Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 30, Issue 4, Pages 447-450Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/S0891-5849(00)00494-9
Keywords
amyloid-beta; Alzheimer disease; free radicals; iron; neurotoxicity; oxidative stress
Funding
- NINDS NIH HHS [NS38648] Funding Source: Medline
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While amyloid-beta toxicity is mediated by oxidative stress and can be attenuated by antioxidants, the actual biochemical mechanism underlying neurotoxicity remains to be established. However, since aggregated amyloid-beta can interact with transition metals, such as iron, both in vitro and in vivo, we suspected that bound iron might be the mediator of toxicity such that holo- and apo-amyloid would have differential effects on cellular viability. Here we demonstrate that when amyloid-beta is pretreated with the iron chelator deferoxamine, neuronal toxicity is significantly attenuated while conversely, incubation of holo-amyloid-beta with excess free iron restores toxicity to original levels. These data, taken together with the known sequelae of amyloid-beta, suggest that the toxicity of amyloid-beta is mediated, at least in part, via redox-active iron that precipitates lipid peroxidation and cellular oxidative stress. (C) 2001 Elsevier Science Inc.
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