Schweizer M, Richter C
Laboratory of Biochemistry I, Swiss Federal Institute of Technology (ETH), Zürich.
Biochem Biophys Res Commun. 1994 Oct 14;204(1):169-75. doi: 10.1006/bbrc.1994.2441.
Nitric oxide (nitrogen monoxide, NO) at low concentrations can potently deenergize isolated liver and brain mitochondria at oxygen concentrations that prevail in cells and tissues. Deenergization is observed when mitochondria utilize respiratory substrates such as pyruvate plus malate, succinate, or ascorbate plus tetramethylphenylenediamine, but not when mitochondria are energized with ATP. The extent and duration of deenergization is determined by the concentration of NO and oxygen, and the kind of respiratory substrate. The NO-induced changes of the mitochondrial energy state are transient and are paralleled by release and reuptake of mitochondrial calcium. These findings reveal a direct action of NO on the mitochondrial respiratory chain and suggest that NO exerts some of its physiological and pathological effects by deenergizing mitochondria.
低浓度的一氧化氮（又称氮 monoxide，NO）能够在细胞和组织中普遍存在的氧浓度下，有效地使分离的肝脏和脑线粒体去极化。当线粒体利用诸如丙酮酸加苹果酸、琥珀酸或抗坏血酸加四甲基对苯二胺等呼吸底物时，会观察到去极化现象，但当线粒体由 ATP 供能时则不会出现。去极化的程度和持续时间由 NO 和氧的浓度以及呼吸底物的种类决定。NO 诱导的线粒体能量状态变化是短暂的，并且与线粒体钙的释放和再摄取同时发生。这些发现揭示了 NO 对线粒体呼吸链的直接作用，并表明 NO 通过使线粒体去极化发挥其部分生理和病理作用。
