Mitochondria as ATP consumers: Cellular treason in anoxia
AUTOR(ES)
St-Pierre, Julie
FONTE
The National Academy of Sciences
RESUMO
In anoxia, mitochondria change from being ATP producers to potentially powerful ATP consumers. This change occurs, because the mitochondrial F1F0-ATPase begins to hydrolyze ATP to avoid the collapse of the proton motive force. Species that can survive prolonged periods of O2 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 F1F0-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 F1F0-ATPase is limited in anoxia by a profound inhibition of the enzyme. Even so, ATP use by the F1F0-ATPase might account for ≈9% of the ATP turnover in anoxic frog skeletal muscle.
ACESSO AO ARTIGO
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=27006Documentos Relacionados
- New consumers: The influence of affluence on the environment
- UNDERSTANDING SOCIAL MEDIA MINDSET OF CONSUMERS: AN INDIAN PERSPECTIVE
- Nutrient loading and consumers: Agents of change in open-coast macrophyte assemblages
- Infrastructure for Reaching Disadvantaged Consumers: Telecommunications in Rural and Remote Nursing in Australia
- Evidence-based medicine for consumers: a role for the Cochrane Collaboration