Faculty of Chemistry, University of Bucharest, Bucharest, Romania.
FEBS J. 2010 Oct;277(19):4027-38. doi: 10.1111/j.1742-4658.2010.07794.x. Epub 2010 Aug 23.
The Ca(2+) -dependent response to oxidative stress caused by H(2)O(2) or tert-butylhydroperoxide (tBOOH) was investigated in Saccharomyces cerevisiae cells expressing transgenic cytosolic aequorin, a Ca(2+) -dependent photoprotein. Both H(2)O(2) and tBOOH induced an immediate and short-duration cytosolic Ca(2+) increase that depended on the concentration of the stressors. Sublethal doses of H(2)O(2) induced Ca(2+) entry into the cytosol from both extracellular and vacuolar sources, whereas lethal H(2)O(2) shock mobilized predominantly the vacuolar Ca(2+). Sublethal and lethal tBOOH shocks induced mainly the influx of external Ca(2+), accompanied by a more modest vacuolar contribution. Ca(2+) transport across the plasma membrane did not necessarily involve the activity of the Cch1p/Mid1p channel, whereas the release of vacuolar Ca(2+) into the cytosol required the vacuolar channel Yvc1p. In mutants lacking the Ca(2+) transporters, H(2)O(2) or tBOOH sensitivity correlated with cytosolic Ca(2+) overload. Thus, it appears that under H(2)O(2)-induced or tBOOH-induced oxidative stress, Ca(2+) mediates the cytotoxic effect of the stressors and not the adaptation process.
研究了在表达转基因细胞质萤光素的酿酒酵母细胞中,钙离子依赖的对由 H2O2 或叔丁基过氧化物(tBOOH)引起的氧化应激的反应。H2O2 和 tBOOH 均诱导即刻和短暂的细胞质钙离子增加,这取决于应激物的浓度。亚致死剂量的 H2O2 诱导来自细胞外和液泡源的钙离子进入细胞质,而致死剂量的 H2O2 休克则主要动员液泡中的钙离子。亚致死和致死 tBOOH 休克主要诱导外部钙离子的流入,同时液泡的贡献较小。质膜上的钙离子转运不一定涉及 Cch1p/Mid1p 通道的活性,而液泡中钙离子释放到细胞质中则需要液泡通道 Yvc1p。在缺乏钙离子转运体的突变体中,H2O2 或 tBOOH 的敏感性与细胞质钙离子过载相关。因此,在 H2O2 诱导或 tBOOH 诱导的氧化应激下,钙离子介导应激物的细胞毒性效应,而不是适应过程。