Mitochondria determine the survival and death in apoptosis by an endogenous neurotoxin, N-methyl(R)salsolinol, and neuroprotection by propargylamines

These results indicate that mitochondria are the site to determine the cell death induced by neurotoxins and the neuroprotection by anti-apoptotic propargylamines

M. Naoi; W. Maruyama; Y. Akao; H. Yi

2003

Scholarcy highlights

  • In neurodegenerative disorders, such as Parkinson's disease, selective neuronal death characterizes clinical signs and symptoms
  • Apoptosis was reported to be a common type of cell death in some disorders, and well-controlled apoptotic cascade is proposed to be a target of neuroprotective therapy
  • In human dopaminergic SH-SY5Y cells, apoptosis was initiated by decline in mitochondrial membrane potential, and anti-apoptotic Bcl-2 family protein regulated apoptotic signal transduction
  • The role of mitochondria and the involvement of Bcl-2 in apoptosis and neuroprotection were clearly demonstrated using isolated mitochondria. These results indicate that mitochondria are the site to determine the cell death induced by neurotoxins and the neuroprotection by anti-apoptotic propargylamines

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