Free radicals and lipid peroxidation do not mediate β-amyloid-induced neuronal cell death

Zhi Xing Yao, Katy Drieu, Luke I. Szweda, Vassilios Papadopoulos

Research output: Contribution to journalArticle

43 Scopus citations

Abstract

'β Amyloid (Aβ)-induced free radical-mediated neurotoxicity' is a leading hypothesis as a cause of Alzheimer's disease (AD). Aβ increased free radical production and lipid peroxidation in PC12 nerve cells, leading to increased 4-hydroxy-2-nonenal (HNE) production and modification of specific mitochondrial target proteins, apoptosis and cell death. Pretreatment of the cells with isolated ginkgolides, the anti-oxidant component of Ginkgo biloba leaves, or vitamin E, prevented the Aβ-induced increase of reactive oxygen species (ROS). Ginkgolides, but not vitamin E, inhibited the Aβ-induced HNE modification of mitochondrial proteins. However, treatment with these anti- oxidants did not rescue the cells from Aβ-induced apoptosis and cell death. These results indicate that free radicals and lipid peroxidation may not mediate Aβ-induced neurotoxicity.

Original languageEnglish (US)
Pages (from-to)203-210
Number of pages8
JournalBrain Research
Volume847
Issue number2
DOIs
StatePublished - Nov 20 1999

Keywords

  • Apoptosis
  • Cell death
  • Ginkgolide
  • Neurotoxicity
  • Vitamin E
  • β Amyloid

ASJC Scopus subject areas

  • Neuroscience(all)
  • Molecular Biology
  • Clinical Neurology
  • Developmental Biology

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