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 Biophys Acta 1782: 280- | |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] | |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 | ||
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|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 dotโ) from rat heart mitochondria (RHM), while O<sub>2</sub>radical dotโ generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dotโ-sensitive spin probes with varying hydrophobicity. The levels of O<sub>2</sub>radical dotโย 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 dotโ levels. Elevated O2radical dotโ levels became sensitive to SOD but in a different manner. The determination of O<sub>2</sub>radical dotโ with water-soluble PPH was fully sensitive to SOD, while the determination of O<sub>2</sub>radical dotโ with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dotโ 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 dotโ) from rat heart mitochondria (RHM), while O<sub>2</sub>radical dotโ generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dotโ-sensitive spin probes with varying hydrophobicity. The levels of O<sub>2</sub>radical dotโย 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 dotโ levels. Elevated O2radical dotโ levels became sensitive to SOD but in a different manner. The determination of O<sub>2</sub>radical dotโ with water-soluble PPH was fully sensitive to SOD, while the determination of O<sub>2</sub>radical dotโ with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dotโ 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= | |mipnetlab=AT Vienna Kozlov AV | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Rat | |organism=Rat | ||
|tissues=Heart | |tissues=Heart | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|instruments=Oxygraph-2k | |||
|discipline=Mitochondrial Physiology | |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 dotโ) from rat heart mitochondria (RHM), while O2radical dotโ generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dotโ-sensitive spin probes with varying hydrophobicity. The levels of O2radical dotโ 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 dotโ levels. Elevated O2radical dotโ levels became sensitive to SOD but in a different manner. The determination of O2radical dotโ with water-soluble PPH was fully sensitive to SOD, while the determination of O2radical dotโ with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dotโ into the surrounding medium. โข Keywords: Mitochondria, Superoxide radical, Electron spin resonance, Spin probe, Endotoxic shock, Apoptosis
โข O2k-Network Lab: AT Vienna Kozlov AV
Labels:
Organism: Rat
Tissue;cell: Heart
Coupling state: OXPHOS
HRR: Oxygraph-2k