Oral administration of diphenyl diselenide protects against cadmium-induced liver damage in rats

Cadmium is an environmental toxic metal implicated in human diseases. In the present study, the effect of diphenyl diselenide, (PhSe)2, on sub-chronic exposure with cadmium chloride (CdCl2) was investigated in rats. Male adult Swiss albino rats received CdCl2 (10 μmol/kg, orally) and (PhSe)2 (5 μmol/kg, orally) for a period of 30 days. A number of parameters were examined as indicators of toxicity, including hepatic and renal damage, glucose and glycogen levels and markers of oxidative stress. Cadmium content, liver histology, δ-aminolevulinate dehydratase (δ-ALA-D) activity, metallothionein (MT) levels were also evaluated. Cadmium content determined in the tissue of rats exposed to CdCl2 provides evidence that the liver is the major cadmium target where (PhSe)2 acts. The concentration of cadmium in liver was about three fold higher than that in kidney, and (PhSe)2 reduced about six fold the levels of this metal in liver of rats exposed. Rats exposed to CdCl2 showed histological alterations abolished by (PhSe)2 administration. (PhSe)2 administration ameliorated plasma malondialdehyde (MDA) levels, aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH) and gamma-glutamyl transferase (GGT) activities increased by CdCl2 exposure. Urea and bilirubin levels increased by CdCl2 exposure were also reduced by (PhSe)2. In conclusion, this study demonstrated that co-treatment with (PhSe)2 ameliorated hepatotoxicity and cellular damage in rat liver after sub-chronic exposure with CdCl2. The proposed mechanisms by which (PhSe)2 acts in this experimental protocol are its antioxidant properties and its capacity to form a complex with cadmium.