Oxidative protein damage in cells engaged in β-amyloidosis is related to apoE genotype

Bozena Mazur-Kolecka, Janusz Frackowiak, Dagmar Kowal, Jolanta Krzeslowska, Dennis Dickson

Research output: Contribution to journalArticle

21 Scopus citations

Abstract

The ε4 allele of apolipoprotein E (apoE) is a risk factor for Alzheimer's disease. The reduced antioxidant defense in ε4 carriers is suggested to contribute to β-amyloidosis. We found that oxidative stress induced by treatment with Fe2+ ions raised more protein carbonyls in vascular smooth muscle cells isolated from human brains with apoE genotype ε4/ε4 than with 3ε/ε3 and ε3/ε4. Antioxidant vitamin E prevented formation of carbonyls but not in cells with genotype ε4/ε4. Treatment with Fe2+ ions induced cellular accumulation of amyloid-β protein (Aβ)-immunoreactive material that co-localized with heme oxygenase, a marker of oxidative stress, and apoE. We hypothesize that the damage caused by oxidation in ε4/ε4 carriers facilitates development of β-amyloidosis.

Original languageEnglish (US)
Pages (from-to)465-468
Number of pages4
JournalNeuroReport
Volume13
Issue number4
DOIs
StatePublished - Mar 25 2002

Keywords

  • ApoE genotype
  • Cell culture
  • Oxidative stress
  • β-Amyloid protein

ASJC Scopus subject areas

  • Neuroscience(all)

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