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Prime, Tracy A; Blaikie, Frances H; Evans, Cameron; Nadtochiy, Sergiy M; James, Andrew M; Dahm, Christina C; Vitturi, Dario A; Patel, Rakesh P; Hiley, C. Robin; Abakumova, Irina; Requejo, Raquel; Chouchani, Edward T; Hurd, Thomas R; Garvey, John F; Taylor, Cormac T; Brookes, Paul S; Smith, Robin A.J; Murphy, Michael P
Proceedings of the National Academy of Sciences - PNAS, 06/2009, Letnik: 106, Številka: 26Journal Article
Nitric oxide (NO{bullet}) competitively inhibits oxygen consumption by mitochondria at cytochrome c oxidase and S-nitrosates thiol proteins. We developed mitochondria-targeted S-nitrosothiols (MitoSNOs) that selectively modulate and protect mitochondrial function. The exemplar MitoSNO1, produced by covalently linking an S-nitrosothiol to the lipophilic triphenylphosphonium cation, was rapidly and extensively accumulated within mitochondria, driven by the membrane potential, where it generated NO{bullet} and S-nitrosated thiol proteins. MitoSNO1-induced NO{bullet} production reversibly inhibited respiration at cytochrome c oxidase and increased extracellular oxygen concentration under hypoxic conditions. MitoSNO1 also caused vasorelaxation due to its NO{bullet} generation. Infusion of MitoSNO1 during reperfusion was protective against heart ischemia-reperfusion injury, consistent with a functional modification of mitochondrial proteins, such as complex I, following S-nitrosation. These results support the idea that selectively targeting NO{bullet} donors to mitochondria is an effective strategy to reversibly modulate respiration and to protect mitochondria against ischemia-reperfusion injury.
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