Heerlein 2005 Am J Respir Cell Mol Biol: Difference between revisions
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{{Publication | {{Publication | ||
|title=Heerlein K, Schulze A, Hotz L, Bartsch P, MairbΓ€url H (2005) Hypoxia decreases cellular ATP demand and inhibits mitochondrial respiration of a549 cells. Am J Respir Cell Mol Biol 32: 44-51. | |title=Heerlein K, Schulze A, Hotz L, Bartsch P, MairbΓ€url H (2005) Hypoxia decreases cellular ATP demand and inhibits mitochondrial respiration of a549 cells. Am J Respir Cell Mol Biol 32:44-51. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/15388515 PMID: 15388515] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/15388515 PMID: 15388515] | ||
|authors=Heerlein K, Schulze A, Hotz L, Bartsch P, Mairbaeurl H | |authors=Heerlein K, Schulze A, Hotz L, Bartsch P, Mairbaeurl H | ||
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|area=Respiration | |area=Respiration | ||
|organism=Rat | |organism=Rat | ||
|tissues=Endothelial; | |tissues=Endothelial;epithelial;mesothelial cell, Blood cells | ||
|model cell lines=Other cell lines | |model cell lines=Other cell lines | ||
|preparations=Intact cells | |preparations=Intact cells |
Revision as of 14:50, 17 February 2015
Heerlein K, Schulze A, Hotz L, Bartsch P, MairbΓ€url H (2005) Hypoxia decreases cellular ATP demand and inhibits mitochondrial respiration of a549 cells. Am J Respir Cell Mol Biol 32:44-51. |
Heerlein K, Schulze A, Hotz L, Bartsch P, Mairbaeurl H (2005) Am J Respir Cell Mol Biol
Abstract: Hypoxia inhibits activity and expression of transporters involved in alveolar Na reabsorption and fluid clearance. We studied whether this represents a mechanism for reducing energy consumption or whether it is the consequence of metabolic dysfunction. Oxygen consumption (JO2) of A549 cells and primary rat alveolar type II cells was measured by microrespirometry during normoxia, hypoxia (1.5% O2), and reoxygenation. In both cell types, acute and 24-h hypoxia decreased total JO2 significantly and reoxygenation restored JO2 after 5 min but not after 24 h of hypoxia in A549 cells, whereas recovery was complete in type II cells. In A549 cells under normoxia Na/K-ATPase accounted for ~ 15% of JO2, whereas Na/K-ATPaseβrelated JO2 was decreased by ~ 25% in hypoxia. Inhibition of other ion transporters did not affect JO2. Protein synthesisβrelated JO2 was not affected by acute hypoxia, but decreased by 30% after 24-h hypoxia. Acute and 24-h hypoxia decreased JO2 of A549 cell mitochondrial complexes I, II, and III by 30β40%. Reoxygenation restored complex I activity after acute hypoxia but not after 24-h hypoxia. ATP was decreased 30% after 24-h hypoxia, but lactate production rate was not affected. Reduced nicotinamine adenine dinucleotide was slightly elevated in acute hypoxia. Our findings indicate that inhibition of the Na/K-ATPase by hypoxia contributes little to energy preservation in hypoxia. It remains unclear to what extent hypoxic inhibition of mitochondrial metabolism affects ATP-consuming processes. β’ Keywords: Energy metabolism, Hypoxia, Mitochondrial electron transfer chain, Na-transport, respirometry
β’ O2k-Network Lab: DE_Heidelberg_Mairbaeurl H
Labels: MiParea: Respiration
Stress:Hypoxia Organism: Rat Tissue;cell: Endothelial;epithelial;mesothelial cell, Blood cells Preparation: Intact cells
Regulation: Ion;substrate transport, O2"O2" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k