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This study aimed to evaluate how excess selenium induces oxidative stress by determining antioxidant enzyme activity and changes in expression of selected selenoproteins in mice.BALB/c mice (n =20 per group)were fed a diet containing 0.045 (Se-marginal), 0.1 (Se-adequate), 0.4 (Se-supernutrition), or 0.8 (Seexcess) mg Se/kg.Gene expression was quantified in RNA samples extracted from the liver, kidney, and testis by real-time quantitative reverse transcription-polymerase chain reaction.We found that glutathione peroxidase (GPx) and catalase activities decreased in livers of mice fed the marginal or excess dose of Se as compared to those in the Se-adequate group.Additionally, superoxide dismutase and glutathione reductase activities were significantly reduced only in mice fed the excess Se diet, compared to animals on the adequate Se diet.Sesupernutrition had no effect on hepatic mRNA levels of GPx isoforms 1 and 4 (GPx1 and GPx4) , down-regulated GPx isoform 3 (GPx3) , and upregulated selenoprotein W (SelW) mRNA expression.The excess Se diet led to decreased hepatic rnRNA levels of GPx1, GPx3 and GPx4 but no change in testicular mRNA levels of GPx1, GPx3 or SelW.Dietary Se had no effect on testicular mRNA levels of GPx4.Thus, our results suggest that Se exposure can reduce hepatic antioxidant capacity and cause liver dysfunction.Dietary Se was found to differentially regulate mRNA levels of the GPx family or SelW, depending on exposure.Therefore, these genes may play a role in the toxicity associated with Se.