Involvement of mitochondria in ischemic cell injury and in regulation of intracellular calcium.
Ischemia causes a pathological drop in the cellular energy state due to inhibition of mitochondrial oxidative phosphorylation. The reversibility of this condition depends on the damage to mitochondrial membrane-linked activities during the period of ischemia or during reoxygenation of the tissue. It is likely that the ischemia-induced damage is due to a combination of factors including an increase in the cytosolic free Ca2+ concentration, a triggering of phospholipase and protease activities, an increase in cellular free fatty acids, and a decrease in pH. Mitochondrial damage that occurs during reperfusion is probably a consequence of excessive mitochondrial Ca2+ accumulation under adverse intracellular conditions. Mitochondria normally have an extremely high capacity for sequestering and buffering cytosolic Ca2+. However, during postischemic reperfusion these processes are inhibited due to existing conditions that potentiate Ca2+ uptake-induced irreversible mitochondrial damage.
D000255:Adenosine Triphosphate / Q000378:metabolism; D002118:Calcium / Q000378:metabolism*; D004734:Energy Metabolism; D006801:Humans; D007424:Intracellular Fluid / Q000378:metabolism; D007511:Ischemia / Q000378:metabolism*; D008928:Mitochondria / Q000378:metabolism*; D010085:Oxidative Phosphorylation; D012119:Respiration
D000255:Adenosine Triphosphate; D002118:Calcium