2001
DOI: 10.1007/s007020170093
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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[microM 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, deltapsi(m), … Show more

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Cited by 60 publications
(45 citation statements)
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“…MAO inhibitors, at lower concentration, have shown antineuronal apoptosis and neuro-protection effects, independent of MAO inhibition (19)(20)(21)(22). Our study using higher concentrations of MAO A inhibitor, which inhibits MAO A catalytic activity, also produced effects on antineuronal apoptosis and neuro-protection.…”
Section: R1 or C-mycer Decreased Mao A Gene Expression But Increased mentioning
confidence: 47%
“…MAO inhibitors, at lower concentration, have shown antineuronal apoptosis and neuro-protection effects, independent of MAO inhibition (19)(20)(21)(22). Our study using higher concentrations of MAO A inhibitor, which inhibits MAO A catalytic activity, also produced effects on antineuronal apoptosis and neuro-protection.…”
Section: R1 or C-mycer Decreased Mao A Gene Expression But Increased mentioning
confidence: 47%
“…So far, Naoi et al demonstrated the cell death caused by salsolinol in human dopaminergic neuroblastoma SH-SY5Y cells to be apoptotic [18]. Apoptosis caused by this neurotoxin is thought to be mediated by an intracellular sequential process, loss of mitochondrial membrane potential, activation of caspases and DNA fragmentation [18,41].…”
Section: Discussionmentioning
confidence: 99%
“…In this context, it is noteworthy that nontumorigenic cell lines, such as the normal HaCaT cells, normally give a relatively low plating efficiency under culture conditions, but this is significantly increased by exposure to l-deprenyl, presumably as a consequence of the induction of Bcl-2. The compounds tested in this work were all MAO inhibitors and other propargylamine-derived MAO inhibitors, such as rasagiline (N-propargyl-[1R]-aminoindan) and N-(2-heptyl)-N-propargylamine (see Finberg et al, 1999;Huang et al, 1999;Maruyama et al, 2001) have also been shown to be neuroprotective. However, the propargylamine derivative CGP 3466 [dibenzo [b,f]oxepin-10-ylmethyl-methyl-prop-2-ynyl-amine], which is about 100 times more potent than l-deprenyl as a neuroprotective or neurorescuing agent is essentially devoid of inhibitory activity towards MAO (Kragten et al, 1998).…”
Section: Discussionmentioning
confidence: 99%