The cytotoxicity and DNA damage caused by thioglycolic acid(TGA)-capped cadmium telluride(CdTe) quantum dots(QDs) to hepatocyte line HL-7702 were investigated.Cell viability was measured by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide(MTT) assay;DNA damage was detected by single cell gel electrophoresis(SCGE);the change of cell cycle progression was examined by propidium iodide(PI)-flow cytometry(FCM);apoptosis was measured by acridine orange/ethidium bromide(AO/EB) assay and Annexin V-FITC/PI-FCM(FITC:fluorescein isothiocyanate).The results show that the cytotoxicity induced by CdTe QDs was increased in a dose-dependent and time-dependent manner;after exposure to QDs for 24 h,as the exposure dose increased,the rate of DNA damage was significantly increased(P<0.05),and the degree of DNA damage was elevated.As the dose of CdTe QDs increased,the percentage of G 0 /G 1 phase cells was significantly decreased(P<0.001),while the percenttages of S and G 2 /M phases cells were significantly increased(P<0.001).In AO/EB assay,apoptotic cells could be observed under a fluorescence microscope,and apoptotic rate was increased as exposure dose increased.In Annexin V-FITC/PI-FCM assay,the apoptotic rates of CdTe QDs treated groups were significantly increased compared with that of control group(P<0.05).Our studies indicate that CdTe QDs could influence cell viability,and induce DNA damage,the S and G2 /M phases arrest and apoptosis of HL-7702. The cytotoxicity and DNA damage caused by thioglycolic acid (TGA) -capped cadmium telluride (CdTe) quantum dots (QDs) to hepatocyte line HL-7702 were investigated. Cell viability was measured by 3- (4,5-dimethylthiazol- ) -2,5-diphenyltetrazolium bromide (MTT) assay; DNA damage was detected by single cell gel electrophoresis (SCGE); the change of cell cycle progression was examined by propidium iodide (PI) -flow cytometry by acridine orange / ethidium bromide (AO / EB) assay and Annexin V-FITC / PI-FCM (FITC: fluorescein isothiocyanate). The results show that the cytotoxicity induced by CdTe QDs was increased in a dose-dependent and time-dependent manner ; after exposure to QDs for 24 h, the rate of DNA damage was significantly increased (P <0.05), and the degree of DNA damage was elevated. As the dose of CdTe QDs increased, the percentage of G 0 / G 1 phase cells was significantly decreased (P <0.001), while the percenttages of S and G 2 / M phases cells were significantly increased (P <0.001) .In AO / EB assay, apoptotic cells could be observed under a fluorescence microscope, and apoptotic rate increased increased as exposure dose increased. In Annexin V-FITC / PI- FCM assay, the apoptotic rates of CdTe QDs treated groups were significantly increased compared to that of control groups (P <0.05) .Our studies indicate that CdTe QDs could influence cell viability, and induce DNA damage, the S and G2 / M arrests and apoptosis of HL-7702.