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Am J Physiol Cell Physiol 280: C517-C526, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 3, C517-C526, March 2001

Regulation of the mitochondrial permeability transition by matrix Ca2+ and voltage during anoxia/reoxygenation

Paavo Korge, Henry M. Honda, and James N. Weiss

Cardiovascular Research Laboratory, Departments of Medicine (Cardiology) and Physiology, University of California at Los Angeles School of Medicine, Los Angeles, California 90095

We studied the interplay between matrix Ca2+ concentration ([Ca2+]) and mitochondrial membrane potential (Delta psi ) in regulation of the mitochondrial permeability transition (MPT) during anoxia and reoxygenation. Without Ca2+ loading, anoxia caused near-synchronous Delta psi dissipation, mitochondrial Ca2+ efflux, and matrix volume shrinkage when a critically low PO2 was reached, which was rapidly reversible upon reoxygenation. These changes were related to electron transport inhibition, not MPT. Cyclosporin A-sensitive MPT did occur when extramitochondrial [Ca2+] was increased to promote significant Ca2+ uptake during anoxia, depending on the Ca2+ load size and ability to maintain Delta psi . However, when [Ca2+] was increased after complete Delta psi dissipation, MPT did not occur until reoxygenation, at which time reactivation of electron transport led to partial Delta psi regeneration. In the setting of elevated extramitochondrial Ca2+, this enhanced matrix Ca2+ uptake while promoting MPT because of less than full recovery of Delta psi . The interplay between Delta psi and matrix [Ca2+] in accelerating or inhibiting MPT during anoxia/reoxygenation has implications for preventing reoxygenation injury associated with MPT.

cardiomyocytes; mitochondrial Ca2+ uptake; Ca2+ efflux; permeability transition pore


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