Mitochondria from anoxia-tolerant animals reveal common strategies to survive without oxygen
Anoxia is the complete absence of oxygen, and various animal species have evolved to tolerate these environments for prolonged periods. The mechanisms allowing this adaptation may allow us to better understand how to combat the effects of reperfusion in cardiac tissue after myocardial infarction. The authors use examples, such as the painted turtle and the common frog, to demonstrate how adaptations to the mitochondria are important in avoiding the onset of cell death during anoxia. The overarching theme is that mitochondria must avoid the collapse of their membrane potential: failing this causes cytosolic calcium to be driven into the mitochondria during reperfusion, which leads to apoptotic signalling and cell death.
Some mechanisms which have been studied include: downregulation of respiratory chain activity; blocking of F1F0-ATPase; tighter membranes to avoid proton leak; blocking of mitochondrial calcium channels; reversal of F1F0-ATPase to maintain membrane potential; and increased ROS-scavenging enzymes. A final noteworthy example is the anoxic turtle brain, where it has been observed that the mitochondrial permeability transition pore can be transiently opened to release calcium from the mitochondria. This protective measure is not associated with mitochondrial swelling, nor release of apoptotic factors.