Amyloid β-peptides increase annular and bulk fluidity and induce lipid peroxidation in brain synaptic plasma membranes

Nicolai A. Avdulov, Svetlana V. Chochina, Urule Igbavboa, Eugene O. O'Hare, Friedhelm Schroeder, James P. Cleary, W. Gibson Wood

Research output: Contribution to journalArticle

97 Scopus citations

Abstract

Amyloid β-peptides (Aβ) may alter the neuronal membrane lipid environment by changing fluidity and inducing free radical lipid peroxidation. The effects of Aβ1-40 and Aβ25-35 on the fluidity of lipids adjacent to proteins (annular fluidity), bulk lipid fluidity, and lipid peroxidation were determined in rat synaptic plasma membranes (SPM). A fluorescent method based on radiationless energy transfer from tryptophan of SPM proteins to pyrene and pyrene monomer-eximer formation was used to determine SPM annular fluidity and bulk fluidity, respectively. Lipid peroxidation was determined by the thiobarbituric acid assay. Annular fluidity end bulk fluidity of SPM were increased significantly (p ≤ 0.02) by Aβ1-40. Similar effects on fluidity were observed for Aβ25-35 (P ≤ 0.002). Increased fluidity was associated with peroxidation. Both Aβ peptides significantly increased (p ≤ 0.006) the amount of malondialdehyde in SPM.The addition of a water-soluble analogue of vitamin E (Trolox) inhibited effects of Aβ on lipid peroxidation and fluidity in SPM. The fluidizing action of Aβ peptides on SPM may be due to the induction of lipid peroxidation by those peptides. Aβ-induced changes in neuronal function, such as ion flux and enzyme activity, that have been reported previously may result from the combined effects of lipid peroxidation and increased membrane fluidity.

Original languageEnglish (US)
Pages (from-to)2086-2091
Number of pages6
JournalJournal of Neurochemistry
Volume68
Issue number5
DOIs
StatePublished - May 1997

Keywords

  • Alzheimer's disease
  • Amyloid β-peptide
  • Antioxidant
  • Lipid peroxidation
  • Membrane fluidity
  • Synaptic plasma membrane

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