To further investigate the biological function of DMS, we observed the effect of DMS on cell lines. ROS production in PC12 cells was stimulated by antimycin A (AA), a mitochondrial respiratory complex III inhibitor. AA increased the levels of O2−·, followed by conversion into other ROS, as judged by the fluorescence signals emitted by the oxidized forms of ROS probes. 2′,7′‐dichlorodihydrofluorescein (H2DCF) was used to evaluate total ROS. Application of AA (100 μg mL−1) for 0.5 h induced an increase of the total ROS level to 256 ± 15% of control (Fig. 2C, P < 0.01). Pretreatment of PC12 cells with DMS (1 and 5 μm) significantly decreased the ROS level to 125 ± 14% and 100 ± 18% of control, respectively (P < 0.01, Fig. 2C). We found that at both low concentration (1 μm) and high concentrations (10 and 100 μm), DMS significantly attenuated H2O2‐induced lipid peroxidation from 159 ± 7% to 131 ± 4%, 123 ± 6% and 120 ± 8% in the brain, respectively (P < 0.01, Fig. 2D). Hydroxyl radical was detected by EPR assay. Cellular radicals were induced as previous report (Ohsawa et al., 2007). DMPO was added to capture the OH˙ radical. As shown in Fig. 2E, AA raised the spin signal to 325 ± 52% of basal level (P < 0.01), and this was reduced to 90 ± 15% of basal level by 5 μm DMS (P < 0.01).