Metallic compounds contribute to the oxidative stress of ambient particulate matter (PM) exposure. The toxicity of redox inert ions of cadmium, mercury, lead and zinc, as well as redox-active ions of vanadium and chromium is underlain by dysregulation of mitochondrial function and loss of signaling quiescence. Central to the initiation of these effects is the interaction of metal ions with cysteinyl thiols on glutathione and key regulatory proteins, which leads to impaired mitochondrial electron transport and persistent pan-activation of signal transduction pathways. The mitochondrial and signaling effects are linked by the production of H2O2, generated from mitochondrial superoxide anion or through the activation of NADPH oxidase, which extends the range and amplifies the magnitude of the oxidative effects of the metals. This oxidative burden can be further potentiated by inhibitory effects of the metals on the enzymes of the glutathione and thioredoxin systems. Along with the better-known Fenton-based mechanisms, the non-redox cycling mechanisms of oxidative stress induced by metals constitute significant pathways for cellular injury induced by PM inhalation.

中文翻译：

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PM金属引起的氧化应激的非氧化还原循环机制。

金属化合物会导致环境颗粒物（PM）暴露的氧化应激。镉，汞，铅和锌的氧化还原惰性离子以及钒和铬的氧化还原活性离子的毒性是由于线粒体功能失调和信号传导性丧失所致。引发这些作用的关键是金属离子与谷胱甘肽和关键调节蛋白上的半胱氨酸硫醇的相互作用，从而导致线粒体电子传递受损和信号转导途径的持续泛激活。线粒体和信号作用与通过线粒体超氧阴离子产生的H2O2或NADPH氧化酶的活化相关，从而扩大了范围并放大了金属的氧化作用。金属对谷胱甘肽和硫氧还蛋白系统酶的抑制作用可以进一步增强这种氧化负担。与众所周知的基于Fenton的机制一起，金属诱导的氧化应激的非氧化还原循环机制构成了PM吸入诱导的细胞损伤的重要途径。