Leist M, Single B, Naumann H, Fava E, Simon B, Kühnle S, Nicotera P
Faculty of Biology, Department of Molecular Toxicology, University of Konstanz, Konstanz, D-78457, Germany.
Biochem Biophys Res Commun. 1999 Apr 29;258(1):215-21. doi: 10.1006/bbrc.1999.0491.
The endogenous mediator nitric oxide (NO) blocked apoptosis of Jurkat cells elicited by staurosporine, anti-CD95 or chemotherapeutics, and switched death to necrosis. The switch in the mode of cell death was dependent on the ATP loss elicited by NO. This affected two distinct steps of the apoptotic cascade. First, the release of cytochrome c from mitochondria was delayed by NO. Second, processing of procaspases-3/7 to the active proteases was prevented even after cytochrome c had been released. Thus, NO interferes with execution steps of apoptosis both upstream and downstream of cytochrome c release.
内源性介质一氧化氮（NO）可阻断由星形孢菌素、抗CD95或化疗药物引发的Jurkat细胞凋亡，并将死亡方式转变为坏死。细胞死亡方式的转变取决于NO引起的ATP损失。这影响了凋亡级联反应的两个不同步骤。首先，NO延迟了细胞色素c从线粒体的释放。其次，即使细胞色素c已经释放，procaspases-3/7向活性蛋白酶的加工过程也被阻止。因此，NO在细胞色素c释放的上游和下游均干扰凋亡的执行步骤。
