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• W2009613708 abstract "Introduction: Mitochondrial reactive oxygen species (mROS) cause significant damage to myocardium after an episode of ischemia-reperfusion (IR). Ischemic preconditioning (IPC) decreases mROS formation and protects myocardium from IR. The mechanism of decreased mROS in IPC is unknown. Proton leak (H+ leak) dissipates mitochondria membrane potential (mΔΨ) and may regulate mROS production by changing the redox status of mitochondria. We hypothesize that increased H+ leak is responsible for decreased mROS production during IPC. Methods: Rat hearts were assigned to CONTROL (30 min of equilibration (EQ), 30 min ischemia (I), and 30 min of reperfusion (RP)) or IPC (10 min EQ, two 5 min episodes of IR, 30 min I, and 30 min RP). Rate pressure product (RPP) was measured throughout. Mitochondria were isolated at end equilibration (end EQ), end ischemia (end I), and end reperfusion (end RP). Respiration was measured by polarography, and mΔΨ with a TPP electrode. H+ leak is the respiratory rate required to maintain mΔΨ of -130mV in the presence of oligomycin-A, and was titrated with FCCP (0-160nM). Complex III mROS production was measured by fluorometry using Amplex-Red at end EQ and by electron paramagnetic resonance at end I and end RP. Results: Induction of IPC increased mROS production at end EQ (59±2 vs. 43±2 nmoles H2O2/mg protein/min, p<0.05, Fig.1) but did not change H+ leak (37±9 vs. 30±10 nmoles O/mg protein/min) when compared to CONTROL. IPC attenuated the increase in H+ leak at end I seen in CONTROL (44±11 vs. 140±11 nmoles O/mg protein/min, p<0.001). At end RP, IPC decreased mROS production (2115±146 vs. 3277±333 arbitrary units/mg protein, p<0.05). There was no difference in H+ leak between IPC and CONTROL at end RP (34±9 vs. 45±9 nmoles O/mg protein/min). IPC mitochondria responded to depolarization with greater reduction in mROS production than CONTROL (Fig.1). Further depolarization led to a trend of increased mROS in both CONTROL and IPC. The inflection point occurred at a higher mΔΨ in IPC mitochondria (-160 vs. -138 mV; Fig. 1). Conclusions: Increased rate of H+ leak is not the mechanism of decreased mROS after IR. While IPC did not lead to increased H+ leak, the induction of IPC increases the sensitivity of mitochondria to changes in mΔΨ leading to greater reduction in mROS per unit of change in mΔΨ. This increased sensitivity explains the greater reduction in mROS at end RP despite a lower H+ leak. Reducing mROS formation after ischemia-reperfusion is important to improving outcomes in patients with acute coronary syndrome." @default.
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• W2009613708 date "2011-02-01" @default.
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• W2009613708 title "Increased Mitochondrial Sensitivity To Proton Leak Is Responsible For Decreased Reactive Oxygen Species Production In Ischemic Preconditioning" @default.
• W2009613708 doi "https://doi.org/10.1016/j.jss.2010.11.443" @default.
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