Editor-in-Chief: Brüne, Bernhard
Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred
IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162
CiteScore 2018: 3.09
SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820
Nitric oxide (NO) and peroxynitrite (ONOO) avidly interact with mitochondrial components, leading to a range of biological responses spanning from the modulation of mitochondrial respiration, mitochondrial dysfunction to the signaling of apoptotic cell death. Physiological levels of NO primarily interact with cytochrome c oxidase, leading to a competitive and reversible inhibition of mitochondrial oxygen uptake. In turn, this leads to alterations in electrochemical gradients, which affect calcium uptake and may regulate processes such as mitochondrial transition pore (MTP) opening and the release of proapoptotic proteins. Large or persistent levels of NO in mitochondria promote mitochondrial oxidant formation. Peroxynitrite formed either extra or intramitochondrially leads to oxidative damage, most notably at complexes I and II of the electron transport chain, ATPase, aconitase and Mnsuperoxide dismutase. Mitochondrial scavenging systems for peroxynitrite and peroxynitritederived radicals such as carbonate (CO3.) and nitrogen dioxide radicals (NO2) include cytochrome c oxidase, glutathione and ubiquinol and serve to partially attenuate the reactions of these oxidants with critical mitochondrial targets. Detection of nitrated mitochondrial proteins in vivo supports the concept that mitochondria constitute central loci of the toxic effects of excess reactive nitrogen species. In this review we will provide an overview of the biochemical mechanisms by which NO and ONOO regulate or alter mitochondrial functions.
Here you can find all Crossref-listed publications in which this article is cited. If you would like to receive automatic email messages as soon as this article is cited in other publications, simply activate the “Citation Alert” on the top of this page.