">S136</biblScope><biblScope unit="page" from="44">44</biblScope><biblScope unit="page" to="59">59</biblScope></imprint><idno type="ISSN">0001-6314</idno></series><idno type="istex">0F587C66D98C964DA1E294BCCD22488A3D1C60AD</idno><idno type="DOI">10.1111/j.1600-0404.1991.tb05020.x</idno><idno type="ArticleID">ANE44</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0001-6314</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>MAO</term><term>MPTP</term><term>free radicals</term><term>interactions</term><term>levoamphetamine</term><term>levodopa</term><term>phenylethylamine</term><term>selegiline</term><term>tyramine</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Selegiline (1‐deprenyl) is an irreversible inhibitor of monoamine oxidase (MAO) type B. Because in the human brain, dopamine is metabolised mainly by MAO‐B, selegiline increases dopamine content in the central nervous system. Besides the inhibition of MAO‐B, selegiline also inhibits the uptake of dopamine and noradrenaline into presynaptic nerve and increases the turnover of dopamine. Thanks to these properties, selegiline significantly potentiates the pharmacological effects of levodopa. These favourable characteristics have been applied in the treatment of Parkinson's disease using selegiline both with levodopa and alone. Unlike earlier MAO‐inhibitors, selegiline does not potentiate the hypertensive effects of tyramine. This is due to the selectivity to MAO‐B, leaving intestinal MAO‐A intact, and also due to the fact that selegiline inhibits the uptake of tyramine into neurons. Selegiline can prevent the parkinsonism caused by MPTP in animals; similar findings have been reported with other toxins like 6‐OHDA and DSP‐4, that destroys noradrenergic nuclei. Furthermore, selegiline reduces oxidative stress caused by degradation of dopamine and increases free radical elimination by enhancing superoxide dismutase and catalase activity. These findings may be important when considering the possible neuroprotective effects of selegiline. Besides the basic pharmacology also the interactions and pharmacokinetics of selegiline are reviewed in this article.</div></front></TEI><affiliations><list><country><li>Finlande</li></country><region><li>Finlande occidentale</li></region><settlement><li>Turku</li></settlement></list><tree><country name="Finlande"><region name="Finlande occidentale"><name sortKey="Heinonen, E H" sort="Heinonen, E H" uniqKey="Heinonen E" first="E. H." last="Heinonen">E. H. Heinonen</name></region><name sortKey="Lammintausta, R" sort="Lammintausta, R" uniqKey="Lammintausta R" first="R." last="Lammintausta">R. Lammintausta</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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