Difference between revisions of "Piskernik 2008 Biochim Biophys Acta"
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|journal=Biochim. Biophys. Acta | |journal=Biochim. Biophys. Acta | ||
|mipnetlab=AT_Vienna_KozlovA | |mipnetlab=AT_Vienna_KozlovA | ||
|abstract=Here we show that both Antimycin A, a respiratory chain inhibitor inducing apoptosis, and endotoxic shock, a syndrome accompanied by both necrosis and apoptosis, cause not only an increase but also the leakage of superoxide radicals (O2radical dot−) from rat heart mitochondria (RHM), while O2radical dot− generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dot−-sensitive spin probes with varying hydrophobicity. The levels of O2radical dot− detected in intact RHM gradually increase as the hydrophobicity of spin probes increases and were not sensitive to superoxide dismutase (SOD) added to the incubation medium. Both Antimycin A and endotoxic shock elevated O2radical dot− levels. Elevated O2radical dot− levels became sensitive to SOD but in a different manner. The determination of O2radical dot− with water-soluble PPH was fully sensitive to SOD, while the determination of O2radical dot− with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dot− into the surrounding medium. | |||
|keywords=Mitochondria, Superoxide radical, Electron spin resonance, Spin probe, Endotoxic shock,Apoptosis | |||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18298959 PMID: 18298959] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18298959 PMID: 18298959] | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|discipline=Mitochondrial Physiology | |||
|organism=Rat | |organism=Rat | ||
|tissues=Cardiac Muscle | |||
|topics=Respiration; OXPHOS; ETS Capacity | |topics=Respiration; OXPHOS; ETS Capacity | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
}} | }} |
Revision as of 10:47, 19 October 2010
Piskernik C, Haindl S, Behling T, Gerald Z, Kehrer I, Redl H, Kozlov AV (2008) Antimycin A and lipopolysaccharide cause the leakage of superoxide radicals from rat liver mitochondria. Biochim. Biophys. Acta 1782: 280-285. |
Piskernik C, Haindl S, Behling T, Gerald Z, Kehrer I, Redl H, Kozlov AV (2008) Biochim. Biophys. Acta
Abstract: Here we show that both Antimycin A, a respiratory chain inhibitor inducing apoptosis, and endotoxic shock, a syndrome accompanied by both necrosis and apoptosis, cause not only an increase but also the leakage of superoxide radicals (O2radical dot−) from rat heart mitochondria (RHM), while O2radical dot− generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dot−-sensitive spin probes with varying hydrophobicity. The levels of O2radical dot− detected in intact RHM gradually increase as the hydrophobicity of spin probes increases and were not sensitive to superoxide dismutase (SOD) added to the incubation medium. Both Antimycin A and endotoxic shock elevated O2radical dot− levels. Elevated O2radical dot− levels became sensitive to SOD but in a different manner. The determination of O2radical dot− with water-soluble PPH was fully sensitive to SOD, while the determination of O2radical dot− with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dot− into the surrounding medium. • Keywords: Mitochondria, Superoxide radical, Electron spin resonance, Spin probe, Endotoxic shock, Apoptosis
• O2k-Network Lab: AT_Vienna_KozlovA
Labels:
Organism: Rat
Tissue;cell: Cardiac Muscle"Cardiac Muscle" is not in the list (Heart, Skeletal muscle, Nervous system, Liver, Kidney, Lung;gill, Islet cell;pancreas;thymus, Endothelial;epithelial;mesothelial cell, Blood cells, Fat, ...) of allowed values for the "Tissue and cell" property.
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" 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