The effects of nitric oxide (NO) in protecting maize (Zea mays) roots against cadmium (Cd) toxicity were investigated. Maize seedlings pretreated for 24 h with 10-40 µM sodium nitroprusside (SNP), an NO donor, and subsequently exposed to 5 µM Cd for 24 h exhibited significantly greater root elongation as compared with the plants without SNP pretreatment. The pretreatment with 20 µM SNP alleviated Cd toxicity most obviously. SNP reduced Cd-induced accumulation of hydrogen peroxide (H2O2) and malonodialdehyde (MDA), which indicated NO alleviated Cd-induced oxidative damage. Cd treatment resulted in an upregulation of activities of superoxide dismutase (SOD), peroxidase (POD) and ascorbate peroxidase (APX) and the contents of glutathione (GSH) and ascorbate (ASC). Though SNP suppresses activities of POD, SOD and APX, it increases the production of non-enzymic antioxidants including glutathione (GSH) and ascorbate (ASC). The protective effect of SNP on Cd toxicity can be reversed by 2-(4-carboxy-2-phenyl)-4,4,5,5 -tetramethylimidazoline-1-oxyl-3-oxide (cPTIO), a NO scavenger, suggesting that the protective effect of SNP is attributable to NO released. These results suggest that NO plays an important role in protecting the plant against Cd-induced oxidative damage.