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 CdCl 2 . Male adult Swiss albino mice received CdCl 2 (10μmol/kg, subcutaneously), 5 times/week, for 4 weeks. (PhSe) 2 (10μmol/kg or 20μmol/kg, orally) was given concomitantly with CdCl 2 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, [ 3 H]glutamate uptake and [ 3 H]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 20μmol/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 CdCl 2 in lungs. At 10μmol/kg, (PhSe) 2 protected cerebral AChE and CAT activities inhibited by CdCl 2 . There were no histopathological alterations in the lung of mice after CdCl 2 exposure. The pulmonary cadmium concentration was higher (2.8-fold) in the group exposed to CdCl 2 than in control mice. (PhSe) 2 at dose of 20μmol/kg reduced cadmium concentration towards the control level. The results suggest that oral administration of (PhSe) 2 attenuated the oxidative damage induced by CdCl 2 in lung and brain of mice.