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• W2077342956 abstract "There is growing evidence that apoptotic mechanisms underlie the neurodegeneration leading to Parkinson's disease. 1-Methyl-4-phenylpyridinium ion (MPP+), the active metabolite of the parkinsonism-inducing drug MPTP, induced apoptosis in cultures of human SH-SY5Y neuroblastoma cells. Nuclear fragmentation, DNA laddering, and a 20% decrease in viability were seen after a 4-day incubation with 5 μM MPP+. Cell viability decreased by 40% at 100 μM MPP+, but the degree of apoptosis was not correlatively increased. The MPP+-induced apoptosis was completely prevented by the broad caspase inhibitor zVAD.fmk but not by the caspase-8 inhibitor IETD.fmk. Furthermore, MPP+ had no effect on the levels of Fas or Fas-L, suggesting lack of activation of the Fas-L/Fas/caspase-8 pathway of apoptosis. There was no evidence of mitochondrial dysfunction at 5 μM MPP+: No differences were seen in transmembrane potential or in cytochrome c release from controls. At 100 μM MPP+, the mitochondrial potential decreased, and cytoplasmic cytochrome c and caspase-9 activation increased slightly. At both low and high concentrations of MPP+, VDVADase and DEVDase activities increased. We conclude that MPP+ can induce caspase-mediated apoptosis, which is prevented by caspase inhibition, at concentrations lower than those needed to trigger mitochondrial dysfunction and closer to those found in the brains of MPTP-treated animals. J. Neurosci. Res. 63:421–428, 2001. © 2001 Wiley-Liss, Inc." @default.
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• W2077342956 date "2001-01-01" @default.
• W2077342956 modified "2023-09-27" @default.
• W2077342956 title "Low concentrations of 1-methyl-4-phenylpyridinium ion induce caspase-mediated apoptosis in human SH-SY5Y neuroblastoma cells" @default.
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• W2077342956 doi "https://doi.org/10.1002/1097-4547(20010301)63:5<421::aid-jnr1037>3.0.co;2-4" @default.
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