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

Abstract

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 (CdCl 2) was investigated in rats. Male adult Swiss albino rats received CdCl 2 (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 CdCl 2 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 CdCl 2 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 CdCl 2 exposure. Urea and bilirubin levels increased by CdCl 2 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 CdCl 2. 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.