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首页> 外文期刊>Bioelectromagnetics. >High frequency electromagnetic fields (GSM signals) affect gene expression levels in tumor suppressor p53-deficient embryonic stem cells.
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High frequency electromagnetic fields (GSM signals) affect gene expression levels in tumor suppressor p53-deficient embryonic stem cells.

机译:高频电磁场(GSM信号)影响肿瘤抑制因子p53缺陷的胚胎干细胞中的基因表达水平。

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Effects of electromagnetic fields (EMF) simulating exposure to the Global System for Mobile Communications (GSM) signals were studied using pluripotent embryonic stem (ES) cells in vitro. Wild-type ES cells and ES cells deficient for the tumor suppressor p53 were exposed to pulse modulated EMF at 1.71 GHz, lower end of the uplink band of GSM 1800, under standardized and controlled conditions, and transcripts of regulatory genes were analyzed during in vitro differentiation. Two dominant GSM modulation schemes (GSM-217 and GSM-Talk), which generate temporal changes between GSM-Basic (active during talking phases) and GSM-DTX (active during listening phases thus simulating a typical conversation), were applied to the cells at and below the basic safety limits for local exposures as defined for the general public by the International Commission on Nonionizing Radiation Protection (ICNIRP). GSM-217 EMF induced a significant upregulation of mRNA levels of the heat shock protein, hsp70 of p53-deficient ES cells differentiating in vitro, paralleled by a low and transient increase of c-jun, c-myc, and p21 levels in p53-deficient, but not in wild-type cells. No responses were observed in either cell type after EMF exposure to GSM-Talk applied at similar slot-averaged specific absorption rates (SAR), but at lower time-averaged SAR values. Cardiac differentiation and cell cycle characteristics were not affected in embryonic stem and embryonic carcinoma cells after exposure to GSM-217 EMF signals. Our data indicate that the genetic background determines cellular responses to GSM modulated EMF. Bioelectromagnetics 25:296-307, 2004.
机译:在体外使用多能胚胎干(ES)细胞研究了模拟暴露于全球移动通信系统(GSM)信号的电磁场(EMF)的影响。在标准化和受控条件下,将野生型ES细胞和缺乏肿瘤抑制物p53的ES细胞暴露于1.71 GHz,GSM 1800上行链路频带下端的脉冲调制EMF,并在体外分析调节基因的转录本差异化。两种主要的GSM调制方案(GSM-217和GSM-Talk)可在GSM基本(通话阶段处于活动状态)和GSM-DTX(在收听阶段处于活动状态,从而模拟典型对话)之间产生时间变化。达到或低于国际非电离辐射防护委员会(ICNIRP)为公众定义的本地暴露的基本安全限值。 GSM-217 EMF诱导热休克蛋白,p53缺失的ES细胞的hsp70的mRNA水平显着上调,并在体外分化,与此同时,p53-中c-jun,c-myc和p21的水平低而短暂的升高缺乏,但不是野生型细胞。在以类似的缝隙平均比吸收率(SAR),但时间平均SAR值较低的情况下,EMF暴露于GSM-Talk后,在任何一种细胞类型中均未观察到响应。暴露于GSM-217 EMF信号后,胚胎干细胞和胚胎癌细胞的心脏分化和细胞周期特征均未受到影响。我们的数据表明遗传背景决定了细胞对GSM调制EMF的反应。生物电磁学25:296-307,2004。

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