Cellular Thiols as a Determinant of Responsiveness to Menadione in Cardiomyocytes

Woan Fang Tzeng, Tzeon Jye Chiou, Chin Peng Wang, Jia Luen Lee, Yee Hsiung Chen

研究成果: 雜誌貢獻文章同行評審

29 引文 斯高帕斯(Scopus)


The role of intracellular thiols in menadione-mediated toxicity was studied in neonatal rat cardiomyocytes. The sensitivity of cardiomyocytes to menadione was greater than that of skeletal muscle cells and 3T3 fibroblasts. Before cell degeneration, menadione induced marked depletion of intracellular thiols and an increase of oxidized glutathione. The sensitivity of these cells to menadione correlated with the level of depletion of intracellular thiols. After incubation of cardiomyocytes with menadione, glutathione reductase activity was inhibited and lipid peroxidation was increased. Both dicumarol (an inhibitor of DT-diaphorase) and diethyldithiocarbamate (an inhibitor of superoxide dismutase) enhanced the capacity of menadione to induce cellular damage and to cause depletion of intracellular glutathione. Decreasing intracellular glutathione by pretreatment of cells with N-ethylmaleimide or buthionine sulphoximine also increased menadione-induced cell degeneration. Preincubation with cysteine or dithiothreitol suppressed the capacity of menadione to damage the cells. Menadione-induced lipid peroxidation was also suppressed by the same treatment. These results show that the oxidative stress induced by menadione in cardiomyocytes results in the depletion of glutathione and protein thiols. Both DT-diaphorase and superoxide dismutase can protect cells from the toxicity of menadione. Cellular thiols are determinants of the responsiveness to menadione.
頁(從 - 到)889-897
期刊Journal of Molecular and Cellular Cardiology
出版狀態已發佈 - 7月 1994

ASJC Scopus subject areas

  • 分子生物學
  • 心臟病學與心血管醫學


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