Protection of cells from menadione-induced apoptosis by inhibition of lipid peroxidation

Tzeon Jye Chiou, Sin Tak Chu, Woan Fang Tzeng

研究成果: 雜誌貢獻文章同行評審

20 引文 斯高帕斯(Scopus)

摘要

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 μM induced cell apoptosis. Menadione at dose of 80 μM induced both apoptosis and necrosis. At a 160 μM dosage, menadione induced cell necrosis. Caspase 3 activation is required for menadione-induced apoptosis. Incubation of cells with 40 μM 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.
原文英語
頁(從 - 到)77-88
頁數12
期刊Toxicology
191
發行號2-3
DOIs
出版狀態已發佈 - 9月 2003
對外發佈

ASJC Scopus subject areas

  • 毒理學

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