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Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells

机译:手机特定的电磁场在缺乏血清的人胶质母细胞瘤细胞中诱导瞬时DNA损伤和核苷酸切除修复

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摘要

Some epidemiological studies indicate that the use of mobile phones causes cancer in humans (in particular glioblastomas). It is known that DNA damage plays a key role in malignant transformation; therefore, we investigated the impact of the UMTS signal which is widely used in mobile telecommunications, on DNA stability in ten different human cell lines (six brain derived cell lines, lymphocytes, fibroblasts, liver and buccal tissue derived cells) under conditions relevant for users (SAR 0.25 to 1.00 W/kg). We found no evidence for induction of damage in single cell gel electrophoresis assays when the cells were cultivated with serum. However, clear positive effects were seen in a p53 proficient glioblastoma line (U87) when the cells were grown under serum free conditions, while no effects were found in p53 deficient glioblastoma cells (U251). Further experiments showed that the damage disappears rapidly in U87 and that exposure induced nucleotide excision repair (NER) and does not cause double strand breaks (DSBs). The observation of NER induction is supported by results of a proteome analysis indicating that several proteins involved in NER are up-regulated after exposure to UMTS; additionally, we found limited evidence for the activation of the γ-interferon pathway. The present findings show that the signal causes transient genetic instability in glioma derived cells and activates cellular defense systems.
机译:一些流行病学研究表明,使用手机会导致人类癌症(尤其是胶质母细胞瘤)。众所周知,DNA损伤在恶性转化中起关键作用。因此,在与用户相关的条件下,我们研究了移动通信中广泛使用的UMTS信号对十种不同人类细胞系(六种脑源性细胞系,淋巴细胞,成纤维细胞,肝和颊组织源性细胞)DNA稳定性的影响(SAR 0.25至1.00 W / kg)。我们发现,当用血清培养细胞时,在单细胞凝胶电泳分析中没有诱导损伤的证据。然而,当这些细胞在无血清条件下生长时,在p53熟练的胶质母细胞瘤系(U87)中观察到明显的阳性作用,而在p53缺乏的胶质母细胞瘤细胞(U251)中未发现作用。进一步的实验表明,损伤在U87中迅速消失,并且暴露引起核苷酸切除修复(NER),并且不会引起双链断裂(DSB)。蛋白质组分析的结果支持了对NER诱导的观察,结果表明,与UMTS接触后,参与NER的几种蛋白质被上调。此外,我们发现γ-干扰素途径激活的证据有限。目前的发现表明,该信号在神经胶质瘤衍生细胞中引起短暂的遗传不稳定性,并激活细胞防御系统。

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