期刊
TOXICOLOGY
卷 191, 期 2-3, 页码 77-88出版社
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0300-483X(03)00189-6
关键词
apoptosis; lipid peroxidation; menadione; oxidative stress; phosphatidylserine translocation
Menadione is a commonly used compound that causes oxidative stress. We investigated the influence of lipid peroxidation on the apoptotic response of mouse myogenic C2C12 cells following menadione-induced oxidative stress. The presence of hypodiploid cells and phosphatidylserine translocation were assayed to detect apoptotic cells. Menadione at 10-40 muM induced cell apoptosis. Menadione at dose of 80 muM induced both apoptosis and necrosis. At a 160 muM dosage, menadione induced cell necrosis. Caspase 3 activation is required for menadione-induced apoptosis. Incubation of cells with 40 muM menadione resulted in the depletion of cellular glutathione and increased lipid peroxidation. Pre-treatment of cells with cysteine suppressed the menadione-induced apoptosis and prevented changes in reactive oxygen species levels, glutathione levels and lipid peroxidation. Pre-treatment of cells with deferoxamine mesylate, an iron chelator, also reduced both menadione-induced apoptosis and lipid peroxidation. However, this did not prevent menadione-induced glutathione depletion. Thus, the inhibition of lipid peroxidation by deferoxamine mesylate prevented apoptosis even though cellular glutathione remained depleted. Our data suggest that menadione-induced apoptosis is directly linked to iron-dependent lipid peroxidation. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
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