Thannickal V J, Fanburg B L
Pulmonary and Critical Care Division, Department of Medicine, New England Medical Center/Tupper Research Institute, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Am J Physiol Lung Cell Mol Physiol. 2000 Dec;279(6):L1005-28. doi: 10.1152/ajplung.2000.279.6.L1005.
Reactive oxygen species (ROS) are generated as by-products of cellular metabolism, primarily in the mitochondria. When cellular production of ROS overwhelms its antioxidant capacity, damage to cellular macromolecules such as lipids, protein, and DNA may ensue. Such a state of "oxidative stress" is thought to contribute to the pathogenesis of a number of human diseases including those of the lung. Recent studies have also implicated ROS that are generated by specialized plasma membrane oxidases in normal physiological signaling by growth factors and cytokines. In this review, we examine the evidence for ligand-induced generation of ROS, its cellular sources, and the signaling pathways that are activated. Emerging concepts on the mechanisms of signal transduction by ROS that involve alterations in cellular redox state and oxidative modifications of proteins are also discussed.
活性氧（ROS）作为细胞代谢的副产物产生，主要在线粒体中。当细胞内ROS的产生超过其抗氧化能力时，可能会导致细胞大分子如脂质、蛋白质和DNA的损伤。这种“氧化应激”状态被认为与包括肺部疾病在内的多种人类疾病的发病机制有关。最近的研究还表明，由特殊的质膜氧化酶产生的ROS参与生长因子和细胞因子的正常生理信号传导。在这篇综述中，我们研究了配体诱导产生ROS的证据、其细胞来源以及被激活的信号通路。还讨论了关于ROS信号转导机制的新观点，这些机制涉及细胞氧化还原状态的改变和蛋白质的氧化修饰。
