Affordable Access

Publisher Website

Methionine oxidation by reactive oxygen species: reaction mechanisms and relevance to Alzheimer's disease

Authors
Journal
Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics
1570-9639
Publisher
Elsevier
Publication Date
Volume
1703
Issue
2
Identifiers
DOI: 10.1016/j.bbapap.2004.09.009
Keywords
  • Methionine
  • Methionine Sulfoxide
  • Sulfide Radical Cation
  • One-Electron Oxidation
  • Hydroxyl Radical
  • β-Amyloid
  • Alzheimer'S Disease
  • Aging
Disciplines
  • Biology
  • Chemistry
  • Medicine

Abstract

Abstract The oxidation of methionine plays an important role in vivo, during biological conditions of oxidative stress, as well as for protein stability in vitro. Depending on the nature of the oxidizing species, methionine may undergo a two-electron oxidation to methionine sulfoxide or one-electron oxidation to methionine radical cations. Both reaction mechanisms derive catalytic support from neighboring groups, which stabilize electron-deficient reaction centers. In vivo, methionine sulfoxide is subject to reduction by the methionine sulfoxide reductase (Msr) system, suggesting that some methionine sulfoxide residues may only be transiently involved in the deactivation of proteins through reactive oxygen species (ROS). Other methionine sulfoxide residues may accumulate, depending on the accessibility to Msr. Moreover, methionine sulfoxide levels may increase as a result of a lower abundance of active Msr and/or the required cofactors as a consequence of pathologies and biological aging. On the other hand, methionine radical cations will enter predominantly irreversible reaction channels, which ultimately yield carbon-centered and/or peroxyl radicals. These may become starting points for chain reactions of protein oxidation. This review will provide detailed mechanistic schemes for the reactions of various prominent, biologically relevant ROS with methionine and organic model sulfides. Emphasis will be given on the one-electron oxidation pathway, characterizing the physico-chemical parameters, which control this mechanism, and its physiological relevance, specifically for the oxidation and neurotoxicity of the Alzheimer's disease β-amyloid peptide (βAP).

There are no comments yet on this publication. Be the first to share your thoughts.

Statistics

Seen <100 times
0 Comments

More articles like this

Methionine oxidation by reactive oxygen species: r...

on Biochimica et Biophysica Acta Jan 17, 2005

Reactive oxygen species and Alzheimer's disease

on Biochemical Pharmacology Jan 01, 1997

Reactive oxygen species and Alzheimer's disease.

on Biochemical Pharmacology Sep 01, 1997

Free radical reactions of methionine in peptides:...

on Journal of the American Chemic... Nov 12, 2003
More articles like this..