Cadmium affects tobacco cells by a series of three waves of reactive oxygen species that contribute to cytotoxicity
Cadmium affects tobacco cells by a series of three waves of reactive oxygen species that contribute to cytotoxicity
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DOI：
10.1111/j.1365-3040.2006.01571.x
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发表时间：
2006-10-01
影响因子：
7.3
通讯作者：
Montillet, Jean-Luc
中科院分区：
文献类型：
--
作者：
Garnier, Lionel;Simon-Plas, Francoise;Montillet, Jean-Luc
镉被怀疑通过氧化损伤对细胞发挥其毒性作用。然而，过渡金属不能在生物环境中通过与分子氧的氧化还原反应直接产生活性氧物质（ROS）。在这里，我们表明，明亮的黄色-2（BY-2）烟草细胞暴露于毫摩尔浓度的氯化镉开发细胞死亡2-3小时内。死亡过程之前有两波连续的活性氧，其性质和亚细胞定位不同。首先，这些包括在短暂的NADPH氧化酶依赖性积累的H2 O2随后积累的O-2（-）。在线粒体中。第三波的活性氧组成的脂肪酸氢过氧化物的积累是伴随着细胞死亡。在H2 O2积累之前，胞质游离钙浓度的增加源于内部池，这是必不可少的激活NADPH氧化酶。细胞系gp 3，受损的NADPH氧化酶的活性，这是无法积累H2 O2响应镉，但中毒的金属。因此，ROS的第一波不足以触发所有镉依赖性有害效应。然而，我们发现，积累的O-2（-）。线粒体起源和膜过氧化是镉诱导细胞死亡的关键球员。
Cadmium is suspected to exert its toxic action on cells through oxidative damage. However, the transition metal is unable to directly generate reactive oxygen species (ROS) via redox reactions with molecular oxygen in a biological environment. Here, we show that bright yellow-2 (BY-2) tobacco cells exposed to millimolar concentrations of CdCl2 developed cell death within 2-3 h. The death process was preceded by two successive waves of ROS differing in their nature and subcellular localization. Firstly, these consisted in the transient NADPH oxidase-dependent accumulation of H2O2 followed by the accumulation of O-2(-). in mitochondria. A third wave of ROS consisting in fatty acid hydroperoxide accumulation was concomitant with cell death. Accumulation of H2O2 was preceded by an increase in cytosolic free calcium concentration originating from internal pools that was essential to activate the NADPH oxidase. The cell line gp3, impaired in NADPH oxidase activity, and that was unable to accumulate H2O2 in response to Cd2+, was nevertheless poisoned by the metal. Therefore, this first wave of ROS was not sufficient to trigger all the cadmium-dependent deleterious effects. However, we show that the accumulation of O-2(-). of mitochondrial origin and membrane peroxidation are key players in Cd2+-induced cell death.