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Complex I Inhibitors Induce Dose‐Dependent Apoptosis in PC12 Cells: Relevance to Parkinson's Disease
Author(s) -
Hartley A.,
Stone J. M.,
Heron C.,
Cooper J. M.,
Schapira A. H. V.
Publication year - 1994
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1994.63051987.x
Subject(s) - substantia nigra , programmed cell death , apoptosis , rotenone , dopaminergic , parkinson's disease , necrosis , neurodegeneration , mptp , microbiology and biotechnology , mitochondrion , disease , biology , neuroscience , dopamine , chemistry , medicine , biochemistry , genetics
The mode of cell death in Parkinson's disease (PD) substantia nigra is uncertain. However, evidence is accumulating that certain of the biochemical abnormalities present in PD nigra at the time of death may precipitate apoptosis. We have investigated the mode of death induced by complex I inhibition of dopaminergic cell cultures, and our results suggest that both 1‐methyl‐4‐phenylpyridinium and rotenone cause apoptosis at low concentrations and necrosis at high concentrations. This dose‐dependent shift in the mode of cell death induced by these mitochondrial toxins may have important implications for the mechanism of neuronal cell death in PD.