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The aim of the present study was to investigate the effects of cadmium (Cd) (5 and 50 mg Cd/l in drinking water) and ethyl alcohol (ethanol, EtOH) (5 g EtOH/kg b.wt., intragastrically), administered alone or simultaneously, on the concentrations of pro-inflammatory (interleukin-1, IL-1α; interleukin-6, IL-6; tumor necrosis factor-α, TNFα and interferon γ, INFγ) and anti-inflammatory (interleukin-4, IL-4) cytokines in the serum of rats. In order to estimate the involvement of Cd- or/and EtOH-induced oxidative stress in damage to cytokines, the concentration of protein carbonyl groups (PC), as a marker of oxidative protein damage, was also determined. Exposure to 5 and 50 mg Cd/l, alone or in combination with EtOH, led to an increase in the serum concentrations of IL-1α, TNFα and INFγ with a simultaneous decrease in IL-4 concentration, compared to the control. The concentration of IL-6 was elevated only after administration of 50 mg Cd/l, both alone and in combination with EtOH. The exposure to EtOH alone resulted in increased concentrations of TNFα and INFγ, as well as in decreased concentrations of IL-4. In rats co-exposed to Cd and EtOH, the changes observed in the concentrations of the cytokines, except in IL-6, were more advanced, compared to the animals treated with these xenobiotics alone. Exposure to Cd and EtOH, both alone and in combination, caused an increase in the serum PC concentration. The concentration of PC positively correlated with the concentrations of IL-1α, IL- 6, TNFα and INFγ and negatively with IL-4 concentration. The results suggest that changes in the cytokines examined are more enhanced after combined exposure to Cd and EtOH, especially at higher Cd dosage. Moreover, it can be hypothesized that oxidative stress may be involved in the mechanism leading to changes in the concentration of cytokines after exposure to Cd and EtOH alone and in combination. [ABSTRACT FROM AUTHOR]

The activity of glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) was investigated in liver and kidney of rats exposed to cadmium (Cd) and ethanol (EtOH) alone and in combination. Rats were treated with 50 mg Cd/dm³ in drinking water and/or 5 g of EtOH/kg body wt/24 h intragastrically, for 12 weeks. Exposure to Cd led to an increase in GPx and GST activity with a simultaneous decrease in GR activity in the liver. In the kidney of rats treated with Cd, an increase in the activity of GPx and GR was noted. In the EtOH-exposed rats, GPx activity decreased in the liver, but increased in the kidney. Exposure to EtOH caused a reduction in GR activity only in the liver. The co-exposure to Cd and EtOH led to an increase in the liver and kidney GPx activity compared to control. In the rats simultaneously exposed to Cd and EtOH liver activity of GR decreased compared to control, whereas the kidney GR activity increased compared to control as well as to the groups treated with Cd and EtOH seperately. The co-exposure to Cd and EtOH led to an increase in the liver activity of GST compared to the control and EtOH groups. Analysis of variance (ANOVA/MANOVA) revealed that the changes noted in the activity of investigated enzymes in the Cd + EtOH group resulted from the independent action of both Cd or EtOH as well as from their interactive action. Numerous correlations (negative or positive) were noted between the activity of GPx, GR and GST, and the concentration of GSH, Cd and MDA in the liver and kidney. On the basis of our results it can be concluded that changes in the activity of GPx, GR and GST in the liver and kidney may be involved in the mechanism leading to a decrease in GSH concentration in these organs due to exposure to Cd and EtOH alone and in conjunction with each other. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]

In the present study, the effect of co-exposure to cadmium (Cd) and ethanol (EtOH) on concentrations of vitamins E and C were evaluated in the liver and kidney homogenates of rats which were administered, singly or in combination, Cd (50 mg Cd/dm³ in drinking water) and EtOH (5 g EtOH/kg b. wt./24 h, intragastrically) for 12 weeks. The exposure to Cd caused a decrease in the concentration of vitamins E and C in the liver, whereas the concentration of vitamin E increased in the kidney, compared to control group. EtOH administration led to a decrease in vitamins E and C concentrations in the liver. Exposure to Cd alone enhanced the concentration of vitamin C in the kidney. In the co-exposed group, the concentration of vitamin E decreased in the liver as compared to control and Cd group but increased in comparison to EtOH group. The concentration of vitamin C in this organ decreased compared to control and Cd- or EtOH-exposed groups. The co-exposure to both substances caused a rise in vitamin E concentration in the kidney compared to control and EtOH groups, whereas the concentration of vitamin C increased compared to control and Cd group. In the liver positive correlation was noted between vitamin E or C concentrations and glutathione (GSH) concentration. In the kidney, negative correlation was found between the concentration of vitamin E and GSH. No correlation was observed between the concentration of vitamin C and GSH in this organ. The results obtained suggest that the change in vitamin E concentration in the liver of rats co-exposed to Cd and EtOH resulted from an independent action of EtOH and its interaction with Cd, whereas in the kidney it was due to an independent Cd effect. In the animals co-exposed to Cd and EtOH, the change in vitamin C detected in the liver was the result of an independent action of either Cd or EtOH. In the kidney, the concentration of vitamin C was only EtOH-dependent. The results of this study together with our previous finding in the model used suggest the involvement of vitamins E and C in the development of Cd- and/or EtOH-induced oxidative stress. [ABSTRACT FROM AUTHOR]

The involvement of some low-molecular thiol compounds in the mechanisms of peroxidative action of cadmium (Cd) and ethanol (EtOH) was studied. Concentrations of reduced glutathione (GSH), metallothionein (Mt) and thiol (-SH) groups in protein and non-protein fractions were assessed in the homogenates of the liver and kidney of rats exposed to Cd (50 Cd/dm³ of drinking water) and EtOH (5 g EtOH/kg body weight/24 h, intragastrically), singly or in combination, for 12 weeks. Exposure to Cd caused a reduction in the concentration of GSH and non-protein SH groups in the liver and kidneys with a simultaneous increase in Mt level in these organs. The concentration of total SH groups increased only in kidneys. Administration of EtOH had no effect on Mt concentration in both organs, but caused a reduction in the concentration of GSH and non-protein SH groups. A reduction in the level of total SH groups following exposure to EtOH was also noted in the liver. In the group of rats with a simultaneous exposure to Cd and EtOH, GSH concentration was decreased in the liver compared to the control and Cd-exposed animals, and in the kidney in comparison to the control and EtOH-receiving rats. Following the combined exposure to Cd and EtOH, the concentration of non-protein SH groups decreased in the liver and kidneys in comparison to the control and Cd-exposed rats, and in the liver also in comparison to the EtOH group. Mt concentration increased in the liver and kidneys of animals exposed to a combination of Cd and EtOH, compared to the control and EtOH group, but was reduced compared to the Cd group. Combined administration of Cd and EtOH caused an increase in the concentration of total SH groups in the kidneys compared to the control, Cd and EtOH groups. A negative correlation was found between GSH concentration and malondialdehyde (MDA) levels and positive correlation between Mt and MDA. The intensity of lipid peroxidation as well as GSH and Mt concentrations influencing this process in the state of combined exposure to Cd and EtOH results both from independent actions of these substances and interactions between them. The study outcome seems to indicate that the Cd-and EtOH-induced reduction in GSH and non-protein SH groups in the liver and kidneys may be one of the mechanisms that leads to lipid peroxidation in these organs. [ABSTRACT FROM AUTHOR]