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Mitochondrial Nitric Oxide Synthase Regulates Mitochondrial Matrix pH

  • P. Ghafourifar and C. Richter
Published/Copyright: June 1, 2005
Biological Chemistry
From the journal Volume 380 Issue 7-8

Abstract

Nitric oxide (nitrogen monoxide, NO) exerts a wide profile of its biological activities via regulation of respiration and respiration-dependent functions. The presence of nitric oxide synthase (NOS) in mitochondria (mtNOS) was recently reported by us (Ghafourifar and Richter, FEBS Lett. 418, 291–296, 1997) and others (Giulivi et al., J. Biol. Chem. 273, 11038–11043, 1998). Here we report that NO, provided by an NO donor as well as by mtNOS stimulation, regulates mitochondrial matrix pH, transmembrane potential and Ca2+ buffering capacity. Exogenously-added NO causes a dose-dependent matrix acidification. Also mtNOS stimulation, induced by loading mitochondria with Ca2+, causes mitochondrial matrix acidification and a drop in mitochondrial transmembrane potential. Inhibition of mtNOS's basal activity causes mitochondrial matrix alkalinization and provides a resistance to the sudden drop of mitochondrial transmembrane potential induced by mitochondrial Ca2+ uptake. We conclude that mtNOS plays a critical role in regulating mitochondrial ∆pH.

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Published Online: 2005-06-01
Published in Print: 1999-07-01

Copyright © 1999 by Walter de Gruyter GmbH & Co. KG

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