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PMID: 7488167 Published · ppublish English Comparative Study Journal Article Research Support, U.S. Gov't, P.H.S.

The role of iron in beta amyloid toxicity.

Biochemical and biophysical research communications ·Vol. 216 ·No. 2 ·1995-11-13 ·Pages 702-7

Schubert D, Chevion M

Abstract

There is evidence that oxidative damage plays a causative role in Alzheimer's disease and amyloid beta protein (A beta) toxicity. Iron is frequently a potent facilitator of free radical production due to its ability to mediate the conversion of H2O2 to hydroxyl radicals via the Fenton reaction or by virtue of hypervalent iron compounds. It is shown here that iron facilitates A beta toxicity to cultured cells.

MeSH Terms
Alzheimer Disease/physiopathology Amyloid beta-Peptides/toxicity Animals Cell Death/drug effects Cell Survival/drug effects Cells, Cultured Cerebral Cortex/cytology,drug effects,pathology Clone Cells Deferoxamine/pharmacology Drug Synergism Humans Hydrogen Peroxide/pharmacology Iron/toxicity Iron Chelating Agents/pharmacology Neurons/cytology,drug effects,pathology Neurotoxins/toxicity Peptide Fragments/toxicity
Chemicals
Amyloid beta-Peptides Iron Chelating Agents Neurotoxins Peptide Fragments amyloid beta-protein (1-40) amyloid beta-protein (25-35) Hydrogen Peroxide Iron Deferoxamine
Authors & Affiliations
2 authors, click to expand affiliations / ORCID
Schubert D
Salk Institute, La Jolla, California 92037, USA.
Chevion M
Article Info
Journal
Biochemical and biophysical research communications
Abbr.
Biochem Biophys Res Commun
ISSN
0006-291X
Published
1995-11-13
Pages
702-7
Language
English
Region
United States
NLM ID
0372516
Subset
IM
Grants
NINDS NIH HHS · P01 NS28121 · United States
NINDS NIH HHS · R01 NS09658 · United States
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