Arsenic is highly toxic naturally occurring element that affects numerous organ systems in humans. Present study was designed to investigate the preventive role of a triterpenoid saponin, arjunolic acid (AA) against arsenic-induced nephrotoxicity in mouse model. For this study, NaAsO 2 was chosen as the source of arsenic. Oral administration of NaAsO 2 at a dose of 10mg/kg body weight for 2 days caused significant accumulation of arsenic in renal tissues as well as altered the activities of serum markers, urea nitrogen (UN) and creatinine, antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione-S-transferase (GST), glutathione reductase (GR) and glutathione peroxidase (GPx), level of cellular metabolites, reduced glutathione (GSH), oxidized glutathione (GSSG) and total thiols, level of lipid peroxidation end products and protein carbonyl content. Treatment with AA at a dose of 20mg/kg body weight for 4 days almost normalized above indices. Histological studies also indicated preventive role of AA against NaAsO 2 -induced nephrotoxicity. The radical scavenging activity and in vivo antioxidant power of AA were determined from its DPPH radical scavenging ability and ferric reducing/antioxidant power (FRAP), respectively. A well-known antioxidant, vitamin C was used as positive control throughout the study. Combining all, results suggest that arsenic could cause kidney damage by inducing oxidative stress in mice and that could be prevented by AA.