Difference between revisions of "St-Pierre 2000 Proc Natl Acad Sci U S A"
(Created page with "{{Publication |title=St-Pierre J, Brand MD, Boutilier RG (2000) Mitochondria as ATP consumers: Cellular treason in anoxia. Proc. Natl. Acad. Sci. USA 97: 8670-8674. |authors=St-P...") |
Beno Marija (talk | contribs) |
||
| (19 intermediate revisions by 7 users not shown) | |||
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=St-Pierre J, Brand MD, Boutilier RG (2000) Mitochondria as ATP consumers: Cellular treason in anoxia. Proc | |title=St-Pierre J, Brand MD, Boutilier RG (2000) Mitochondria as ATP consumers: Cellular treason in anoxia. Proc Natl Acad Sci U S A 97:8670-4. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/10890886 PMID: 10890886 Open Access] | |||
|authors=St-Pierre J, Brand MD, Boutilier RG | |authors=St-Pierre J, Brand MD, Boutilier RG | ||
|year=2000 | |year=2000 | ||
|journal=Proc | |journal=Proc Natl Acad Sci U S A | ||
|abstract=In anoxia, mitochondria change from being ATP producers to | |abstract=In anoxia, mitochondria change from being ATP producers to | ||
potentially powerful ATP consumers. This change occurs, because | potentially powerful ATP consumers. This change occurs, because | ||
| Line 21: | Line 22: | ||
ATP use by the F1F0-ATPase might account for '9% of the ATP | ATP use by the F1F0-ATPase might account for '9% of the ATP | ||
turnover in anoxic frog skeletal muscle. | turnover in anoxic frog skeletal muscle. | ||
| | |mipnetlab=UK Cambridge Boutilier RG | ||
|discipline=Mitochondrial Physiology | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration, Comparative MiP;environmental MiP | |||
|organism=Amphibians | |||
|tissues=Skeletal muscle | |||
|preparations=Isolated mitochondria | |||
|enzymes=Complex V;ATP synthase | |||
|topics=ADP, ATP, Oxygen kinetics | |||
|instruments=Oxygraph-2k | |||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
Latest revision as of 09:30, 9 November 2016
| St-Pierre J, Brand MD, Boutilier RG (2000) Mitochondria as ATP consumers: Cellular treason in anoxia. Proc Natl Acad Sci U S A 97:8670-4. |
St-Pierre J, Brand MD, Boutilier RG (2000) Proc Natl Acad Sci U S A
Abstract: 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.
• O2k-Network Lab: UK Cambridge Boutilier RG
Labels: MiParea: Respiration, Comparative MiP;environmental MiP
Organism: Amphibians
Tissue;cell: Skeletal muscle
Preparation: Isolated mitochondria
Enzyme: Complex V;ATP synthase
Regulation: ADP, ATP, Oxygen kinetics
HRR: Oxygraph-2k
