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Background and purpose: Hepatocellular carcinoma (HCC) is one of the most fatal cancers, so, proposing new anticancer agents is highly valuable. Production of reactive oxygen species (ROS) is increased in majority of cancers. Increase in ROS leads to cell damage and death. Aminoguanidine (AG) (pimagedine) is one of the compounds that can produce ROS at high concentrations. The present study was conducted to evaluate the effect of aminoguanidine on HepG-2 cell survival and ROS production. Materials and methods: HepG-2 cell were cultured in complete culture medium. To evaluate the viability, MTT assay was done through spectrophotometry. ROS production was measured by fluorimetry using DCFDA dye, and photographs were taken using fluorescent microscope. Results: MTT assay showed 50% decrease in metabolic activity in the cells treated with aminoguanidine 40 mM (54.8±5.2) after 24 hours. Additionally, the results of ROS measurements showed that ROS formation increased by the elevation of aminoguanidine at concentrations above 40 mM. Conclusion: Aminoguanidine could increase ROS production and decrease the cell viability at 40 mM and higher concentrations, therefore, it can induce other cellular pathways including oxidative and nitrosative stress, apoptosis, and necrosis in HepG-2 cells. Interestingly, AG showed antioxidant potentials in concentrations lower than 40 mM and further investigations are needed to clarify this pattern. [ABSTRACT FROM AUTHOR]