Superoxide flashes, reactive oxygen species, and the mitochondrial permeability transition pore: potential implications for hematopoietic stem cell function

2011 ◽  
Vol 18 (4) ◽  
pp. 208-213 ◽  
Author(s):  
Charlie Mantel ◽  
Steven V Messina-Graham ◽  
Hal E Broxmeyer
Keyword(s):  
Reactive Oxygen Species ◽  
Stem Cell ◽  
Mitochondrial Permeability Transition Pore ◽  
Cell Function ◽  
Mitochondrial Permeability Transition ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Oxygen Species ◽  
Hematopoietic Stem ◽  
Mitochondrial Permeability

Transient opening of mitochondrial permeability transition pore by reactive oxygen species protects myocardium from ischemia-reperfusion injury

2009 ◽  
Vol 296 (4) ◽  
pp. H1125-H1132 ◽  
Author(s):  
Masao Saotome ◽  
Hideki Katoh ◽  
Yasuhiro Yaguchi ◽  
Takamitsu Tanaka ◽  
Tsuyoshi Urushida ◽  
...  
Keyword(s):  
Mitochondrial Permeability Transition Pore ◽  
Mitochondrial Permeability Transition ◽  
Ischemia Reperfusion ◽  
Permeability Transition Pore ◽  
Permeability Transition ◽  
Oxygen Species ◽  
Mitochondrial Permeability ◽  
Mptp Opening ◽  
Rat Hearts ◽  
Perfused Rat Hearts

Reactive oxygen species (ROS) production during ischemia-reperfusion (I/R) is thought to be a critical factor for myocardial injury. However, a small amount of ROS during the ischemic preconditioning (IPC) may provide a signal for cardioprotection. We have previously reported that the repetitive pretreatment of a small amount of ROS [hydrogen peroxide (H2O2), 2 μM] mimicked the IPC-induced cardioprotection in the Langendorff-perfused rat hearts. We further investigated the mechanisms of the ROS-induced cardioprotection against I/R injury and tested the hypothesis whether it could mediate the mitochondrial permeability transition pore (mPTP) opening. The Langendorff-perfused rat hearts were subjected to 35 min ischemia and 40 min reperfusion, and the pretreatment of H2O2 (2 μM) significantly improved the postischemic recoveries in left ventricular developed pressure, intracellular phosphocreatine, and ATP levels. A specific mPTP inhibitor cyclosporin A (CsA; 0.2 μM) canceled these H2O2-induced effects. In isolated permeabilized myocytes, H2O2 (1 μM) accelerated the calcein leakage from mitochondria in a CsA-sensitive manner, indicating the opening of mPTP by H2O2. However, H2O2 did not depolarize mitochondrial membrane potential (ΔΨm) even in the presence of oligomycin (F1/F0 ATPase inhibitor; 1 μM) and decreased mitochondrial Ca2+ concentration ([Ca2+]m) by accelerating the mitochondrial Ca2+ extrusion via an mPTP. We conclude that the transient mPTP opening could be involved in the H2O2-induced cardioprotection against reperfusion injury, and the reduction of [Ca2+]m without the change in ΔΨm might be a possible mechanism for the protection.

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