MsrA promotes the radical‐scavenging capacity of DMS. (A) We proposed the oxygen atom on the sulfenic acid was derived from H2O2 or other ROS. A lone pair of electrons on the DMS sulfur attacked the sulfenic sulfur to form the positively charged sulfonium intermediate. Glu115 and Tyr103 acted as a proton donor and stabilized by hydrogen bonding with DMS. With the release of DMSO, the reduced form of MsrA was formed. (B) The working hypothesis of DMS‐DMSO recycle system was illustrated. (C) PC12 cells were pretreated with 0, 1, or 5 μm DMS for 30 min and then incubated with AA (100 μg mL−1 for 30 min). The levels of intracellular ROS were detected with H2 DCFDA. The fluorescence intensity of DCF was determined (n = 6–9, one‐way ANOVA, ## P < 0.01 vs. control, **P < 0.01 vs. AA.). The scale bar represented 100 μm. (D) Rat brain tissues were pretreated with DMS (0, 1, 10, or 100 μm for 30 min) and then incubated with H2O2 (250 μm for 30 min). The MDA contents were determined by a MDA test kit. n = 8, one‐way ANOVA, ## P < 0.01 vs. control, **P < 0.01 vs. H2O2 group. (E) Cell culture medium with or without DMS (5 μM) was added into the culture wells for 30 min. And then, PC12 cells were incubated with AA (100 μg mL−1 for 10 min) in the presence of DMPO. Then, EPR signal of DMPO‐OH spin adduct was detected (n = 4, Student's t‐test, ## P < 0.01 vs. control, **P < 0.01 vs. AA). The levels of EPR peak intensity were expressed as a relative change in comparison with the untreated control, which was set to 100%.