The present study was conducted to investigate whether the combined treatment with Se and Zn offers more beneficial effects than that provided by either of them alone in reversing Cd-induced oxidative stress in the kidney of rat. For this purpose, 30 adult male Wistar albino rats, equally divided into control and four treated groups, received either 200 ppm Cd (as CdCl(2)), 200 ppm Cd + 500 ppm Zn (as ZnCl(2)), 200 ppm Cd + 0.1 ppm Se (as Na(2)SeO(3)), or 200 ppm Cd + 500 ppm Zn + 0.1 ppm Se in their drinking water for 35 days. The results showed that Cd treatment decreased significantly the catalase (CAT) and glutathione peroxidase (GSH-Px) activities, whereas the superoxide dismutase (SOD) activity and the renal levels of lipid peroxidation (as malondialdehyde, MDA) were increased compared to control rats. The treatment of Cd-exposed rats with Se alone had no significant effect on the Cd-induced increase in the MDA concentrations but increased significantly the CAT activities and reversed Cd-induced increase in SOD activity. It also partially prevented Cd-induced decrease in GSH-Px activity. The treatment of Cd-exposed animals with Zn alone increased significantly the CAT activity and partially protected against Cd-induced increase in the MDA concentrations, whereas it had no significant effect on the Cd-induced increase in SOD activity and decrease in GSH-Px activity. The combined treatment of Cd-exposed animals with Se and Zn was more effective than that with either of them alone in reversing Cd-induced decrease in CAT and GSH-Px activities and Cd-induced increase in MDA concentrations. Results demonstrated beneficial effects of combined Se and Zn treatment in Cd-induced oxidative stress in kidney and suggest that Se and Zn can have a synergistic role against Cd toxicity.

Cadmium (Cd), one of the most widely distributed heavy metals, is highly toxic to humans and animals. It is well known that zinc (Zn) and selenium (Se) administration reduce the Cd-induced toxicity and that metallothioneins can have a protective effect to mitigate Cd toxicity in biological systems. In this study we report the expression analysis of the two metallothioneines gene classes MT-1 and MT-2 as well as the total metalloprotein content in the liver of rats exposed to Cd (200 ppm), Cd + Zn (200 ppm + 500 ppm), Cd + Se (200 ppm + 0.1 ppm) or Cd + Zn + Se (200 ppm + 500 ppm + 0.1 ppm) in their drinking water for 35 days. Metals accumulation was quantified in rat liver. Cd decreased significantly the hepatic concentrations of Se and increased those of Zn. The treatment of Cd-exposed rats with Se alone or combined with Zn reversed the Cd-induced depletion of Se concentrations in the liver. However, Zn or Zn + Se administration significantly increased the liver Cd uptake and had no effect on the Cd-induced increase in hepatic concentrations of Zn. The molecular assay showed a decreasing trend of MT-1 relative gene expression levels in animals supplemented with Zn (6.87-fold), Se (3.58-fold), and their combination (1.69-fold) when compared to Cd-treated animals (16.22-fold). Upregulation of the MT-2 expression were recorded in all conditions, although fold induction levels were less pronounced than MT-1 expressions. Our data suggest that the well-established protective effect of Zn and Se against Cd-induced toxicity passes through non-MT gene expression mechanisms, being more dependent on the oxidative stress status of the cell.

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