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.