In previous studies we demonstrated that radiofrequency (RF) electromagnetic fields (EMF) is able to reduce DNA damage induced by a subsequent treatment with genotoxic agents, resembling the adaptive response, a phenomenon well known in radiobiology. In this study we report on the capability of the culture medium from SH-SY5Y neuroblastoma cells exposed to 1950 MHz to elicit, in recipient non-exposed cells, a reduction of menadione-induced DNA damage (P < 0.05; comet assay), indicating the capability of non-ionizing radiation to elicit a bystander effect. A comparable reduction was also detected in cultures directly exposed to the same EMF conditions (P < 0.05), confirming the adaptive response. In the same exposure conditions, we also evidenced an increase of heat shock protein 70 (hsp70) in culture medium of cells exposed to RF with respect to sham exposed ones (P < 0.05; western blot analysis), while no differences were detected in the intracellular content of hsp70. On the whole, our results evidence a protective effect of RF against menadione-induced DNA damage in directly and non-directly exposed cells, and suggest hsp70 pathway to be investigated as one of the potential candidate underpinning the interaction between RF exposure and biological systems.

在以前的研究中，我们证明了射频 (RF) 电磁场 (EMF) 能够减少随后用基因毒剂治疗引起的 DNA 损伤，类似于适应性反应，这是放射生物学中众所周知的一种现象。在这项研究中，我们报告了暴露于 1950 MHz 的 SH-SY5Y 神经母细胞瘤细胞的培养基在受体非暴露细胞中引起甲萘醌诱导的 DNA 损伤减少的能力（P < 0.05；彗星试验），表明非电离辐射引起旁观者效应的能力。在直接暴露于相同 EMF 条件的培养物中也检测到类似的减少 (P < 0.05)，证实了适应性反应。在相同的曝光条件下，我们还证明了与假暴露细胞相比，暴露于 RF 的细胞培养基中的热休克蛋白 70 (hsp70) 增加（P < 0.05；蛋白质印迹分析），而 hsp70 的细胞内含量未检测到差异。总体而言，我们的结果证明了 RF 对直接和非直接暴露细胞中甲萘醌诱导的 DNA 损伤具有保护作用，并建议将 hsp70 途径作为支持 RF 暴露与生物系统之间相互作用的潜在候选者之一进行研究。