Myocardial ischemia reperfusion is associated with mitochondrial dysfunction and increased formation of reactive oxygen/nitrogen species. The main purpose of this study was to assess the role of tyrosine nitration of mitochondrial proteins in postischemic contractile dysfunction known as myocardial stunning. Isolated Langendorff-perfused rat hearts were subjected to 20-min global ischemia followed by 30-min reperfusion. The reperfused hearts showed marked decline in left ventricular developed pressure, maximal rate of contraction (+dP/dt), and maximal rate of relaxation (−dP/dt). Immunofluorescence and ELISA assays demonstrated enhanced protein tyrosine nitration in reperfused hearts. Using two-dimensional gel electrophoresis and MALDI-TOF/TOF mass spectrometry, eight mitochondrial proteins were identified to be nitrated after ischemia reperfusion. These proteins are crucial in mitochondrial electron transport, fatty acid oxidation, tricarboxylic acid cycle, ATP synthesis, and control of high-energy phosphates. The proteome data also indicated reduced abundance in several of nitrated proteins. The results suggest that these changes may contribute to inhibition of aconitase activity but are unlikely to affect electron transport chain activity. Whether tyrosine nitration of mitochondrial proteins can be considered the contributing factor of postischemic contractile dysfunction remains to be explored.

中文翻译：

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心肌缺血和再灌注期间线粒体蛋白的酪氨酸硝化。

心肌缺血再灌注与线粒体功能障碍和活性氧/氮物质形成增加有关。这项研究的主要目的是评估线粒体蛋白的酪氨酸硝化在缺血性收缩功能障碍（称为心肌震颤）中的作用。离体的Langendorff灌注大鼠心脏经历20分钟的整体缺血，然后再进行30分钟的再灌注。再灌注的心脏显示左心室发育压力，最大收缩率（+ dP / dt）和最大放松率（-dP / dt）明显下降。免疫荧光和ELISA分析表明，再灌注心脏中的蛋白酪氨酸硝化增强。使用二维凝胶电泳和MALDI-TOF / TOF质谱，缺血再灌注后鉴定出8种线粒体蛋白被硝化。这些蛋白质在线粒体电子传输，脂肪酸氧化，三羧酸循环，ATP合成以及高能磷酸盐的控制中至关重要。蛋白质组数据还表明，某些硝化蛋白质的丰度降低了。结果表明，这些变化可能有助于乌头酸酶活性的抑制，但不太可能影响电子转运链的活性。线粒体蛋白的酪氨酸硝化是否可以被认为是缺血后收缩功能障碍的因素。结果表明，这些变化可能有助于乌头酸酶活性的抑制，但不太可能影响电子转运链的活性。线粒体蛋白的酪氨酸硝化是否可以被认为是缺血后收缩功能障碍的因素。结果表明，这些变化可能有助于乌头酸酶活性的抑制，但不太可能影响电子转运链的活性。线粒体蛋白的酪氨酸硝化是否可以被认为是缺血后收缩功能障碍的因素。