Difference between revisions of "Piskernik 2008 Biochim Biophys Acta"
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|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|organism=Rat | |organism=Rat | ||
|tissues= | |tissues=Heart | ||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|discipline=Mitochondrial Physiology | |discipline=Mitochondrial Physiology | ||
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Revision as of 12:08, 27 February 2013
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_Kozlov AV
Labels:
Organism: Rat
Tissue;cell: Heart
Coupling state: OXPHOS
HRR: Oxygraph-2k