Increased O-2(center dot-) and NO production is a key mechanism of mitochondrial dysfunction in mycocardial ischemia/reperfusion injury. In complex impairment and enhanced tyrosine nitration of the 70 kDa FAD-binding protein occur in the…
Extracting and concentrating mitochondrial protein complexes from gel strips after blue native PAGE (BN-PAGE) can be daunting tasks using the traditional methods, such as electroelution, passive diffusion and centrifugal concentration. We present a…
Lee HL, Chen CL, Yeh ST, Zweier JL, Chen YR. Biphasic modulation of the mitochondrial electron transport chain in myocardial ischemia and reperfusion. Am J Physiol Heart Circ Physiol 302: H1410-H1422, 2012. First published January 20, 2012; doi:…
Reactive oxygen species and reactive nitrogen species are biological molecules that play important roles in cardiovascular physiology and contribute to disease initiation, progression, and severity. Because of their ephemeral nature and rapid…
Complex I (NQR) is a critical site of superoxide (O-2(radical anion)) production and the major host of redox protein thiols in mitochondria. In response to oxidative stress, NQR-derived protein thiols at the 51- and 75-kDa subunits are known to be…
Mitochondria-derived oxygen-free radical(s) are important mediators of oxidative cellular injury. It is widely hypothesized that excess NO enhances O(2)(center dot-) generated by mitochondria under certain pathological conditions. In the…
Cai M, Li Y, Xu Y, Swartz HM, Chen C, Chen Y, He G. Endothelial NOS activity and myocardial oxygen metabolism define the salvageable ischemic time window for ischemic postconditioning. Am J Physiol Heart Circ Physiol 300: H1069-H1077, 2011. First…
