Ahmadianpour Mohammad Reza, Abdolmaleki Parviz, Mowla Seyed Javad, Hosseinkhani Saman
Department of Biophysics, Tarbiat Modares University, Tehran, Iran.
Electromagn Biol Med. 2013 Mar;32(1):9-19. doi: 10.3109/15368378.2012.692748. Epub 2013 Jan 15.
This study aimed to investigate the effect of 6 milliTesla (mT) static magnetic field (SMF) on apoptosis induction and cell cycle alteration in T-lymphoblastoid Jurkat E6.1 cells. Exposure of human p53 mutant Jurkat cells to 6 mT SMF resulted in apoptosis, which was detected by luminometric and flow cytometric analysis also, phosphorylated ATM and E2F1 proteins were detected by western blot analysis. Based on luminescence detection data, apoptosis initiated 36 h after exposure to 6 mT SMF. Apoptosis also reached its maximum rate 48 h after treatment. Flow cytometric analysis revealed a temporary G2 arrest after exposure to 6 mT SMF. Indeed, cellular population of S and G2 phases was increased. Based on reports of other investigations on the effect of magnetic fields on Ca2+flux changes in cell membranes and the effect of MFs on free radical formation, it can be suggested that the magnetic fields may induce the apoptosis and alter the cell population in different cell cycle phases of Jurkat cells via changing the Ca2+fluxes through cell membranes and playing a role in free radical formation. Western blot analysis showed that the amount of phosphorylated ATM and E2F1 proteins were increased in treated cells. The results of luminometric and flow cytometric detection did not show a significant difference in the apoptosis rate between 6 h-treated and 24 h-treated cells by 6 mT SMF. Thus, 6 mT SMF can induce apoptosis and alter cell cycle in Jurkat cells via a p53-independent pathway.
本研究旨在探讨6毫特斯拉(mT)静磁场(SMF)对T淋巴细胞样Jurkat E6.1细胞凋亡诱导及细胞周期改变的影响。将人p53突变型Jurkat细胞暴露于6 mT SMF后会导致细胞凋亡,这也通过发光法和流式细胞术分析得以检测,同时通过蛋白质印迹分析检测到磷酸化的ATM和E2F1蛋白。根据发光检测数据,凋亡在暴露于6 mT SMF后36小时开始。凋亡在处理后48小时也达到最高速率。流式细胞术分析显示,暴露于6 mT SMF后出现短暂的G2期阻滞。实际上,S期和G2期的细胞群体增加。基于其他关于磁场对细胞膜中Ca2+通量变化的影响以及磁场对自由基形成的影响的研究报道,可以推测磁场可能通过改变细胞膜的Ca2+通量并在自由基形成中发挥作用,从而诱导Jurkat细胞凋亡并改变其在不同细胞周期阶段的细胞群体。蛋白质印迹分析表明,处理后的细胞中磷酸化的ATM和E2F1蛋白量增加。发光法和流式细胞术检测结果显示,6 mT SMF处理6小时和24小时的细胞之间的凋亡率没有显著差异。因此,6 mT SMF可通过p53非依赖途径诱导Jurkat细胞凋亡并改变细胞周期。