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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-1?; interleukin-6, IL-6; tumor necrosis factor-?, TNF? and interferon ?, INF?) 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-1?, TNF? and INF? 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 TNF? and INF?, 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-1?, IL- 6, TNF? and INF? 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.
Specificity of targeting of the oxidative stress towards lipid and protein fractions in a model of estrogen-induced Syrian hamster nephrocarcinogenesis was evaluated. The amount of proteins modified by oxidative stress was significantly elevated as early as one month after the initial implantation of estradiol to the experimental ver­sus the control group, while the stress did not affect lipids. Subcellular localization of the oxidative stress target was determined by the analysis of protein oxidation in subcellular fractions of kidney cells. The endoplasmic reticulum membranes were the fraction most affected by the oxidative stress.
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