Park Y, Devlin T M, Majde J A, Jones D P
Department of Biochemistry, Emory University School of Medicine, Atlanta, Georgia 30322.
Ren Fail. 1992;14(3):303-6. doi: 10.3109/08860229209106633.
Mammalian cells differ considerably in the duration of anoxia which they can tolerate despite the fact that dramatic bioenergetic changes occur rapidly. Previous studies indicate that the ability to tolerate anoxia is at least partly due to an endogenous signal transduction system that senses O2 deficiency and signal altered ion transport functions in the mitochondria. The responses included inhibition of ATP synthase, ADP/ATP exchange, inorganic phosphate uptake, mitochondrial swelling, and loss of the mitochondrial proton-motive force. An important distinction between KCN toxicity and anoxia is that KCN does not elicit these protective mechanisms. Thus, the ability of a compound to elicit these mechanisms in KCN-treated cells provides an assay for potential agonists of the endogenous protective mechanisms.
哺乳动物细胞在可耐受的缺氧持续时间上有很大差异，尽管剧烈的生物能量变化会迅速发生。先前的研究表明，耐受缺氧的能力至少部分归因于一种内源性信号转导系统，该系统能感知氧气缺乏并调节线粒体中离子转运功能的改变。这些反应包括对ATP合酶的抑制、ADP/ATP交换、无机磷酸盐摄取、线粒体肿胀以及线粒体质子动力的丧失。KCN毒性与缺氧之间的一个重要区别在于，KCN不会引发这些保护机制。因此，一种化合物在KCN处理的细胞中引发这些机制的能力，为内源性保护机制的潜在激动剂提供了一种检测方法。
