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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