Extracellular toxicity of 6-hydroxydopamine on PC12 cells
Identifieur interne : 003B91 ( Main/Curation ); précédent : 003B90; suivant : 003B92Extracellular toxicity of 6-hydroxydopamine on PC12 cells
Auteurs : D. Blum [Belgique, France] ; S. Torch [France] ; M.-F. Nissou [France] ; A.-L. Benabid [France] ; J.-M. Verna [France]Source :
- Neuroscience letters [ 0304-3940 ] ; 2000.
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- Pascal (Inist)
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Abstract
6-hydroxydopamine (6-OHDA) is usually thought to cross cell membrane through dopamine uptake transporters, to inhibit mitochondrial respiration and to generate intracellular reactive oxygen species. In this study, we show that the anti-oxidants catalase, glutathion and N-acetyl-cystein are able to reverse the toxic effects of 6-OHDA. These two latter compounds considerably slow down 6-OHDA oxidation in a cell free system suggesting a direct chemical interaction with the neurotoxin. Moreover, desipramine does not protect PC12 cells and 6-OHDA is also strongly toxic towards non-catecholaminergic C6 and NIH3T3 cells. These results thus suggest that 6-OHDA toxicity on PC12 cells mainly involves an extracellular process.
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Cell death</term>
<term>Cell line</term>
<term>Extracellular</term>
<term>In vitro</term>
<term>Neuron</term>
<term>Oxidative stress</term>
<term>Oxidopamine</term>
<term>Parkinson disease</term>
<term>Toxicity</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Extracellulaire</term>
<term>Oxidopamine</term>
<term>Toxicité</term>
<term>Lignée cellulaire</term>
<term>Neurone</term>
<term>In vitro</term>
<term>Stress oxydatif</term>
<term>Parkinson maladie</term>
<term>Mort cellulaire</term>
<term>Lignée PC12</term>
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<front><div type="abstract" xml:lang="en">6-hydroxydopamine (6-OHDA) is usually thought to cross cell membrane through dopamine uptake transporters, to inhibit mitochondrial respiration and to generate intracellular reactive oxygen species. In this study, we show that the anti-oxidants catalase, glutathion and N-acetyl-cystein are able to reverse the toxic effects of 6-OHDA. These two latter compounds considerably slow down 6-OHDA oxidation in a cell free system suggesting a direct chemical interaction with the neurotoxin. Moreover, desipramine does not protect PC12 cells and 6-OHDA is also strongly toxic towards non-catecholaminergic C6 and NIH3T3 cells. These results thus suggest that 6-OHDA toxicity on PC12 cells mainly involves an extracellular process.</div>
</front>
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