Antioxidant assay and ESEM observation were carried out to investigate the antioxidant and anti-bladder cancer activities of myricetin． The results show that myricetin can effectively inhibit the AAPH-induced hemolysis of erythrocytes in a dose-dependent manner． The hemolysis inhibition rate of myricetin increases to ( 93. 67 ± 0. 01) % at a concentration of 80 μmol /L． A further experiment confirms that SOD and GPx antioxidant enzyme activities are enhanced to control ＲOS and MDA generation when erythrocytes are preconditioned by myricetin． Moreover，MTT tests indicate that myricetin could suppress the EJ and T24 bladder cancer cells proliferation in a dose-related manner with the half-maximal inhibitory concentration ( IC50 ) of ( 39. 8 ± 1. 0) μmol /L and ( 49. 0 ± 0. 9) μmol /L，as well as a lower cytotoxicity on normal bladder cell SV-HUC-1 with the IC50 of ( 75. 9 ± 1. 8) μmol /L． In addition， myricetin exhibits higher antitumor activity in EJ cell than that in T24 cells due to higher intracellular uptake amount of myricetin in EJ cells． Further flow cytometric studies of EJ cell cycle distribution show that myricetin inhibits the proliferation of EJ cancer cells mainly through induction of apoptosis and S cycle arrest．