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Overexpression of superoxide dismutase 1 protects against β-amyloid peptide toxicity: Effect of estrogen and copper chelators

TitoloOverexpression of superoxide dismutase 1 protects against β-amyloid peptide toxicity: Effect of estrogen and copper chelators
Tipo di pubblicazioneArticolo su Rivista peer-reviewed
Anno di Pubblicazione2004
AutoriCelsi, F., Ferri A., Casciati Arianna, D'Ambrosi N., Rotilio G., Costa A., Volonté C., and Carrì M.T.
RivistaNeurochemistry International
Volume44
Paginazione25-33
ISSN01970186
Parole chiaveamyloid beta protein, Amyloid beta-Protein, Antioxidant, Apoptosis, article, Benzimidazoles, Blotting, Brain Neoplasms, Caspase 1, caspase 3, Caspases, cell differentiation, Cell Line, chelating agent, Chelating Agents, Coloring Agents, Copper, copper derivative, Cultured, drug effect, Electrophoresis, enzyme activity, estradiol, Fluorescent Antibody Technique, Fluorescent Dyes, human, human cell, Humans, interleukin 1beta converting enzyme, Neuroblastoma, neuroblastoma cell, neuroprotection, neurotoxicity, Polyacrylamide Gel, priority journal, protein expression, reactive oxygen metabolite, Reactive Oxygen Species, superoxide dismutase, Tetrazolium Salts, Thiazoles, Tumor Cells, Western
Abstract

β-Amyloid peptides (Aβ) are major constituents of senile plaques in Alzheimer's disease (AD) brain and contribute to neurodegeneration, operating through activation of apoptotic pathways. It has been proposed that Aβ induces death by oxidative stress, possibly through the generation of peroxynitrite from superoxide and nitric oxide. Estrogen is thought to play a protective role against neurodegeneration through a variety of mechanisms including scavenging of reactive oxygen species (ROS). In this study, we have challenged with Aβ, either in the presence or in the absence of 17β-estradiol, differentiated human neuroblastoma SH-SY5Y cells (named line SH) and the same line overexpressing anti-oxidant enzyme superoxide dismutase 1 (SOD1; named line WT). We have observed that: (1) WT cells are less susceptible than SH cells to Aβ insult; (2) caspase-3, but not caspase-1, is involved in Aβ-induced apoptosis in this system; (3) estrogen protects both lines, without significantly affecting SOD activity; and (4) copper chelators prevent Aβ-induced toxicity. Our results further support the notion that anti-oxidant therapy might be beneficial in the treatment of AD by preventing activation of selected apoptotic pathways. © 2003 Elsevier Science Ltd. All rights reserved.

Note

cited By 40

URLhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-0042328239&doi=10.1016%2fS0197-0186%2803%2900101-3&partnerID=40&md5=57dc39219be2aff48551f1d5df8276a2
DOI10.1016/S0197-0186(03)00101-3
Citation KeyCelsi200425