Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission
Identifieur interne : 000221 ( France/Analysis ); précédent : 000220; suivant : 000222Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission
Auteurs : Federico A. Dajas-Bailador [Uruguay, Royaume-Uni] ; Marcelo Asencio [Chili] ; Carolina Bonilla [Uruguay] ; Ma. Cecilia Scorza [Uruguay] ; Carolina Echeverry [Uruguay] ; Miguel Reyes-Parada [Uruguay] ; Rodolfo Silveira [Uruguay] ; Philippe Protais [France] ; Graeme Russell [Nouvelle-Zélande] ; Bruce K. Cassels [Chili] ; Federico Dajas [Uruguay]Source :
- General Pharmacology [ 0306-3623 ] ; 1998.
Abstract
The dopaminergic and antioxidant properties of pukateine [(R)-11-hydroxy-1,2-methylenedioxyaporphine, PUK], a natural aporphine derivative, were analyzed in the rat central nervous system. At dopamine (DA) D1 ([3H]-SCH 23390) and D2 ([3H]-raclopride) binding sites, PUK showed IC50 values in the submicromolar range (0.4 and 0.6 μM, respectively). When the uptake of tritiated dopamine was assayed by using a synaptosomal preparation, PUK showed an IC50 = 46 μM. In 6-hydroxydopamine unilaterally denervated rats, PUK (8 mg/kg but not 4 mg/kg) elicited a significant contralateral circling, a behavior classically associated with a dopaminergic agonist action. When perfused through a microdialysis probe inserted into the striatum, PUK (340 μM) induced a significant increase in dopamine levels. In vitro experiments with a crude rat brain mitochondrial suspension showed that PUK did not affect monoamine oxidase activities, at concentrations as high as 100 μM. PUK potently IC50 = 15 μM and dose-dependently inhibited the basal lipid peroxidation of a rat brain membrane preparation. As a whole, PUK showed a unique profile of action, comprising an increase in extracellular DA, an agonist-like interaction with DA receptors, and antioxidant activity. Thus, PUK may be taken as a lead compound for the development of novel therapeutic strategies for Parkinson disease.
Url:
DOI: 10.1016/S0306-3623(98)00210-9
Affiliations:
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Tel./Fax: 598 2 4872603</wicri:noCountry></affiliation><affiliation wicri:level="1"><country wicri:rule="url">Royaume-Uni</country></affiliation></author><author><name sortKey="Asencio, Marcelo" sort="Asencio, Marcelo" uniqKey="Asencio M" first="Marcelo" last="Asencio">Marcelo Asencio</name><affiliation wicri:level="1"><country xml:lang="fr">Chili</country><wicri:regionArea>Department of Chemistry, Faculty of Sciences, Universidad de Chile, Santiago</wicri:regionArea><wicri:noRegion>Santiago</wicri:noRegion></affiliation></author><author><name sortKey="Bonilla, Carolina" sort="Bonilla, Carolina" uniqKey="Bonilla C" first="Carolina" last="Bonilla">Carolina Bonilla</name><affiliation wicri:level="1"><country xml:lang="fr">Uruguay</country><wicri:regionArea>Division of Neurochemistry, Instituto de Investigaciones Biológicas Clemente Estable, Av. 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At dopamine (DA) D1 ([3H]-SCH 23390) and D2 ([3H]-raclopride) binding sites, PUK showed IC50 values in the submicromolar range (0.4 and 0.6 μM, respectively). When the uptake of tritiated dopamine was assayed by using a synaptosomal preparation, PUK showed an IC50 = 46 μM. In 6-hydroxydopamine unilaterally denervated rats, PUK (8 mg/kg but not 4 mg/kg) elicited a significant contralateral circling, a behavior classically associated with a dopaminergic agonist action. When perfused through a microdialysis probe inserted into the striatum, PUK (340 μM) induced a significant increase in dopamine levels. In vitro experiments with a crude rat brain mitochondrial suspension showed that PUK did not affect monoamine oxidase activities, at concentrations as high as 100 μM. PUK potently IC50 = 15 μM and dose-dependently inhibited the basal lipid peroxidation of a rat brain membrane preparation. As a whole, PUK showed a unique profile of action, comprising an increase in extracellular DA, an agonist-like interaction with DA receptors, and antioxidant activity. Thus, PUK may be taken as a lead compound for the development of novel therapeutic strategies for Parkinson disease.</div></front></TEI><affiliations><list><country><li>Chili</li><li>France</li><li>Nouvelle-Zélande</li><li>Royaume-Uni</li><li>Uruguay</li></country><region><li>Région Bourgogne</li></region><settlement><li>Rouen</li></settlement><orgName><li>Université de Rouen</li></orgName></list><tree><country name="Uruguay"><noRegion><name sortKey="Dajas Bailador, Federico A" sort="Dajas Bailador, Federico A" uniqKey="Dajas Bailador F" first="Federico A" last="Dajas-Bailador">Federico A. Dajas-Bailador</name></noRegion><name sortKey="Bonilla, Carolina" sort="Bonilla, Carolina" uniqKey="Bonilla C" first="Carolina" last="Bonilla">Carolina Bonilla</name><name sortKey="Dajas, Federico" sort="Dajas, Federico" uniqKey="Dajas F" first="Federico" last="Dajas">Federico Dajas</name><name sortKey="Echeverry, Carolina" sort="Echeverry, Carolina" uniqKey="Echeverry C" first="Carolina" last="Echeverry">Carolina Echeverry</name><name sortKey="Reyes Parada, Miguel" sort="Reyes Parada, Miguel" uniqKey="Reyes Parada M" first="Miguel" last="Reyes-Parada">Miguel Reyes-Parada</name><name sortKey="Scorza, Ma Cecilia" sort="Scorza, Ma Cecilia" uniqKey="Scorza M" first="Ma. Cecilia" last="Scorza">Ma. 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