Biochemistry and physiology of heart mitochondrial nitric oxide synthase

ZAOBORNYJ T; IGLESIAS DE; BOMBICINO SS; RUKAVINA MIKUSIC IA; VALDEZ LB

Advances in Biochemistry in Health and Disease. Biochemistry of oxidative stress: Physiopathology and clinical aspects

Springer

Lugar: New York; Año: 2016; p. 37 - 48

Heart mitochondria are the major source of reactive oxygen and nitrogen species and play a central role in cell energy provision and signaling. The NO produced by cardiac mtNOS is allowed to interact restrictedly with the co-localized effectors. NO exerts a high affinity, reversible and physiological inhibition of cytochrome c oxidase activity. A second effect of NO on the respiratory chain is accomplished through its interaction with ubiquinol-cytochrome coxidoreductase. The ability of mtNOS to regulate mitochondrial O2 uptake and O2- and H2O2 productions is named mtNOS functional activity.Several situations, including chronic hypoxia and ischemia-reperfusion, can modify heart mtNOS activity or expression.The regulation of heart mtNOS by the distinctive mitochondrial environment includes the effects of Ca2+, O2, L-arginine, NADPH, mitochondrial membrane potential () and the metabolic states. Together, this enzyme seems to be critical during the adaptation of heart mitochondria to changes in cellular bioenergetics.