中华放射医学与防护杂志
中華放射醫學與防護雜誌
중화방사의학여방호잡지
Chinese Journal of Radiological Medicine and Protection
2008年
5期
466-470
,共5页
CdCl2%适应性反应%γ辐射%DNA修复
CdCl2%適應性反應%γ輻射%DNA脩複
CdCl2%괄응성반응%γ복사%DNA수복
CdCl2%Adaptive response%γ-irradiation%DNA repair
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PI3K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2 h,再对细胞进行50、100 μmol/L CdCl2或1、2 Gy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20 μmol/L woamannin处理细胞.结果 低浓度能够诱导细胞对随后50 μmol/L CdCl2或1 Gy γ射线照射产生适应性反应.当攻击剂量为50 μmol/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.
目的 探討不同的脩複能力在鎘誘導的細胞適應性反應中的作用,併對PI3K傢族參與細胞適應性信號傳導的作用做初步探索.方法 0.1或 1μmol/LCdCl2預處理細胞後.間隔2 h,再對細胞進行50、100 μmol/L CdCl2或1、2 Gy輻射處理,微覈法檢測細胞錶達適應性反應程度.另外,在預處理和間隔時間中,用20 μmol/L woamannin處理細胞.結果 低濃度能夠誘導細胞對隨後50 μmol/L CdCl2或1 Gy γ射線照射產生適應性反應.噹攻擊劑量為50 μmol/L CdCl2,EM-C11細胞的適應反應程度低于另外兩株細胞.三種細胞的適應性反應均可被wortmannin抑製.結論 細胞適應性程度的大小與其DNA損傷的脩複能力、預處理和攻擊處理劑量相關,相對于DSB,SSB在誘導細胞錶達適應性反應中起主要作用.ATM激酶參與細胞適應性信號通路的信號傳導.
목적 탐토불동적수복능력재력유도적세포괄응성반응중적작용,병대PI3K가족삼여세포괄응성신호전도적작용주초보탐색.방법 0.1혹 1μmol/LCdCl2예처리세포후.간격2 h,재대세포진행50、100 μmol/L CdCl2혹1、2 Gy복사처리,미핵법검측세포표체괄응성반응정도.령외,재예처리화간격시간중,용20 μmol/L woamannin처리세포.결과 저농도능구유도세포대수후50 μmol/L CdCl2혹1 Gy γ사선조사산생괄응성반응.당공격제량위50 μmol/L CdCl2,EM-C11세포적괄응반응정도저우령외량주세포.삼충세포적괄응성반응균가피wortmannin억제.결론 세포괄응성정도적대소여기DNA손상적수복능력、예처리화공격처리제량상관,상대우DSB,SSB재유도세포표체괄응성반응중기주요작용.ATM격매삼여세포괄응성신호통로적신호전도.
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.
