The inhibition effect of continuous low dose rate radiation by 125I radioactive seeds on Hep-2 larynx cancer cell line
10.3760/cma.j.issn.0254-5098.2013.06.006
- VernacularTitle:125Ⅰ粒子持续低剂量率照射对人喉癌细胞系Hep-2的抑制作用
- Author:
Yuliang JIANG
;
Jingjia LIU
;
Jinna LI
;
Hao WANG
;
Ang QU
;
Yong ZHAO
;
Junjie WANG
- Publication Type:Journal Article
- Keywords:
Radiosensitivity;
DNA damage repair;
Cell apoptosis;
G2/M arrest
- From:
Chinese Journal of Radiological Medicine and Protection
2013;33(6):593-596
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibition effect of continuous low dose rate radiation by 125Ⅰ 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 by125Ⅰ-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.
