Nitric oxide regulation of mitochondrial oxygen consumption I: cellular physiology

被引:89
|
作者
Giulivi, Cecilia
Kato, Kazunobu
Cooper, Christopher Eric
机构
[1] Univ Calif Davis, Dept Mol Biosci, Davis, CA 95616 USA
[2] Univ Essex, Dept Biol Sci, Colchester CO4 3SQ, Essex, England
来源
基金
英国惠康基金;
关键词
nitric oxide synthase; cytochrome c oxidase;
D O I
10.1152/ajpcell.00307.2006
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Mitochondrial biochemistry is complex, expanding from oxygen consumption, oxidative phosphorylation, lipid catabolism, heme biosynthesis, to apoptosis, calcium homeostasis, and production of reactive oxygen species, including nitric oxide (NO). The latter molecule is produced by a mitochondrial NO synthase (mtNOS). The rates of consumption and production determine the steady-state concentration of NO at subcellular levels, leading to regulation of mitochondrial events. Temporospatial processes tightly regulate production of NO in mitochondria to maximize target effects and minimize deleterious reactions. Temporal regulatory mechanisms of mtNOS include activation by calcium signaling and transcriptional/translational regulations. Calcium-activated mtNOS inhibits mitochondrial respiration, resulting in a decrease of the oxygen consumption. This negative regulation antagonizes the effects of calcium on calcium-dependent dehydrogenases in the citric acid cycle, preventing the formation of anoxic foci. Temporal regulation of NO production by intracellular calcium signaling is a complex process, considering the heterogeneous intracellular calcium response and distribution. NO production in mitochondria is spatially regulated by mechanisms that determine subcellular localization of mtNOS, likely acylation and protein-protein interactions, in addition to transcriptional regulation as neuronal NOS. Because NO rapidly decays in mitochondria, subcellular localization of mtNOS is crucial for NO to function as a signal molecule. These temporospatial processes are biologically important to allow NO to act as an effective signal molecule to regulate mitochondrial events such as oxygen consumption and reactive oxygen species production.
引用
收藏
页码:C1225 / C1231
页数:7
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