Mitochondria as ATP consumers: Cellular treason in anoxia

In anoxia. mitochondria change from being ATP producers to potentially powe rful ATP consumers. This change occurs, because the mitochondrial F1F0-ATPa se begins to hydrolyze ATP to avoid the collapse of the proton motive force . Species that can survive prolonged periods of O-2 lack must limit such AT P use; otherwise. this process would dominate glycolytic metabolism and thr eaten ATP delivery to essential ATE-consuming processes of the cell (e.g.. ion-motive ATPases). There are two ways to limit ATP hydrolysis by the F1F0 -ATPase. namely (i) reduction of the proton conductance of the mitochondria l inner membrane and (ii) inhibition of the enzyme. We assessed these two p ossibilities by using intact mitochondria isolated from the skeletal muscle of anoxia-tolerant frogs. Our results show that proton conductance is unal tered between normoxia and anoxia. However, ATP use by the F1F0-ATPase is l imited in anoxia by a profound inhibition of the enzyme. Even so. ATP use b y the F1F0-ATPase might account for approximate to 9% of the ATP turnover i n anoxic frog skeletal muscle.