Difference between revisions of "Huetter 2002 Mol Biol Rep"
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{{Labeling | {{Labeling | ||
|organism=Human | |organism=Human | ||
|model cell lines=Fibroblast | |model cell lines=Fibroblast | ||
|preparations=Intact | |preparations=Intact cells | ||
|injuries=Hypoxia | |||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|kinetics=Oxygen | |kinetics=Oxygen | ||
|instruments=Oxygraph-2k | |||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} |
Revision as of 08:15, 8 August 2013
Hรผtter E, Renner K, Jansen-Dรผrr P, Gnaiger E (2002) Biphasic oxygen kinetics of cellular respiration and linear oxygen dependence of antimycin A inhibited oxygen consumption. Mol Biol Rep 29: 83-87. |
Huetter E, Renner K, Jansen-Duerr P, Gnaiger E (2002) Mol Biol Rep
Abstract: Oxygen kinetics in fibroblasts was biphasic. This was quantitatively explained by a major mitochondrial hyperbolic component in the low-oxygen range and a linear increase of rotenone- and antimycin A- inhibited oxygen consumption in the high-oxygen range. This suggest an increased production of reactive oxygen species and oxidative stress at elevated, air-level oxygen concentrations. The high oxygen activity of mitochondrial respiration provides the basis for the maintenance of a high aerobic scope at physiological low-oxygen levels, whereas further pronounced depression induces energetic stress under hypoxia.
โข O2k-Network Lab: AT_Innsbruck_Gnaiger E, AT_Innsbruck_Jansen-Duerr P, AT Innsbruck MitoCom
Labels:
Stress:Hypoxia Organism: Human
Preparation: Intact cells
Coupling state: OXPHOS
HRR: Oxygraph-2k