| JIANG Yu-liang,LIU Jing-jia,LI Jin-na,et al.The inhibition effect of continuous low dose rate radiation by 125I radioactive seeds on Hep-2 larynx cancer cell line[J].Chinese Journal of Radiological Medicine and Protection,2013,33(6):593-596 |
| The inhibition effect of continuous low dose rate radiation by 125I radioactive seeds on Hep-2 larynx cancer cell line |
| Received:March 25, 2013 |
| DOI：10.3760/cma.j.issn.0254-5098.2013.06.006 |
| KeyWords:Radiosensitivity DNA damage repair Cell apoptosis G2/M arrest |
| FundProject: |
| Author Name | Affiliation | E-mail | | JIANG Yu-liang | Cancer Center, Peking University Third Hospital, Beijing 100191, China | | | LIU Jing-jia | Cancer Center, Peking University Third Hospital, Beijing 100191, China | | | LI Jin-na | Cancer Center, Peking University Third Hospital, Beijing 100191, China | | | WANG Hao | Cancer Center, Peking University Third Hospital, Beijing 100191, China | | | QU Ang | Cancer Center, Peking University Third Hospital, Beijing 100191, China | | | ZHAO Yong | 中国科学院动物研究所 生物膜与膜生物工程国家重点实验室 | | | WANG Jun-jie | Cancer Center, Peking University Third Hospital, Beijing 100191, China | junjiew920@sohu.com |
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| Abstract:: |
| Objective To investigate the inhibition effect of continuous low dose rate radiation by125I radioactive seeds on Hep-2 cells and the corresponding mechanisms. Methods Hep-2 cells were divided into three groups, control group, single dose radiation group with high dose rate form X-rays (SDR) and continuous low dose rate radiation by 125I seeds group (125I-CLDR). After exposure to SDR and 125I-CLDR, colony formation assay was used to determine the radiosensitivity and RBE, trypan blue exclusion assay was used to determine cell proliferation, and flow cytometry was used to detect cell apoptosis and cell cycle arrest. Results The radiosensitivity of Hep-2 cells to 125I-CLDR was higher than that to SDR. The RBE of 125I-CLDR versus SDR was approximately 1.61. The α/β ratio of 125I-CLDR group was higher than that of SDR group. Both SDR and 125I-CLDR inhibited cell proliferation (t=30.9,40.7, P<0.05), in which 125I-CLDR was stronger than SDR (t=9.8, P<0.05). In addition, the incidences of apoptosis and G2/M arrest induced by 125I-CLDR were also stronger than those induced by SDR (t=5.8,19.8,P<0.05). Conclusions 125I-CLDR generates more serious inhibition effects than SDR on reducing cellular DNA repair capacity, inducing cell apoptosis and G2/M arrest and inhibiting proliferation of Hep-2 cells. |
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