Efficacy of diphenyl diselenide against cerebral and pulmonary damage induced by cadmium in mice

This study was designed to examine if diphenyl diselenide (PhSe)2, an organoselenium compound, attenuates pulmonar and cerebral oxidative stress caused by sub-chronic exposure to CdCl2. Male adult Swiss albino mice received CdCl2 (10 μmol/kg, subcutaneously), 5 times/week, for 4 weeks. (PhSe)2 (10 μmol/kg or 20 μmol/kg, orally) was given concomitantly with CdCl2 to mice. A number of toxicological parameters in lung and brain of mice were examined including δ-aminolevulinic acid dehydratase (δ-ALA-D), superoxide dismutase (SOD) and catalase activities, lipid peroxidation, non-protein thiols (NPSH) and ascorbic acid content. Na+,K+-ATPase activity, acetylcholinesterase (AChE) activity, [3H]glutamate uptake and [3H]glutamate release were also carried out in brain. Cadmium concentration and histopathological analysis were carried out in lung tissue. (PhSe)2 at the dose of 20 μmol/kg protected the inhibition of δ-ALA-D, SOD and CAT activities, the reduction of vitamin C content and the increase of lipid peroxidation levels caused by CdCl2 in lungs. At 10 μmol/kg, (PhSe)2 protected cerebral AChE and CAT activities inhibited by CdCl2. There were no histopathological alterations in the lung of mice after CdCl2 exposure. The pulmonary cadmium concentration was higher (2.8-fold) in the group exposed to CdCl2 than in control mice. (PhSe)2 at dose of 20 μmol/kg reduced cadmium concentration towards the control level. The results suggest that oral administration of (PhSe)2 attenuated the oxidative damage induced by CdCl2 in lung and brain of mice.