Abstract: Microcystins are a family of toxins produced by freshwater cyanobacteria.They are cyclic heptapeptides, composed of seven amino acids.They exert a toxic effect by being specific inhibitors of the protein phosphatases 1 and 2A (PP1 and PP2A), but recent evidences also indicate its potential to generate oxidative stress.Oxidative stress is a general term used to describe the steady state level of oxidative damage in cells,tissues, or organs, caused by the reactive oxygen species(ROS).In this experiment, the toxic mechanism of MC-RR inducing oxidative stress was evaluated in tobacco BY-2 suspension cells.Changes of ROS formation and antioxidant system of tobacco BY-2 suspension cellswere studied under the treatment of 2 μg/mLMC-RR,2 μg/mLMC-RR +0.5 % DMSO and 2 μg/mLMC-RR +2 mmol/L ASA.Under the treatment of 2 μg/mL MC-RR,the contents of ROS ,MDA and ASA as well as the activities of SOD and POD were higher than those in control after 5 days treatment.GSH content first decreased and then increased, and at the 6th day of treatment GSH content significantly increased compared with the control.The abundant accumulation of ROS and the change of antioxidant system both indicated that the cells suffered from oxidative stress induced by MC-RR.ROS may play an important role in its toxic effect on the cells.The MC-RR-induced oxidative stress in cellswas further confirmed by exposing the cells to MC-RR in the presence of two ROS scavengers ,ASA or DMSO.ASA has significant capacity of scavenging O2- and H2O2, and DMSO is a kind of hydroxyl radical scavengers.When tobacco BY-2 suspension cells were exposed to 2 μg/mLMCRRwith 0.5%DMSO or 2 mmol/L ASA , the formation of ROS and MDA were prevented and the contents of GSH ,ASA and activities of SOD and POD all decreased in contrast to MC-RR treatment.It concluded that tobacco BY-2 suspension cells suffered oxidative stress after MC-RR treatment and the exogenous ASA and DMSO can protect the cells fromMC-RR induced oxidative stress.