Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, is mediated by activation of caspase 3

Yukihiko Akao, Yoshihito Nakagawa, Wakako Maruyama, Tsutomu Takahashi, Makoto Naoi

Research output: Contribution to journalArticle

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Abstract

An endogenous neurotoxin, N-methyl(R)salsolinol, has been proved to be involved in the pathogenesis of Parkinson's disease. Increased level of N- methyl(R)salsolinol in the cerebrospinal fluid and high activity of its synthesizing (R)salsolinol N-methyltransferase in lymphocytes were confirmed in the majority of parkinsonian patients. Recently this neurotoxin was found to induce apoptosis in human dopaminergic neuroblastoma SH-SY5Y cells. In this study, we tried to elucidate the intracellular mechanism of apoptosis induced by N-methyl(R)salsolinol, and proved activation of caspase 3 after incubation with this toxin by Western blot analysis. Further, a caspase 3 inhibitor, acetyl-L-aspartyl-L-glutamyl-L-valyl-L-aspartic aldehyde, prevented the nucleosomal DNA fragmentation completely. These results demonstrate that caspase 3 mediates apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, which may cause apoptotic cell death of dopamine neurons in Parkinson's disease.

Original languageEnglish
Pages (from-to)153-156
Number of pages4
JournalNeuroscience Letters
Volume267
Issue number3
DOIs
Publication statusPublished - 04-06-1999

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Neurotoxins
Caspase 3
Apoptosis
Parkinson Disease
Caspase Inhibitors
Dopaminergic Neurons
DNA Fragmentation
Neuroblastoma
Aldehydes
Cerebrospinal Fluid
Cell Death
Western Blotting
Lymphocytes
salsoline

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Akao, Yukihiko ; Nakagawa, Yoshihito ; Maruyama, Wakako ; Takahashi, Tsutomu ; Naoi, Makoto. / Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, is mediated by activation of caspase 3. In: Neuroscience Letters. 1999 ; Vol. 267, No. 3. pp. 153-156.
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Apoptosis induced by an endogenous neurotoxin, N-methyl(R)salsolinol, is mediated by activation of caspase 3. / Akao, Yukihiko; Nakagawa, Yoshihito; Maruyama, Wakako; Takahashi, Tsutomu; Naoi, Makoto.

In: Neuroscience Letters, Vol. 267, No. 3, 04.06.1999, p. 153-156.

Research output: Contribution to journalArticle

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