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. Author manuscript; available in PMC: 2011 Jan 15.
Published in final edited form as: Free Radic Biol Med. 2009 Nov 5;48(2):306. doi: 10.1016/j.freeradbiomed.2009.11.001

Figure 6.

Figure 6

Reduction of mitochondrial O2․- suppresses NO-mediated mitochondrial dysfunction. Permeabilized HPMVECs were exposed to DeaNONOate (10 μM) for 30 min. HPMVECs were infected with Ad5CMVMnSOD for 48 hr and these cells were exposed to DeaNONOate. (A) Immunoprecipitation was performed with NDUFB8 antibody and immunoblotted with an anti-nitrotyrosine antibody. (B) DeaNONOate induced a significant reduction in complex I activity that was restored by overexpression of MnSOD (mean±S.E.M., n=3). (C) Endothelial cells overexpressing MnSOD prevented the DeaNONOate-induced reduction in complex IV mitochondrial oxygen consumption. (D) MnSOD overexpressing HPMVECs were exposed to 10 μM DeaNONOate and ATP levels were assessed 12 hr following NO addition and normalized to untreated RPMVECs.