St-Pierre J, Brand M D, Boutilier R G
Department of Zoology, University of Cambridge, Cambridge, England CB2 3EJ.
Proc Natl Acad Sci U S A. 2000 Jul 18;97(15):8670-4. doi: 10.1073/pnas.140093597.
In anoxia, mitochondria change from being ATP producers to potentially powerful ATP consumers. This change occurs, because the mitochondrial F(1)F(0)-ATPase 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 ATP use; otherwise, this process would dominate glycolytic metabolism and threaten ATP delivery to essential ATP-consuming processes of the cell (e.g., ion-motive ATPases). There are two ways to limit ATP hydrolysis by the F(1)F(0)-ATPase, namely (i) reduction of the proton conductance of the mitochondrial inner membrane and (ii) inhibition of the enzyme. We assessed these two possibilities by using intact mitochondria isolated from the skeletal muscle of anoxia-tolerant frogs. Our results show that proton conductance is unaltered between normoxia and anoxia. However, ATP use by the F(1)F(0)-ATPase is limited in anoxia by a profound inhibition of the enzyme. Even so, ATP use by the F(1)F(0)-ATPase might account for approximately 9% of the ATP turnover in anoxic frog skeletal muscle.
在缺氧状态下，线粒体从ATP的产生者转变为潜在的强大ATP消耗者。这种变化之所以发生，是因为线粒体F(1)F(0)-ATP酶开始水解ATP，以避免质子动力势的崩溃。能够在长时间缺氧环境下存活的物种必须限制这种ATP的消耗；否则，这个过程将主导糖酵解代谢，并威胁到ATP向细胞中重要的ATP消耗过程（如离子动力ATP酶）的供应。有两种方法可以限制F(1)F(0)-ATP酶的ATP水解，即（i）降低线粒体内膜的质子传导性和（ii）抑制该酶。我们通过使用从耐缺氧青蛙的骨骼肌中分离出的完整线粒体来评估这两种可能性。我们的结果表明，常氧和缺氧状态下质子传导性未发生改变。然而，在缺氧状态下，F(1)F(0)-ATP酶对ATP的消耗因该酶受到深度抑制而受到限制。即便如此，F(1)F(0)-ATP酶对ATP的消耗可能占缺氧青蛙骨骼肌中ATP周转的约9%。
