极低频磁场抑制细胞间隙连接通讯的分子机制  

Molecular mechanism of inhibition of gap junctional intercellular communication induced by extremely low frequency(ELF) magnetic fields

作　　者：胡根林[1] 姜槐[1] 吴瑞英[1] 鲁德强[1] 

机构地区：[1]浙江大学医学院微波研究室,杭州310031

出　　处：《中华劳动卫生职业病杂志》2001年第3期166-168,共3页Chinese Journal of Industrial Hygiene and Occupational Diseases

基　　金：国家自然科学基金重点资助项目 ( 3 963 0 10 0 )

摘　　要：目的　研究极低频 (ELF)磁场抑制细胞间隙连接通讯 (GJIC)的分子机制。方法　NIH3T3小鼠成纤维细胞受 5 0Hz、0 .8mTELF(2 4h)、12 氧 14 酰佛波 13酯 (TPA ,2h)或ELF加TPA的作用后 ,用Northern和Western印迹法检测连接蛋白 (Cx43)的基因转录水平及其磷酸化状态。结果　各处理组的Cx43基因转录水平与对照组比较 ,差异无显著性 (P >0 .0 5 )。Cx43的非磷酸化条带在正常组为 10 7.33± 2 7.42 (以样本Cx43基因条带的特异吸光度值与相对应的GAPDH吸光度值之比来表示 ) ,与ELF处理组 (6 4.6 9± 2 7.88)、TPA处理组 (45 .5 4± 2 0 .5 9)和ELF +TPA处理组 (39.96±11.93)比较 ,差异有显著或极显著性 (P <0 .0 5、P <0 .0 1) ,在各处理组间则差异无显著性 (P >0 .0 5 )。各处理组均出现了过磷酸化的P3 条带。结论　ELF和 (或 )TPA不影响Cx43基因的转录 ;ELF和 (或 )TPA抑制GJIC的主要机制是Cx43蛋白的过磷酸化。Objective To explore the molecular mechanism of suppression of gap junctional intercellular communication(GJIC) by extremely low frequency(ELF) magnetic fields. Methods NIH3T3 fibroblast cells were exposed to 0.8 mT,50 Hz magnetic fields for 24 h,in the presence or absence of phorbol ester(TPA),then using Northern and Western blot,connexin 43 gene transcription and the state of the protein phosphorylation were detected respectively. Results The connexin 43 gene transcriptional level did not change significantly in any exposure groups( P >0.05).However,ELF and(or) TPA and ELF+TPA could obviously decrease the quantity of non phosphorylated connexin 43 [(64.69±27.88),(45.54±20.59) and (39.96±11.93) respectively vs normal control(107.33±27.42), P <0.05 or P <0.01].Hyperphosphorylation pattern(P 3) appeared in both exposed groups. Conclusion ELF magnetic fields did not influence connexin 43 gene transcription.The main inhibition mechanism of GJIC is related to the hyperphosphorylation of connexin 43.

关 键 词：磁场 连接蛋白 基因转录 磷酸化 肿瘤 潜在危害 GJIC 

分 类 号：R730.2[医药卫生—肿瘤]