Amyloid β-induced erythrocytic damage and its attenuation by carotenoids

FEBS Lett. 2011 Apr 20;585(8):1249-54. doi: 10.1016/j.febslet.2011.03.060. Epub 2011 Apr 1.

Abstract

The presence of amyloid β-peptide (Aβ) in human blood has recently been established, and it has been hypothesized that Aβ readily contacts red blood cells (RBC) and oxidatively impairs RBC functions. In this study, we conducted in vitro and in vivo studies, which provide evidence that Aβ induces oxidative injury to RBC by binding to them, causing RBC phospholipid peroxidation and diminishing RBC endogenous carotenoids, especially xanthophylls. This type of damage is likely to injure the vasculature, potentially reducing oxygen delivery to the brain and facilitating Alzheimer's disease (AD). As a preventive strategy, because the Aβ-induced RBC damage could be attenuated by treatment of RBC with xanthophylls, we suggest that xanthophylls may contribute to the prevention of AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Antioxidants / metabolism
  • Carotenoids / pharmacology*
  • Erythrocytes / drug effects*
  • Erythrocytes / metabolism
  • Flow Cytometry
  • Hemolysis / drug effects
  • Humans
  • Lipid Peroxides / metabolism
  • Lutein / pharmacology
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Oxidation-Reduction / drug effects
  • Oxidative Stress / drug effects
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology*
  • Phospholipids / metabolism
  • Protein Binding
  • Xanthophylls / pharmacology

Substances

  • Amyloid beta-Peptides
  • Antioxidants
  • Lipid Peroxides
  • Peptide Fragments
  • Phospholipids
  • Xanthophylls
  • amyloid beta-protein (1-40)
  • Carotenoids
  • astaxanthine
  • Lutein