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- W2101899991 abstract "Le but de ce travail était d’évaluer la toxicité du 3,4-dihydroxyphénylacétaldéhyde (DOPAL) in vitro et in vivo. Cet aldéhyde résulte de l’action des monoamine-oxydases (MAO) sur la dopamine (DA) et il est généralement oxydé en acide 3,4-dihydroxyphénylacétique (DOPAC) par les aldéhyde déshydrogénases cérébrales (ALDH), ou éventuellement réduit par les aldéhyde/aldose réductases. In vitro, des cellules SH-SY5Y ont été incubées avec de la DA et du disulfirame (DSF), un inhibiteur irréversible d’ALDH. Le test MTT révèle qu’un traitement de 24 h avec la DA 104 M et/ou le DSF106 M suivi d’une incubation de 24 h dans un milieu sans réactif se traduit par une potentialisation de l’effet toxique de chacun des réactifs par le second. Des mesures HPLC démontent que cette association induit une formation précoce de DOPAL qui pourrait se traduire par une toxicité cellulaire différée de quelques dizaines d’heures. Pour les essais in vivo, des rats mâles Sprague-Dawley ont été traités par la L-DOPA/bensérazide, qui accroît la production de DOPAL par les MAO, et le DSF. Une administration aigue de DSF (100 mg/kg i.p.) et de L-DOPA/bensérazide (100 mg/kg + 25 mg/kg, 24 h plus tard) augmente significativement le taux de DOPAL striatal. Cependant, un traitement de 30 jours par le DSF (100 mg/kg i.p., une fois tous les deux jours) et la L-DOPA/bensérazide (100 mg/kg + 25 mg/kg, deux fois par jour) n’affecte pas deux index de l’intégrité des terminaisons striatales des neurones dopaminergiques (le contenu striatal de DA et la liaison au transporteur vésiculaire présent dans ces terminaisons). Ces résultats ne confortent pas l’hypothèse d’une toxicité du DOPAL et vont à l’encontre d’une toxicité de la L-DOPA. This work was carried out in order to evaluate the in vitro and invivo toxicity of 3,4-dihydroxyphenylacetaldehyde (DOPAL). This aldehyde is formed from dopamine (DA) by monoamine oxidases (MAO) and is mainly oxidised to 3,4-dihydroxyphenylacetic acid by brain aldehyde dehydrogenases (ALDH), or eventually reduced to 3,4-dihydroxyphenylethanol by aldose/aldehyde reductases. In vitro, catecholaminergic SH-SY5Y cells were incubated with DA and disulfiram (DSF), an irreversible inhibitor of ALDH. As evidenced by MTT assays, a 24-h treatment with 10-4 M DA and/or 10-6 M DSF followed by a 24-h incubation in a drug-free medium evidenced that the toxicity of each of these drugs was potentiated by the second drug. HPLC measurements demonstrated that this drug association induced an early DOPAL production that could result in a delayed cell toxicity. For in vivo studies, male Sprague-Dawley rats were treated with L-DOPA-benserazide, which increases the production of DOPAL by MAO, and DSF. An acute injection of DSF (100mg/kg i.p.) and L-DOPA/benserazide (100mg/kg+25mg/kg, 24h later) significantly increased the DOPAL striatal level. However, a 30-day treatment with DSF (100mg/kg i.p., once every two days) and L-DOPA/benserazide (100mg/kg+25mg/kg, twice a day) did not affect both indexes used to assess the integrity of the nigro-striatal dopaminergic terminals (i.e. the striatal content in DA and the binding to the vesicular monoamine transporter on striatal membranes). These results do not support the hypothesis of a DOPAL toxicity and argue against the toxicity of L-DOPA therapy." @default.
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- W2101899991 date "2004-09-01" @default.
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- W2101899991 title "Recherche d’une toxicité du 3,4-dihydroxyphénylacétaldéhyde (DOPAL) in vitro et in vivo" @default.
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