Piskernik 2008 Biochim Biophys Acta
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 dotβ) from rat heart mitochondria (RHM), while O2radical dotβ generated in intact RHM do not escape from mitochondria. This was shown by a set of O2radical dotβ-sensitive spin probes with varying hydrophobicity. The levels of O2radical dotβ 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 dotβ levels. Elevated O2radical dotβ levels became sensitive to SOD but in a different manner. The determination of O2radical dotβ with water-soluble PPH was fully sensitive to SOD, while the determination of O2radical dotβ with the more hydrophobic CMH and CPH was only partially sensitive to SOD, suggesting the release of a portion of O2radical dotβ into the surrounding medium. β’ Keywords: Mitochondria, Superoxide radical, Electron spin resonance, Spin probe, Endotoxic shock, Apoptosis
β’ O2k-Network Lab: AT_Vienna_Kozlov AV
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.
Coupling state: OXPHOS
HRR: Oxygraph-2k