Piskernik 2008 Biochim Biophys Acta: Difference between revisions
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{{Publication | {{Publication | ||
|title=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 | |title=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 1782:280-5. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18298959 PMID: 18298959 Open Access] | |||
|authors=Piskernik C, Haindl S, Behling T, Gerald Z, Kehrer I, Redl H, Kozlov AV | |authors=Piskernik C, Haindl S, Behling T, Gerald Z, Kehrer I, Redl H, Kozlov AV | ||
|year=2008 | |year=2008 | ||
|journal=Biochim | |journal=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 (O<sub>2</sub>radical dot−) from rat heart mitochondria (RHM), while O<sub>2</sub>radical 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 O<sub>2</sub>radical 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 O<sub>2</sub>radical dot− with water-soluble PPH was fully sensitive to SOD, while the determination of O<sub>2</sub>radical 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. | |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 (O<sub>2</sub>radical dot−) from rat heart mitochondria (RHM), while O<sub>2</sub>radical 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 O<sub>2</sub>radical 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 O<sub>2</sub>radical dot− with water-soluble PPH was fully sensitive to SOD, while the determination of O<sub>2</sub>radical 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 | |keywords=Mitochondria, Superoxide radical, Electron spin resonance, Spin probe, Endotoxic shock,Apoptosis | ||
| | |mipnetlab=AT Vienna Kozlov AV | ||
|discipline=Mitochondrial Physiology | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |organism=Rat | ||
|tissues= | |tissues=Heart | ||
| | |couplingstates=OXPHOS | ||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|discipline=Mitochondrial Physiology | |||
}} | }} | ||
Latest revision as of 15:59, 20 March 2015
| 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 1782:280-5. |
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 Kozlov AV
Labels:
Organism: Rat
Tissue;cell: Heart
Coupling state: OXPHOS
HRR: Oxygraph-2k
