Heavy metal pollution has become one of the major problems the world, with cadmium (Cd) the most widespread pollution. Cd is a heavy metal without biological functions and highly toxic to plants and animals. Its accumulation in soil is becoming a severe threat to crop production as well as human health. The presence of excessive amount of Cd may cause toxicity to plants, resulting in stunted growth, strong reduction in biomass production, damage of the photosynthetic apparatus, reduction in chlorophyll content and disturbance of mineral nutrition and carbohydrate metabolism. Nitric oxide (NO) is a bioactive gas and is an important signaling molecule with diverse physiological functions in plants. Recently, a lot of researchers found that NO plays an important role in mediating some biotic and abiotic stress-induced oxidative stresses in plant kingdom. To understand the regulative effect of exogenous nitric oxide on the physiological and biochemical responses of rice seedlings under cadmium stress, in the present study, two rice cultivars, ZF802 (indica) and ZH11 (japonica) grown in IRRI's nutrient solution were used to investigate the effects of exogenous nitric oxide (sodium nitroprusside as NO donor) on the growth of seedlings, activities of antioxidant enzymes (SOD and POD) and microelements accumulation in two rice genotypes under 100 μmol/L cadmium stress. The results showed that addition of 1.5 mmol/L exogenous SNP significantly alleviated the inhibitory effect of Cd²⁺ stress on the growth of rice seedlings. Exogenous SNP also decreased the activities of superoxide dismutase (SOD) and peroxidase (POD), and the contents of malondialdehyde (MDA) in the leaves of rice seedlings under Cd stress, despite of certain genotype difference, suggesting that SNP could alleviate oxidative damage of rice seedlings caused by Cd. In addition, exogenous NO supply affected Cd and microelements accumulation of the shoots and roots of rice seedlings under Cd stress. The effects had significant genotypic difference and complex mechanism.