Mechanism and subpopulation specificity of mitochondrial reactive oxygen species release in the post-ischemic hyperthyroid myocardium
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Hyperthyroidism (HT) augments release of reactive oxygen species (ROS) from cardiac mitochondria following myocardial ischemia/reperfusion (I/R). The present study examined the mechanisms of this phenomenon and determined whether subsarcolemmal (SSM) and intermyofibrillar mitochondria (IFM) are differentially affected. Male SD rats received 10 daily injections of thyroid hormone (30ug/kg i.p.; HT) or vehicle (CON) before hearts were excised and exposed to a 20/25 min global I/R protocol ex vivo. Following I/R, ROS release was assessed in freshly isolated SSM and IFM using the Amplex Red assay ...