Journal of molecular and cellular cardiology
-
J. Mol. Cell. Cardiol. · Jun 2009
Postconditioning inhibits mPTP opening independent of oxidative phosphorylation and membrane potential.
Mitochondrial permeability transition pore (mPTP) inhibition plays a relevant role in postconditioning (PostC). Ischemia damages the electron transport chain, and the potential contribution of additional modifications in mitochondrial function caused by PostC remains unknown. We sought to determine which mitochondrial functions are involved in the inhibition of mPTP opening during the first minutes of reperfusion. ⋯ Control, PostC and CsA mitochondria exhibited a comparable significant dissipation of DeltaPsi(m), together with a comparable significant decrease in state 3 and an increase in state 4 respiration, in both SSM and IFM. However, PostC but not CsA treatment reduced total heart oxidative stress. These data suggest that during the early minutes of reperfusion, PostC reduces oxidative stress and inhibits mPTP opening, independent of alteration of oxidative phosphorylation or of DeltaPsi(m).