Mitochondria as ATP consumers: cellular treason in anoxia.

TitleMitochondria as ATP consumers: cellular treason in anoxia.
Publication TypeJournal Article
Year of Publication2000
AuthorsSt-Pierre, J, Brand, MD, Boutilier, RG
JournalProc Natl Acad Sci U S A
Date Published2000 Jul 18
KeywordsAdenosine Triphosphate, Animals, Cell Hypoxia, Electron Transport, Male, Mitochondria, Muscle, Muscle, Skeletal, Proton-Translocating ATPases, Protons, Rana temporaria

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.

Alternate JournalProc. Natl. Acad. Sci. U.S.A.
Citation Key10.1073/pnas.140093597
PubMed ID10890886
PubMed Central IDPMC27006