Objective To investigate cadmium induced adaptive responses (AR) to either toxicant challenge or irradiation and also the role of PI3K family in the AR. Methods Cells were pre-treated with 0.1 or 1 μmol/L cadmium and then challenged by 50, 100 μmol/L cadmium or 1, 2 Gy γ-rays irradiation. Micronucleus induction was measured to evaluate the magnitude of AR. In some experiments, cells were treated with wortmannin during and after pretreatment. Results Cadmium of sub-lethal concentration could induce AR in all the cells toward 50 μmol/L cadmium or 1 Gy irradiation. When challenged by 50 μmol/L CdCl1, EM-C11 cells had an AR less apparent than the other two cell lines. Moreover, treatment of cells with wortmannin eliminated the AR in all three cell lines. Conclusions The magnitudes of AR in adapted cells may be related to multiple factors, such as DNA repair capacity, the priming and challenging dose of cadmium or irradiation. SSB rather than DSB repair is mainly involved in the cadmium induced AR and this cellular response may be mediated through ATM pathway.

Cumulative evidence demonstrated that the chromatin modification plays important roles in the processes of DNA replication,transcription,repair and recombination.Both of the generation of DNA lesions and the activation of DNA damage response (DDR) to ionizing radiation could be affected by the chromatin modifications.This paper reviewed the recent research progresses in the chromatin structure modifications and its role in DDR,especially the influence of characteristic chromatin structure and histone modification on the radiation sensitivity of tumor cells.

Objective To investigate the effects of long-term low-dose radiation (LDR) of γ-rays on the proliferation and radiosensitivity of human lymphoblast cells HMy2.CIR (HMy) and to elucidate the underlying mechanism.Methods HMy cells were divided into control group and long-term LDR group.For the long-term LDR treatment,HMy cells were fractionally exposed to a low dose of γ-rays,which could enhance cell proliferation,3 times per week for 4 weeks.After the long-term LDR exposure,part of the control and long-term LDR exposed cells were further irradiated with a challenging dose (2 Gy) of γ-rays.Then cell proliferation and radiosensitivity were assayed by CCK-8 kit,cell apoptosis,and γ-H2AX formation was measured by flow cytometry.Gene expressions of cyclinD1,PCNA,bcl-2 and bax were detected by RT-PCR.Results The long-term LDR significantly increased cell proliferation (t =9.607,P ＜ 0.01) accompanied with up-regulation of cell cycle regulation gene cyclinD1 (t =6.869,P ＜ 0.01),proliferation regulation gene PCNA (proliferating cell nuclear antigen) (t =9.229,P ＜ 0.01) and bcl-2 gene (t =2.662,P ＜ 0.05),but decreased the expression of pro-apoptotic gene bax (t =19.908,P ＜0.01) in HMy cells.Compared to untreated cells,the long-term LDR decreased cell radiosensitivity (t =8.896,P ＜ 0.01),including apoptosis induction (t =4.762,P ＜ 0.01) and γ-H2AX formation (t =10.264,P＜0.01).Conclusions The long-term LDR promoted cell proliferation by up-regulating cell cycle related genes,while it reduced the radiosensitivity of HMy cells with acquisition of apoptotic resistance.