Free radicals and lipid peroxidation do not mediate β-amyloid-induced neuronal cell death |
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| Authors: | Zhi-Xing Yao Katy Drieu Luke I. Szweda Vassilios Papadopoulos |
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| Affiliation: | a Division of Hormone Research, Departments of Cell Biology and Pharmacology, Georgetown University Medical Center, 3900 Reservoir Road, NW, Washington, DC 20007, USA;b Institute Henri Beaufour-IPSEN, 24 rue Erlanger, Paris 75116, France;c Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, 10900 Euclid Avenue, Cleveland, OH 44106, USA |
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| 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. |
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| Keywords: | β Amyloid Neurotoxicity Vitamin E Ginkgolide Apoptosis Cell death |
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