Toxicity of Annonaceae for dopaminergic neurons: Potential role in atypical parkinsonism in Guadeloupe
Identifieur interne : 000B32 ( Istex/Curation ); précédent : 000B31; suivant : 000B33Toxicity of Annonaceae for dopaminergic neurons: Potential role in atypical parkinsonism in Guadeloupe
Auteurs : Annie Lannuzel [France] ; Patrick P. Michel [France] ; Dominique Caparros-Lefebvre [France] ; Jacqueline Abaul ; Reynald Hocquemiller ; Merle Ruberg [France]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-01.
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Abstract
In the French West Indies there is an abnormally high frequency of levodopa‐resistant parkinsonism, suggested to be caused by consumption of fruit and infusions of tropical plants, especially Annona muricata (corossol, soursop). To determine whether toxic substances from this plant can cause the neuronal degeneration or dysfunction underlying the syndrome, we exposed mesencephalic dopaminergic neurons in culture to the total extract (totum) of alkaloids from Annona muricata root bark and to two of the most abundant subfractions, coreximine and reticuline. After 24 hours, 50% of dopaminergic neurons degenerated with 18 μg/ml totum, 4.3 μg/ml (13 μM) coreximine, or 100 μg/ml (304 μM) reticuline. The effects of the alkaloid totum were not restricted to the population of dopaminergic cells since GABAergic neurons were also affected by the treatment. Nuclei in dying neurons showed DNA condensation or fragmentation, suggesting that neuronal death occurred by apoptosis. Cell death was not excitotoxic and did not require toxin uptake by the dopamine transporter. Neurodegeneration was attenuated by increasing the concentration of glucose in the culture medium, which also reduced the effect of the dopaminergic neurotoxin MPP+, a mitochondrial respiratory chain inhibitor. Toxin withdrawal after short‐term exposure arrested cell death. Acute treatment with totum, coreximine, or reticuline reversibly inhibited dopamine uptake by a mechanism that was distinct from that causing neuronal death. GABA uptake was not reduced under the same conditions. This study suggests that alkaloids from A. muricata can modulate the function and the survival of dopaminergic nerve cells in vitro. It is therefore conceivable that repeated consumption could cause the neuronal dysfunction and degeneration underlying the West Indian parkinsonian syndrome. © 2002 Movement Disorder Society.
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DOI: 10.1002/mds.1246
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Jacqueline Abaul<affiliation><mods:affiliation>Laboratoire COVACHIM, UFR des Sciences Exactes et Naturelles, Université des Antilles et de la Guyane, Pointe‐à‐Pitre, Guadeloupe; France</mods:affiliation><wicri:noCountry code="subField">Guadeloupe; France</wicri:noCountry></affiliation><affiliation><mods:affiliation>Laboratoire de Pharmacognosie, UPRES‐A 8076 CNRS, Faculté de Pharmacie, Châtenay‐Malabry; France</mods:affiliation><wicri:noCountry code="subField">Châtenay‐Malabry; France</wicri:noCountry></affiliation>Le document en format XML
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Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>John Wiley & Sons, Inc.</publisher><pubPlace>New York</pubPlace><date type="published" when="2002-01">2002-01</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="84">84</biblScope><biblScope unit="page" to="90">90</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">AD39733D539A8E3F82FD91ECED1722F0F74B48A5</idno><idno type="DOI">10.1002/mds.1246</idno><idno type="ArticleID">MDS1246</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>apoptosis</term><term>movement disorders</term><term>neurotoxicology</term><term>parkinsonism</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">In the French West Indies there is an abnormally high frequency of levodopa‐resistant parkinsonism, suggested to be caused by consumption of fruit and infusions of tropical plants, especially Annona muricata (corossol, soursop). To determine whether toxic substances from this plant can cause the neuronal degeneration or dysfunction underlying the syndrome, we exposed mesencephalic dopaminergic neurons in culture to the total extract (totum) of alkaloids from Annona muricata root bark and to two of the most abundant subfractions, coreximine and reticuline. After 24 hours, 50% of dopaminergic neurons degenerated with 18 μg/ml totum, 4.3 μg/ml (13 μM) coreximine, or 100 μg/ml (304 μM) reticuline. The effects of the alkaloid totum were not restricted to the population of dopaminergic cells since GABAergic neurons were also affected by the treatment. Nuclei in dying neurons showed DNA condensation or fragmentation, suggesting that neuronal death occurred by apoptosis. Cell death was not excitotoxic and did not require toxin uptake by the dopamine transporter. Neurodegeneration was attenuated by increasing the concentration of glucose in the culture medium, which also reduced the effect of the dopaminergic neurotoxin MPP+, a mitochondrial respiratory chain inhibitor. Toxin withdrawal after short‐term exposure arrested cell death. Acute treatment with totum, coreximine, or reticuline reversibly inhibited dopamine uptake by a mechanism that was distinct from that causing neuronal death. GABA uptake was not reduced under the same conditions. This study suggests that alkaloids from A. muricata can modulate the function and the survival of dopaminergic nerve cells in vitro. It is therefore conceivable that repeated consumption could cause the neuronal dysfunction and degeneration underlying the West Indian parkinsonian syndrome. © 2002 Movement Disorder Society.</div></front></TEI></record>Pour manipuler ce document sous Unix (Dilib)
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