Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells : Suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine
Identifieur interne : 000176 ( PascalFrancis/Curation ); précédent : 000175; suivant : 000177Enantio-specific induction of apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, in dopaminergic SH-SY5Y cells : Suppression of apoptosis by N-(2-heptyl)-N-methylpropargylamine
Auteurs : W. Maruyama [Japon] ; A. A. Boulton [Canada] ; B. A. Davis [Canada] ; P. Dostert [France] ; M. Naoi [Japon]Source :
- Journal of neural transmission [ 0300-9564 ] ; 2001.
Descripteurs français
- Pascal (Inist)
English descriptors
- KwdEn :
Abstract
Endogenous N-methyl(R)salsolinol, which caused parkinsonism in rats by injection in the striatum, was found to induce apoptosis in dopaminergic neuroblastoma SH-SY5Y cells. After 12-h incubation with 500 μM N-methyl(R)salsolinol, almost all the cells died with apoptosis and necrotic cell death was negligible. N-Methyl(R)salsolinol was much more potent to induce apoptosis than the (S)-enantiomer. The mechanism of apoptosis was studied in relation to changes in mitochondrial membrane potential, ΔΨm, using a fluorescent indicator, JC-1. Red fluorescence of J-aggregates representing hyperpolarized ΔΨm was found to decrease significantly within 60min after incubation with N-methyl(R)salsolinol, but not by the (S)-enantiomer at the same concentration. It suggests that mitochondria may recognize the stereo-chemical structure of N-methyl(R) salsolinol. Aliphatic propargylamines, (R)-N-(2-heptyl)-N-methylpropargyl-amine and (R)-N-(2-heptyl)propargylamine, were found to prevent ΔΨm loss and subsequent apoptosis induced by N-methyl(R)salsolinol. These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines.
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<front><div type="abstract" xml:lang="en">Endogenous N-methyl(R)salsolinol, which caused parkinsonism in rats by injection in the striatum, was found to induce apoptosis in dopaminergic neuroblastoma SH-SY5Y cells. After 12-h incubation with 500 μM N-methyl(R)salsolinol, almost all the cells died with apoptosis and necrotic cell death was negligible. N-Methyl(R)salsolinol was much more potent to induce apoptosis than the (S)-enantiomer. The mechanism of apoptosis was studied in relation to changes in mitochondrial membrane potential, ΔΨm, using a fluorescent indicator, JC-1. Red fluorescence of J-aggregates representing hyperpolarized ΔΨm was found to decrease significantly within 60min after incubation with N-methyl(R)salsolinol, but not by the (S)-enantiomer at the same concentration. It suggests that mitochondria may recognize the stereo-chemical structure of N-methyl(R) salsolinol. Aliphatic propargylamines, (R)-N-(2-heptyl)-N-methylpropargyl-amine and (R)-N-(2-heptyl)propargylamine, were found to prevent ΔΨm loss and subsequent apoptosis induced by N-methyl(R)salsolinol. These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines.</div>
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