期刊
ACTA BIOCHIMICA ET BIOPHYSICA SINICA
卷 38, 期 11, 页码 765-772出版社
BLACKWELL PUBLISHING
DOI: 10.1111/j.1745-7270.2006.00228.x
关键词
Alzheimer's disease; Cu(II)-A beta 1-40 complex; neuron injury; A beta secondary structure
Mounting evidence has shown that dyshomeostasis of the redox-active biometals such as Cu and Fe can lead to oxidative stress, which plays a key role in the neuropathology of Alzheimer's disease (AD). Here we demonstrate that with the formation of Cu(II)-A(31-40 complexes, copper markedly potentiates the neurotoxicity exhibited by beta-amyloid peptide (A beta). A greater amount of hydrogen peroxide was released when Cu(II)-A(31-40 complexes was added to the xanthine oxidase/xanthine system detected by potassium iodide spectrophotometry. Copper bound to A beta 1-40 was observed by electron paramagnetic resonance (EPR) spectroscopy. Circular dichroism (CD) studies indicated that copper chelation could cause a structural transition of A beta. The addition of copper to A beta introduced an increase on beta-sheet as well as alpha-helix, which may be responsible for the aggregation of A beta. We hypothesized that A beta aggregation induced by copper may be responsible for local injury in AD. The interaction between Cu2+ and A beta also provides a possible mechanism for the enrichment of metal ions in amyloid plaques in the AD brain.
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