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 CdCl(2) 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 H(2)O(2) 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 H(2)O(2) 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 H(2)O(2) in response to Cd(2+), 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 Cd(2+)-induced cell death.

译文

:镉被怀疑通过氧化损伤对细胞产生毒性作用。然而,在生物环境中,过渡金属不能通过与分子氧的氧化还原反应直接产生活性氧(ROS)。在这里,我们显示暴露于毫摩尔浓度的CdCl(2)的亮黄色2(BY-2)烟草细胞在2-3小时内发展出细胞死亡。死亡过程之前是连续两次的ROS,其性质和亚细胞定位各不相同。首先,这些包括线粒体中H(2)O(2)的瞬时NADPH氧化酶依赖性积累,然后是线粒体中O(2)(-*)的积累。 ROS的第三波涉及脂肪酸氢过氧化物的积累,并伴随着细胞死亡。 H(2)O(2)的积累之前是来自内部池的胞质游离钙浓度的增加,这对于激活NADPH氧化酶是必不可少的。然而,细胞系gp3在NADPH氧化酶活性中受损,并且无法响应Cd(2)积聚H(2)O(2),但仍被金属中毒。因此,ROS的第一波不足以触发所有依赖镉的有害作用。但是,我们表明,线粒体起源的O(2)(-*)积累和膜过氧化是Cd(2)诱导的细胞死亡的关键因素。

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