UCD Conway Institute, University College Dublin, Ireland.
Arterioscler Thromb Vasc Biol. 2010 Apr;30(4):643-7. doi: 10.1161/ATVBAHA.108.181628. Epub 2009 Aug 27.
Cytochrome c oxidase (CcO; complex IV of the mitochondrial electron transport chain) is the primary site of cellular oxygen consumption and, as such, is central to oxidative phosphorylation and the generation of adenosine-triphosphate. Nitric oxide (NO), an endogenously-generated gas, modulates the activity of CcO. Depending on the intracellular oxygen concentration and the resultant dominant redox state of CcO, the interaction between CcO and NO can have a range of signaling consequences for cells in the perception of changes in oxygen concentration and the initiation of adaptive responses. At higher oxygen concentrations, when CcO is predominantly in an oxidized state, it consumes NO. At lower oxygen concentrations, when CcO is predominantly reduced, NO is not consumed and accumulates in the microenvironment, with implications for both the respiratory rate of cells and the local vascular tone. Changes in the availability of intracellular oxygen and in the generation of reactive oxygen species that accompany these interactions result in cell signaling and in regulation of oxygen-sensitive pathways that ultimately determine the nature of the cellular response to hypoxia.
细胞色素 c 氧化酶（CcO；线粒体电子传递链的复合物 IV）是细胞耗氧量的主要部位，因此是氧化磷酸化和三磷酸腺苷生成的核心。一氧化氮（NO）是一种内源性气体，可调节 CcO 的活性。根据细胞内氧浓度和 CcO 的主要还原状态，CcO 与 NO 之间的相互作用会对细胞感知氧浓度变化和启动适应性反应产生一系列信号后果。在较高的氧浓度下，当 CcO 主要处于氧化状态时，它会消耗 NO。在较低的氧浓度下，当 CcO 主要处于还原状态时，NO 不会被消耗，而是在微环境中积累，这对细胞的呼吸速率和局部血管张力都有影响。这些相互作用伴随着细胞内氧可用性的变化和活性氧的产生，导致细胞信号转导和氧敏感途径的调节，最终决定细胞对缺氧的反应性质。
