Résumé : Background. Antioxidant enzyme status changes in experimental models of chronic renal disease with glomerulosclerosis. Most of the studies are performed in rats. We now investigate whether a mouse model with more rapid development of glomerulosclerosis is suitable for the study of radical-associated renal disease. Methods. Female BALB/c mice are injected intravenously with a single dose of adriamycin (10 mg/kg). The development of glomerular and interstitial injury is evaluated by means of renal function parameters and histology. Renal cortex activities of catalase, Cu/Zn and Mn superoxide dismutase and glutathione peroxidase are measured by enzymatic techniques, and their mRNA levels by Northern blot analysis. Results. The mice develop proteinuria and hypercholesterolaemia; glomerulosclerosis is present 20 days after adriamycin injection. Involvement of reactive oxygen intermediates in the disease process is supported by an increased cortex level of glutathione (1.77±0.13 vs 1.31±0.12 μmol/g kidney; P=0.021) and ferric iron deposition in the tubulointerstitial compartment. Glomerulosclerosis and tubulointerstitial lesions are accompanied by decreased cortex activities of catalase (0.19±0.01 vs 0.23±0.01 U/mg protein; P=0.024), glutathione peroxidase (0.28±0.01 vs 0.32±0.01 U/mg protein; P=0.049) and Mn superoxide dismutase (6.61±0.91 vs 9.25 ± 0.99 U/mg protein, P=0.020). We find decreased cortex mRNA levels only for glutathione peroxidase. Conclusion. The fast development of glomerulosclerosis combined with an altered antioxidant status makes this mouse adriamycin model a suitable alternative for the slower rat models.