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暴露于分配给移动无线电基站的2.1425吉赫兹频段连续波(CW)或W-CDMA调制辐射下的人体细胞中,p53的磷酸化和基因表达不受影响。

Phosphorylation and gene expression of p53 are not affected in human cells exposed to 2.1425 GHz band CW or W-CDMA modulated radiation allocated to mobile radio base stations.

作者信息

Hirose H, Sakuma N, Kaji N, Suhara T, Sekijima M, Nojima T, Miyakoshi J

机构信息

Research Division for Advanced Technology, Kashima Laboratory, Mitsubishi Chemical Safety Institute Ltd., Kamisu, Japan.

出版信息

Bioelectromagnetics. 2006 Sep;27(6):494-504. doi: 10.1002/bem.20238.

Abstract

A large-scale in vitro study focusing on low-level radiofrequency (RF) fields from mobile radio base stations employing the International Mobile Telecommunication 2000 (IMT-2000) cellular system was conducted to test the hypothesis that modulated RF fields induce apoptosis or other cellular stress response that activate p53 or the p53-signaling pathway. First, we evaluated the response of human cells to microwave exposure at a specific absorption rate (SAR) of 80 mW/kg, which corresponds to the limit of the average whole-body SAR for general public exposure defined as a basic restriction by the International Commission on Non-Ionizing Radiation Protection (ICNIRP) guidelines. Second, we investigated whether continuous wave (CW) and wideband code division multiple access (W-CDMA) modulated signal RF fields at 2.1425 GHz induced apoptosis or any signs of stress. Human glioblastoma A172 cells were exposed to W-CDMA radiation at SARs of 80, 250, and 800 mW/kg, and CW radiation at 80 mW/kg for 24 or 48 h. Human IMR-90 fibroblasts from fetal lungs were exposed to both W-CDMA and CW radiation at a SAR of 80 mW/kg for 28 h. Under the RF field exposure conditions described above, no significant differences in the percentage of apoptotic cells were observed between the test groups exposed to RF signals and the sham-exposed negative controls, as evaluated by the Annexin V affinity assay. No significant differences in expression levels of phosphorylated p53 at serine 15 or total p53 were observed between the test groups and the negative controls by the bead-based multiplex assay. Moreover, microarray hybridization and real-time RT-PCR analysis showed no noticeable differences in gene expression of the subsequent downstream targets of p53 signaling involved in apoptosis between the test groups and the negative controls. Our results confirm that exposure to low-level RF signals up to 800 mW/kg does not induce p53-dependent apoptosis, DNA damage, or other stress response in human cells.

摘要

开展了一项大规模体外研究,该研究聚焦于采用国际移动通信2000(IMT - 2000)蜂窝系统的移动无线电基站产生的低水平射频(RF)场,以检验以下假设:调制RF场会诱导细胞凋亡或激活p53或p53信号通路的其他细胞应激反应。首先,我们评估了人类细胞在80 mW/kg的比吸收率(SAR)下对微波暴露的反应,该比吸收率对应于国际非电离辐射防护委员会(ICNIRP)指南定义为基本限制的公众全身平均SAR限值。其次,我们研究了2.1425 GHz的连续波(CW)和宽带码分多址(W - CDMA)调制信号RF场是否会诱导细胞凋亡或任何应激迹象。将人胶质母细胞瘤A172细胞暴露于80、250和800 mW/kg的SAR下的W - CDMA辐射以及80 mW/kg的CW辐射中24或48小时。将来自胎儿肺的人IMR - 90成纤维细胞暴露于80 mW/kg的SAR下的W - CDMA和CW辐射中28小时。在上述RF场暴露条件下,通过膜联蛋白V亲和力测定评估,暴露于RF信号的测试组与假暴露阴性对照组之间凋亡细胞百分比无显著差异。通过基于微珠的多重分析,测试组与阴性对照组之间在丝氨酸15处磷酸化p53或总p53的表达水平无显著差异。此外,微阵列杂交和实时RT - PCR分析表明,测试组与阴性对照组之间在参与细胞凋亡的p53信号下游后续靶标的基因表达上无明显差异。我们的结果证实,暴露于高达800 mW/kg的低水平RF信号不会在人类细胞中诱导p53依赖性细胞凋亡、DNA损伤或其他应激反应。

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