Espey M G, Miranda K M, Feelisch M, Fukuto J, Grisham M B, Vitek M P, Wink D A
Radiation Biology Branch, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.
Ann N Y Acad Sci. 2000;899:209-21. doi: 10.1111/j.1749-6632.2000.tb06188.x.
Many cellular functions in physiology are regulated by the direct interaction of NO with target biomolecules. In many pathophysiologic and toxicologic mechanisms, NO first reacts with oxygen, superoxide or other nitrogen oxides to subsequently elicit indirect effects. The balance between nitrosative stress and oxidative stress within a specific biological compartment can determine whether the presence of NO will be ultimately deleterious or beneficial. Nitrosative stress can be defined primarily through reactions mediated by N2O3, a reactive nitrogen oxide species generated by high fluxes of NO in an aerobic environment. In contrast, oxidative stress is mediated primarily by superoxide and peroxides. In addition to reactive oxygen species, several reactive nitrogen oxide species such as peroxynitrite, nitroxyl, and nitrogen dioxide can also impose oxidative stress to a cell. We here describe how the mechanisms of cell death are interwoven in the balance between the different chemical intermediates involved in nitrosative and oxidative stress.
生理学中的许多细胞功能是由一氧化氮（NO）与靶生物分子的直接相互作用来调节的。在许多病理生理和毒理机制中，NO首先与氧气、超氧化物或其他氮氧化物反应，随后引发间接效应。特定生物区室内亚硝化应激和氧化应激之间的平衡可以决定NO的存在最终是有害还是有益。亚硝化应激主要可以通过由N2O3介导的反应来定义，N2O3是在有氧环境中由高通量的NO产生的一种活性氮氧化物。相比之下，氧化应激主要由超氧化物和过氧化物介导。除了活性氧物种外，一些活性氮氧化物，如过氧亚硝酸盐、硝酰基和二氧化氮，也会对细胞施加氧化应激。我们在此描述细胞死亡机制是如何在亚硝化应激和氧化应激所涉及的不同化学中间体之间的平衡中相互交织的。
