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Resistance of guinea pig cardiac cytochrome c oxidase (complex IV) to extended ischemic time during global ischemia and reperfusion

Reactive oxygen species (ROS) produced from cardiac mitochondria during ischemia and reperfusion (IR) injury can damage respiratory complexes I–V. We reported that complexes I and III, but not IV, were damaged after 30 min global ischemia. Here we examined for damaging effects of extended ischemic time on complex IV. Guinea pig heart mitochondria were isolated after 30 min reperfusion in four groups: time control (TC), 35 min ischemia alone, 45 min ischemia alone, and 45 min ischemia plus a cocktail of ROS scavengers (MnTBAP, catalase, glutathione, resveratrol) given 10 min before ischemia and throughout reperfusion. Complex IV enzyme activity was assessed by the conversion of reduced cytochrome c to oxidized cytochrome c in a spectrophotometer at 550 nm. Phasic (systolic – diastolic) left ventricular pressures (LVP) were 92±1 (SEM), 47±7, 17±5, 23±3 mmHg, and diastolic LVPs were 0, 9±4, 41±5, 22±2 mmHg, for TC and ischemia lasting 35, 45, and 45 min + ROS scavengers, respectively. Despite differences in cardiac function, complex IV activity was not different among groups including TC. Respiratory complexes that are most susceptible to ischemic damage are important for developing targeted strategies to protect them. Understanding why and how complex IV is resistant to oxidative stress could provide insight into better strategies to protect the more susceptible complexes against IR injury. (supported by NIH HL89514)