Trumbeckaite 2001 Eur J Biochem: Difference between revisions
No edit summary |
No edit summary |
||
Line 50: | Line 50: | ||
|tissues=Cardiac muscle, Skeletal muscle | |tissues=Cardiac muscle, Skeletal muscle | ||
|preparations=Permeabilized tissue | |preparations=Permeabilized tissue | ||
|couplingstates=OXPHOS | |||
|enzymes=Complex I, Complex III | |enzymes=Complex I, Complex III | ||
|discipline=Biomedicine, Pharmacology; Biotechnology | |discipline=Biomedicine, Pharmacology; Biotechnology | ||
}} | }} |
Revision as of 15:36, 27 November 2012
Trumbeckaite S, Opalka JR, Neuhof C, Zierz S, Gellerich FN (2001) Different sensitivity of rabbit heart and skeletal muscle to endotoxin-induced impairment of mitochondrial function. Eur J Biochem 268: 1422-1429. |
Trumbeckaite S, Opalka JR, Neuhof C, Zierz S, Gellerich FN (2001) Eur J Biochem
Abstract: The involvement of mitochondrial dysfunction in septic disturbances of tissues is controversial. The aim of this study was to investigate the effects of endotoxininduced sepsis on the function of heart and skeletal muscle mitochondria. Rabbits were made septic by subcutaneous injection of endotoxin (lipopolysaccharide, LPS) from Escherichia coli at concentrations of 100 or 150 mg LPSยดkg21 24 h prior to the experiments. Mitochondrial respiration was measured in saponin-skinned muscle fibers and compared with photometrically detected activities of respiratory chain enzymes as well as with function of perfused hearts. In heart fibers a dosage of 100 mg LPSยดkg21 caused a significant decrease of state 3-respiration for the substrates pyruvate (238%), octanoyl-carnitine (238%) and succinate (230%) with correspondingly decreased respiratory control indexes (RCI). In addition, endotoxin caused a decreased temporal stability of the rate of state 3-respiration. At least in part these changes can be attributed to a reduced activity of complex I 1 III (250%) of the respiratory chain. State 4-respiration rates were not significantly altered. The lowered state 3-respiration in heart mitochondria seems to contribute to the impairment of heart muscle function as detected by an increase of coronary vascular resistance (CVR) in endotoxin-treated hearts. Functional properties of mitochondria from M. Vastus lasteralis were not affected by 100 mg LPSยดkg21 but a higher dosage of 150 mg LPSยดkg21 caused decreased RCI for the substrates pyruvate (229%) and octanoyl-carnitine (232%). Also the activity of complex I 1 III was not significantly affected at lower dose of endotoxin but decreased (242%) after treatment with 150 mg LPSยดkg21. Results demonstrate the involvement of impaired mitochondria in the pathophysiology of septic organ failure and a tissue specifity of endotoxaemia. โข Keywords: Sepsis, Endotoxin, Mitochondria, Heart, Skeletal muscle
โข O2k-Network Lab: DE Magdeburg Gellerich FN
Labels:
Organism: Other Mammal"Other Mammal" is not in the list (Human, Pig, Mouse, Rat, Guinea pig, Bovines, Horse, Dog, Rabbit, Cat, ...) of allowed values for the "Mammal and model" property.
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., Skeletal muscle
Preparation: Permeabilized tissue
Enzyme: Complex I, Complex III
Coupling state: OXPHOS
HRR: Oxygraph-2k