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The aim of the study was the evaluation of cadmium effects on the activity of antioxidant enzymes in rat hepatocytes. The studies were conducted with isolated rat hepatocytes incubated for 1 or 2 hours in a modified (deprived of carbonates with phosphates) Williams’ E medium (MWE) in the presence of cadmium chloride (25, 50 and 200 μM). Hepatocytes incubated in the MWE medium without cadmium chloride were used as a control. The application of the modified Williams’ E medium allowed for the appearance of cadmium compounds in a soluble form that is indispensable for suitable estimation of its toxic action. There were evaluated markers of the oxidative stress such as: concentration of thiobarbiturate reactive substances (TBARS) – proportional to the level of lipid peroxidation, concentration of reduced glutathione (GSH), and the activity of antioxidant enzymes, including superoxide dismutase (SOD1 and SOD2), catalase (CAT), total glutathione peroxidase (GSHPx), selenium – dependent glutathione peroxidase (SeGSHPx), glutathione transferase (GST) and glutathione reductase (GSHR). Alterations of antioxidant enzymes activity, the level of TBARS and GSH in isolated rat hepatocytes caused by cadmium in vitro, were shown to depend on the concentration and time of exposure of cells to this metal. The increased level of TBARS and GSH was observed as well as changes in the activity of antioxidant enzymes. The activity of SOD isoenzymes and CAT was increased, whereas GSHPx and GST were decreased. These results indicate that cadmium induces oxidative stress followed by alterations in the cellular antioxidant enzyme system in isolated rat hepatocytes.
The aim of our study was to evaluate oxidative stress in hepatic mitochondria of rats exposed for 12 weeks alone and in conjunction to cadmium (Cd) (50 mg Cd/dm3, in drinking water) and ethanol (EtOH) (5g of EtOH/kg body wt, intragastrically). In hepatic mitochondria the concentrations of malondialdehyde (MDA), hydrogen peroxide (H2O2), reduced glutathione (GSH) and the activities of manganese superoxide dismutase (MnSOD), glutathione peroxidase (GPx) and glutathione reductase (GR) were measured. After exposure to Cd, an increase in MDA and H2O2 concentrations with a simultaneous decrease in GSH concentration and the activities of MnSOD, GPx and GR were noted. Exposure to EtOH caused an increase in MDA and H2O2 concentration, as well as MnSOD and GPx activities and a decrease in GSH concentration and GR activity. Co-exposure to Cd and EtOH caused an increase in MDA and H2O2 con­centration as well as in MnSOD activity and resulted in a decrease in GSH concentration as well as GPx and GR activities in comparison to the control group. The increase in H2O2 concentration and MnSOD activity as well as the decrease in GSH concentration were significant compared to the animals exposed to Cd alone. The changes noted in the investigated parameters in hepatic mitochondria of the rats co-exposed to Cd and EtOH resulted from an independent action of Cd (H2O2, GSH and GPx) or EtOH (H2O2, GSH and MnSOD) as well as from their mutual interaction (GSH, MnSOD and GPx). Based on all results, it can be concluded that exposure to Cd and EtOH, both alone and in conjunction, leads mainly to changes in the concentration of H2O2 and GSH and MnSOD activity in the liver mitochon­dria.
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