Al-Serori Halh, Kundi Michael, Ferk Franziska, Mišík Miroslav, Nersesyan Armen, Murbach Manuel, Lah Tamara T, Knasmüller Siegfried
Institute of Cancer Research, Department of Internal Medicine 1, Medical University of Vienna, Vienna, Austria.
Center for Public Health, Institute of Environmental Health, Medical University of Vienna, Vienna, Austria.
Toxicol In Vitro. 2017 Apr;40:264-271. doi: 10.1016/j.tiv.2017.01.012. Epub 2017 Jan 24.
Some epidemiological studies indicate that mobile phones cause glioblastomas in humans. Since it is known that genomic instability plays a key role in the etiology of cancer, we investigated the effects of the universal mobile telecommunications system radiofrequency (UMTS-RF) signal, which is used in "smart" phones, on micronucleus (MN) formation and other anomalies such as nuclear buds (NBUDs) and nucleoplasmatic bridges (NPBs). MN are formed by structural and numerical aberrations, NBs reflect gene amplification and NPBs are formed from dicentric chromosomes. The experiments were conducted with human glioblastoma cell lines, which differ in regard to their p53 status, namely U87 (wild-type) and U251 (mutated). The cells were cultivated for 16h in presence and absence of fetal calf serum and exposed to different SAR doses (0.25, 0.50 and 1.00W/kg), which reflect the exposure of humans, in presence and absence of mitomycin C as former studies indicate that RF may cause synergistic effects in combination with this drug. We found no evidence for induction of MN and other anomalies. However, with the highest dose, induction of apoptosis was observed in U251 cells on the basis of the morphological features of the cells. Our findings indicate that the UMTS-RF signal does not cause chromosomal damage in glioblastoma cells; the mechanisms which lead to induction of programmed cell death will be investigated in further studies.
一些流行病学研究表明，手机会导致人类患胶质母细胞瘤。由于已知基因组不稳定在癌症病因中起关键作用，我们研究了“智能”手机中使用的通用移动通信系统射频（UMTS-RF）信号对微核（MN）形成以及其他异常情况（如核芽（NBUDs）和核质桥（NPBs））的影响。微核由结构和数量畸变形成，核芽反映基因扩增，核质桥由双着丝粒染色体形成。实验使用了人胶质母细胞瘤细胞系，它们在p53状态方面有所不同，即U87（野生型）和U251（突变型）。细胞在有和没有胎牛血清的情况下培养16小时，并暴露于不同的比吸收率（SAR）剂量（0.25、0.50和1.00W/kg）下，这些剂量反映了人类的暴露情况，同时在有和没有丝裂霉素C的情况下进行实验，因为先前的研究表明射频可能与这种药物产生协同作用。我们没有发现诱导微核和其他异常的证据。然而，在最高剂量下，根据细胞的形态特征，在U251细胞中观察到了凋亡诱导现象。我们的研究结果表明，UMTS-RF信号不会在胶质母细胞瘤细胞中引起染色体损伤；导致程序性细胞死亡诱导的机制将在进一步研究中进行探讨。
