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Biochemistry and Physiology of Heart Mitochondrial Nitric Oxide Synthase

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Biochemistry of Oxidative Stress

Abstract

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 c oxidoreductase. 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, modify heart mtNOS activity or expression. The regulation of heart mtNOS by distinctive mitochondrial environments includes the effects of Ca2+, O2, L-arginine, NADPH, mitochondrial membrane potential (Δψ) and the metabolic states. Together, this enzyme seems to be critical during the adaptation of heart mitochondria to changes in cellular bioenergetics.

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Acknowledgments

This work was supported by research grants from the University of Buenos Aires (UBACYT 20020110100140, 20020130100731), Agencia Nacional de Promoción Científica y Tecnológica (PICT 2014-0964), and Consejo Nacional de Investigaciones Científicas y Técnicas (PIP 11220110100444).

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Correspondence to Tamara Zaobornyj .

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Zaobornyj, T., Iglesias, D.E., Bombicino, S.S., Rukavina-Mikusic, I.A., Valdez, L.B. (2016). Biochemistry and Physiology of Heart Mitochondrial Nitric Oxide Synthase. In: Gelpi, R., Boveris, A., Poderoso, J. (eds) Biochemistry of Oxidative Stress. Advances in Biochemistry in Health and Disease, vol 16. Springer, Cham. https://doi.org/10.1007/978-3-319-45865-6_4

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