Mechanisms participating in oxidative damage of isolated rat hepatocytes
Language English Country Germany Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Cytosol drug effects metabolism MeSH
- Glutathione metabolism MeSH
- Hepatocytes drug effects metabolism MeSH
- Mitochondria, Liver drug effects enzymology physiology MeSH
- Rats MeSH
- Cells, Cultured MeSH
- L-Lactate Dehydrogenase metabolism MeSH
- Malondialdehyde metabolism MeSH
- Membrane Potential, Mitochondrial drug effects MeSH
- Oxidative Stress drug effects physiology MeSH
- Oxidants toxicity MeSH
- Lipid Peroxidation drug effects MeSH
- Rats, Wistar MeSH
- Oxygen Consumption drug effects MeSH
- tert-Butylhydroperoxide toxicity MeSH
- Cell Survival drug effects MeSH
- Dose-Response Relationship, Drug MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Glutathione MeSH
- L-Lactate Dehydrogenase MeSH
- Malondialdehyde MeSH
- Oxidants MeSH
- tert-Butylhydroperoxide MeSH
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.
References provided by Crossref.org
In vitro toxicity of epigallocatechin gallate in rat liver mitochondria and hepatocytes