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首页> 外文期刊>International Journal of Cell Biology >The Chemical Interplay between Nitric Oxide andMitochondrial Cytochrome c Oxidase: Reactions, Effectors and Pathophysiology
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The Chemical Interplay between Nitric Oxide andMitochondrial Cytochrome c Oxidase: Reactions, Effectors and Pathophysiology

机译：一氧化氮和线粒体细胞色素c氧化酶之间的化学相互作用：反应，效应子和病理生理学。

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Nitric oxide (NO) reacts with Complex I and cytochrome c oxidase (CcOX, Complex IV), inducing detrimental or cytoprotective effects. Two alternative reaction pathways (PWs) have been described whereby NO reacts with CcOX, producing either a relatively labile nitrite-bound derivative (CcOX-NO_2~?, PW1) or a more stable nitrosyl-derivative (CcOX-NO, PW_2). The two derivatives are both inhibited, displaying different persistency and O_2 competitiveness. In the mitochondrion, during turnover with O_2, one pathway prevails over the other one depending on NO, cytochrome c~(2+) and O_2 concentration. High cytochrome c~(2+), and low O_2_ proved to be crucial in favoring CcOX nitrosylation, whereas under-standard cell-culture conditions formation of the nitrite derivative prevails. All together, these findings suggest that NO can modulate physiologically the mitochondrial respiratory/OXPHOS efficiency, eventually being converted to nitrite by CcOX, without cell detrimental effects. It is worthy to point out that nitrite, far from being a simple oxidation byproduct, represents a source of NO particularly important in view of the NO cell homeostasis, the NO production depends on the NO synthases whose activity is controlled by different stimuli/effectors; relevant to its bioavailability, NO is also produced by recycling cell/body nitrite. Bioenergetic parameters, such as mitochondrial ΔΨ, lactate, and ATP production, have been assayed in several cell lines, in the presence of endogenous or exogenous NO and the evidence collected suggests a crucial interplay between CcOX and NO with important energetic implications.
机译：一氧化氮（NO）与复合物I和细胞色素C氧化酶（CcOX，复合物IV）反应，诱导有害或细胞保护作用。已经描述了两种替代反应途径（PW），其中NO与CcOX反应，产生相对不稳定的亚硝酸盐结合衍生物（CcOX-NO_2〜β，PW1）或更稳定的亚硝酰基衍生物（CcOX-NO，PW_2）。两种衍生物均被抑制，表现出不同的持久性和O_2竞争性。在线粒体中，在与O_2交换期间，取决于NO，细胞色素c〜（2+）和O_2的浓度，一种途径优先于另一种途径。高细胞色素c〜（2+）和低O_2_被证明是促进CcOX亚硝化的关键，而亚硝酸盐衍生物的标准培养条件则普遍存在。总之，这些发现表明NO可以在生理上调节线粒体呼吸/ OXPHOS效率，最终被CcOX转化为亚硝酸盐，而没有细胞有害作用。值得指出的是，考虑到NO细胞的动态平衡，亚硝酸盐不是简单的氧化副产物，而是代表NO的特别重要，NO的产生取决于NO的合成酶，其合成酶的活性受不同刺激/效应物的控制。与它的生物利用度有关，NO也可以通过回收细胞/体内亚硝酸盐来产生。在存在内源性或外源性NO的情况下，已经在几种细胞系中测定了生物能参数，例如线粒体ΔΨ，乳酸和ATP的产生，并且收集到的证据表明CcOX和NO之间的重要相互作用具有重要的能量意义。

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