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

These results suggest that mitochondria play a key role in the induction of apoptosis by the neurotoxin and the prevention by aliphatic propargylamines

W. Maruyama; A. A. Boulton; B. A. Davis; P. Dostert; M. Naoi

2003

Scholarcy highlights

  • 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
  • The mechanism of apoptosis was studied in relation to changes in mitochondrial membrane potential, ΔΨm, using a fluorescent indicator, JC-1
  • Aliphatic propargylamines,-N-(2-heptyl)-N-methylpropargyl-amine and-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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