Piskernik 2008 Biochim Biophys Acta: Difference between revisions

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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.

» PMID: 18298959

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

@@ Line 5: / Line 5: @@
 |journal=Biochim. Biophys. Acta
 |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.
+|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
 |info=[http://www.ncbi.nlm.nih.gov/pubmed/18298959 PMID: 18298959]