Extracellular toxicity of 6-hydroxydopamine on PC12 cells
Identifieur interne : 001392 ( PascalFrancis/Corpus ); précédent : 001391; suivant : 001393Extracellular toxicity of 6-hydroxydopamine on PC12 cells
Auteurs : D. Blum ; S. Torch ; M.-F. Nissou ; A.-L. Benabid ; J.-M. VernaSource :
- Neuroscience letters [ 0304-3940 ] ; 2000.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
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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Format Inist (serveur)
NO : | PASCAL 00-0242455 INIST |
---|---|
ET : | Extracellular toxicity of 6-hydroxydopamine on PC12 cells |
AU : | BLUM (D.); TORCH (S.); NISSOU (M.-F.); BENABID (A.-L.); VERNA (J.-M.) |
AF : | ULB-Campus Erasme, Laboratory of Neurophysiology, Department of Neurosciences, 808 Rte de Lennik, CP601/1070 Brussels/Belgique (1 aut.); NDP-LAPSEN, CHU Michallon, Pavillon de Neurologie, BP 217/38043 Grenoble/France (1 aut., 2 aut., 3 aut., 5 aut.); INSERM U318, Neurobiologie Préclinique, CHU Michallon, Pavillon B, BP 217/38043 Grenoble/France (4 aut.) |
DT : | Publication en série; Niveau analytique |
SO : | Neuroscience letters; ISSN 0304-3940; Coden NELED5; Irlande; Da. 2000; Vol. 283; No. 3; Pp. 193-196; Bibl. 16 ref. |
LA : | Anglais |
EA : | 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. |
CC : | 002A25C |
FD : | Extracellulaire; Oxidopamine; Toxicité; Lignée cellulaire; Neurone; In vitro; Stress oxydatif; Parkinson maladie; Mort cellulaire; Lignée PC12 |
ED : | Extracellular; Oxidopamine; Toxicity; Cell line; Neuron; In vitro; Oxidative stress; Parkinson disease; Cell death |
SD : | Extracelular; Oxidopamina; Toxicidad; Línea celular; Neurona; In vitro; Stress oxidativo; Parkinson enfermedad; Muerte celular |
LO : | INIST-17240.354000087126230080 |
ID : | 00-0242455 |
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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>
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<EA>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.</EA>
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