AIM:To determine the mechanism of the radiationinduced biological effects of 125I seeds on pancreatic carcinoma cells in vitro.METHODS:SW1990 and PANC-1 pancreatic cancer cell lines were cultured in DMEM in a suitable environment.Gray’s model of iodine-125(125I)seed irradiation was used.In vitro,exponential phase SW1990,and PANC-1cells were exposed to 0,2,4,6,and 8 Gy using 125I radioactive seeds,with an initial dose rate of 12.13c Gy/h.A clonogenic survival experiment was performed to observe the ability of the cells to maintain their clonogenic capacity and to form colonies.Cell-cycle and apoptosis analyses were conducted to detect the apoptosis percentage in the SW1990 and PANC-1 cells.DNA synthesis was measured via a tritiated thymidine(3H-Td R)incorporation experiment.After continuous low-dose-rate irradiation with 125I radioactive seeds,the survival fractions at 2 Gy(SF2),percentage apoptosis,and cell cycle phases of the SW1990 and PANC-1 pancreatic cancer cell lines were calculated and compared.RESULTS:The survival fractions of the PANC-1 andSW1990 cells irradiated with 125I seeds decreased exponentially as the dose increased.No significant difference in SF2 was observed between SW1990 and PANC-1 cells(0.766±0.063 vs 0.729±0.045,P<0.05).The 125I seeds induced a higher percentage of apoptosis than that observed in the control in both the SW1990and PANC-1 cells.The rate of apoptosis increased with increasing radiation dosage.The percentage of apoptosis was slightly higher in the SW1990 cells than in the PANC-1 cells.Dose-dependent G2/M cellcycle arrest was observed after 125I seed irradiation,with a peak value at 6 Gy.As the dose increased,the percentage of G2/M cell cycle arrest increased in both cell lines,whereas the rate of DNA incorporation decreased.In the 3H-Td R incorporation experiment,the dosimetry results of both the SW1990 and PANC-1cells decreased as the radiation dose increased,with a minimum at 6 Gy.There were no significant differences in the dosimetry results of the two cell lines when they were exposed to the same dose of radiation.CONCLUSION:The pancreatic cancer cell-killing effects induced by 125I radioactive seeds mainly occurred via apoptosis and G2/M cell cycle arrest. AIM: To determine the mechanism of the radiation induced biological effects of 125I seeds on pancreatic carcinoma cells in vitro. METHODS: SW1990 and PANC-1 pancreatic cancer cell lines were cultured in DMEM in a suitable environment. Gray’s model of iodine-125 (125I) seed irradiation was used in vitro, exponential phase SW1990, and PANC-1 cells were exposed to 0, 2, 4, 6, and 8 Gy using 125I radioactive seeds with an initial dose rate of 12.13c Gy / hA clonogenic survival experiment was performed to observe the ability of the cells to maintain their clonogenic capacity and to form colonies. Cell-cycle and apoptosis analyzes were conducted to detect the apoptosis percentage in the SW1990 and PANC-1 cells. DNA synthesis was measured via a tritiated thymidine (3H -Td R) incorporation experiment. After continuous low-dose-rate irradiation with 125I radioactive seeds, the survival fractions at 2 Gy (SF2), percentage apoptosis, and cell cycle phases of the SW1990 and PANC-1 pancreatic cancer cell lines were calcu lated and compared .RESULTS: The survival fractions of the PANC-1 and SW1990 cells irradiated with 125 seeds were exponentially as the dose increased. No significant difference in SF2 was observed between SW1990 and PANC-1 cells (0.766 ± 0.063 vs 0.729 ± 0.045, P <0.05). The 125I seeds induced a higher percentage of apoptosis than that observed in the control in both the SW1990 and PANC-1 cells. The rate of apoptosis increased with increasing radiation dosage. Percentage of apoptosis was slightly higher in the SW1990 cells than in the PANC-1 cells. Focus-dependent G2 / M cellcycle arrest was observed after 125 I seed irradiation, with a peak value at 6 Gy. As the dose increased, the percentage of G2 / M cell cycle arrest increased in both cell lines , the rate of DNA incorporation decreased. In the 3H-Td R incorporation experiment, the dosimetry results of both the SW1990 and PANC-1 cells decreased as the radiation dose increased, with a minimum at 6 Gy. There were no significant differences in th e dosimetry results of the two cell lines when they were exposed to the same dose of radiation. CONCLUSION: The pancreatic cancer cell-killing effects induced by 125I radioactive seeds in the event of apoptosis via G2 / M cell cycle arrest.