Difference between revisions of "Cervinkova 2009 Arch Toxicol"
| Line 1: | Line 1: | ||
{{Publication | {{Publication | ||
|title=Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z ( | |title=Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z (2009) Mechanisms participating in oxidative damage of isolated rat hepatocytes. Arch Toxicol 83: 363-372. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19020865 PMID: 19020865] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/19020865 PMID: 19020865] | ||
|authors=Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z | |authors=Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z | ||
|year= | |year=2009 | ||
|journal=Arch. Toxicol. | |journal=Arch. Toxicol. | ||
|abstract=The aim of the study was to evaluate time course and dose dependence of peroxidative damage induced by ''tert''-butyl hydroperoxide (tBHP) in rat hepatocytes cultured in suspension and in monolayer. At the lowest (0.1 mM) concentration, decrease of cytosolic glutathione and discharge of mitochondrial membrane potential (MMP) could be detected. Significant increases in leakage of lactate dehydrogenase and in malondialdehyde concentrations together with decrease of pyruvate-dependent respiration were detected at higher tBHP concentrations (above 0.5 mM) and after longer periods of incubation. Changes in plasma membrane integrity were observed at 1 mM concentration of tBHP. Succinate-dependent oxidation was most resistant to peroxidative damages. Opening of the mitochondrial permeability transition pore was responsible for the discharge of mitochondria membrane potential. In the presence of cyclosporine A and succinate, the membrane potential could be restored. Our data showed that the most sensitive indicators of the peroxidative damage are changes of cytosolic glutathione concentration and MMP. | |abstract=The aim of the study was to evaluate time course and dose dependence of peroxidative damage induced by ''tert''-butyl hydroperoxide (tBHP) in rat hepatocytes cultured in suspension and in monolayer. At the lowest (0.1 mM) concentration, decrease of cytosolic glutathione and discharge of mitochondrial membrane potential (MMP) could be detected. Significant increases in leakage of lactate dehydrogenase and in malondialdehyde concentrations together with decrease of pyruvate-dependent respiration were detected at higher tBHP concentrations (above 0.5 mM) and after longer periods of incubation. Changes in plasma membrane integrity were observed at 1 mM concentration of tBHP. Succinate-dependent oxidation was most resistant to peroxidative damages. Opening of the mitochondrial permeability transition pore was responsible for the discharge of mitochondria membrane potential. In the presence of cyclosporine A and succinate, the membrane potential could be restored. Our data showed that the most sensitive indicators of the peroxidative damage are changes of cytosolic glutathione concentration and MMP. | ||
Revision as of 17:33, 14 February 2012
| Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z (2009) Mechanisms participating in oxidative damage of isolated rat hepatocytes. Arch Toxicol 83: 363-372. |
Cervinkova Z, Krivakova P, Labajova A, Rousar T, Lotkova H, Kucera O, Endlicher R, Cervinka M, Drahota Z (2009) Arch. Toxicol.
Abstract: The aim of the study was to evaluate time course and dose dependence of peroxidative damage induced by tert-butyl hydroperoxide (tBHP) in rat hepatocytes cultured in suspension and in monolayer. At the lowest (0.1 mM) concentration, decrease of cytosolic glutathione and discharge of mitochondrial membrane potential (MMP) could be detected. Significant increases in leakage of lactate dehydrogenase and in malondialdehyde concentrations together with decrease of pyruvate-dependent respiration were detected at higher tBHP concentrations (above 0.5 mM) and after longer periods of incubation. Changes in plasma membrane integrity were observed at 1 mM concentration of tBHP. Succinate-dependent oxidation was most resistant to peroxidative damages. Opening of the mitochondrial permeability transition pore was responsible for the discharge of mitochondria membrane potential. In the presence of cyclosporine A and succinate, the membrane potential could be restored. Our data showed that the most sensitive indicators of the peroxidative damage are changes of cytosolic glutathione concentration and MMP. • Keywords: Hepatocytes, Oxidative damage, Mitochondrial enzymes
• O2k-Network Lab: CZ_Hradec Kralove_Cervinkova Z
Labels:
Organism: Rat
Tissue;cell: Hepatocyte; Liver"Hepatocyte; Liver" 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.
Preparation: Intact Cell; Cultured; Primary"Intact Cell; Cultured; Primary" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.
HRR: Oxygraph-2k
