DNA损伤修复在镉诱导的细胞辐射适应性中的作用

Role of DNA repair capacity in cadmium induced cellular adaptive response

目的探讨不同的修复能力在镉诱导的细胞适应性反应中的作用，并对P13K家族参与细胞适应性信号传导的作用做初步探索。方法0．1或1μmol／LCdCl2预处理细胞后，间隔2h，再对细胞进行50、100μmol／L CdCl2或1、2Gy辐射处理，微核法检测细胞表达适应性反应程度。另外，在预处理和间隔时间中，用20μmol／L wortmannin处理细胞。结果低浓度能够诱导细胞对随后50μmol／L Cdcl2或1Gyγ射线照射产生适应性反应。当攻击剂量为50μmol／L CdCl2，EM—C11细胞的适应反应程度低于另外两株细胞。三种细胞的适应性反应均可被wortmannin抑制。结论细胞适应性程度的大小与其DNA损伤的修复能力、预处理和攻击处理剂量相关，相对于DSB，SSB在诱导细胞表达适应性反应中起主要作用。ATM激酶参与细胞适应性信号通路的信号传导。

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 Ceils 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 CdCl2 , EM-Cll ceils had an AR less apparent than the other two cell lines. Moreover, treatment of ceils with wortmannin eliminated the AR in all three ceil 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.