Cadmium and cadmium compounds have a wide variety of industrial applications such as electroplating, pigments, plastics and Cd-Ni batteries. In animals, acute Cd poisoning produces primarily hepatic and testicular injury, whereas chronic exposure results in renal damage and osteotoxicity. Several lines of evidence indicate that reactive oxygen species are involved in cadmium-mediated tissues damage, which could cause oxidative stress as assessed by increased lipid oxidation and decrease in antioxidant defenses. Selenium is an essential dietary trace element that plays a crucial role in gluthatione peroxidase and thioredoxin redutase activities. The concept that selenium-containing molecules may be better nucleophiles (and therefore antioxidants) than classical antioxidants, has led to design synthetic organoselenium compounds. In this investigation we evaluated the possible protector role of ebselen, an organoselenium compound, on cadmium-induced testicular damage in Swiss mice. Animals were injected intraperitoneally with a single dose of CdCl₂ (2.5 and 5 mg/kg) and 30 minutes later they were subcutaneously injected with ebselen (100 mmol/kg). Mice were killed 24 hours after cadmium administration and blood and testes were removed. Thus, we determined lipid peroxidation (Ohkawa et al., 1979), ascorbic acid (Jacques-Silva et al., 2001) levels and d-aminolevulinic acid dehydratase (d-ALA-D) activity (Sassa, 1982). Data were statistically analyzed by two-way ANOVA, followed by Duncan’s Multiple Range Test when appropriate. The results demonstrated that animals exposed to 2.5 and 5 mg/kg cadmium presented a reduction in testicular d- ALA-D activity (36 and 38 %, respectively), an increase in lipid peroxidation levels (150 and 160 %, respectively) and a reduction in ascorbic acid levels (43 and 30 %, respectively). Ebselen was effective in restoring enzyme activity at the control levels, while this therapy did not ameliorate lipid peroxidation and ascorbic acid levels.  We suggest that ebselen was effective, at least in part, in protecting against cadmium-induced testes damage in mice, since it restored d- ALA-D activity at the control levels.