期刊
NEUROCHEMICAL RESEARCH
卷 27, 期 6, 页码 501-505出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1023/A:1019800703683
关键词
Acetyl-L-carnitine; ATP; neuronal degeneration; Abeta; oxidative stress; Alzheimer's disease
Acetyl-L-carnitine (ALCAR), normally produced in mitochondria, is a precursor of acetyl-CoA in the tricarboxylic (TCA) cycle. Since mitochondrial compromise and ATP depletion have been considered to play a role in neuronal degeneration in Alzheimer's disease (AD), we examined whether ALCAR attenuated oxidative stress and/or ATP depletion after exposure of cells to beta-amyloid (Abeta), a neurotoxic peptide that accumulates in AD brain. Differentiated SH-SY-5Y human neuroblastoma cells were exposed for 2-24 h to 20 muM Abeta in the presence and absence of 50 muM ALCAR. ALCAR attenuated oxidative stress and cell death induced by Abeta neurotoxicity. Abeta depleted ATP levels, suggesting Abeta may induce neurotoxicity in part by compromising neuronal energy. ALCAR prevented ATP depletion; therefore, ALCAR may mediate its protective effect by buffering oxidative stress and maintaining ATP levels.
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