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首页> 外文期刊>Journal of cellular biochemistry. >Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: Possible immune cell activation.
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Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: Possible immune cell activation.

机译：极低频电磁场作为体外细胞反应的效应物：可能的免疫细胞活化。

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There is presently an intense discussion if electromagnetic field (EMF) exposure has consequences for human health. This include exposure to structures and appliances that emit in the extremely low frequency (ELF) range of the electromagnetic spectrum, as well as emission coming from communication devices using the radiofrequency part of the spectrum. Biological effects of such exposures have been noted frequently, although the implication for specific health effects is not that clear. The basic interaction mechanism(s) between such fields and living matter is unknown. Numerous hypotheses have been suggested, although none is convincingly supported by experimental data. Various cellular components, processes, and systems can be affected by EMF exposure. Since it is unlikely that EMF can induce DNA damage directly, most studies have examined EMF effects on the cell membrane level, general and specific gene expression, and signal transduction pathways. In addition, a large number of studies have been performed regarding cell proliferation, cell cycle regulation, cell differentiation, metabolism, and various physiological characteristics of cells. Although 50/60 Hz EMF do not directly lead to genotoxic effects, it is possible that certain cellular processes altered by exposure to EMF indirectly affect the structure of DNA causing strand breaks and other chromosomal aberrations. The aim of this article is to present a hypothesis of a possible initial cellular event affected by exposure to ELF EMF, an event which is compatible with the multitude of effects observed after exposure. Based on an extensive literature review, we suggest that ELF EMF exposure is able to perform such activation by means of increasing levels of free radicals. Such a general activation is compatible with the diverse nature of observed effects. Free radicals are intermediates in natural processes like mitochondrial metabolism and are also a key feature of phagocytosis. Free radical release is inducible by ionizing radiation or phorbolester treatment, both leading to genomic instability. EMF might be a stimulus to induce an "activated state" of the cell such as phagocytosis, which then enhances the release of free radicals, in turn leading to genotoxic events. We envisage that EMF exposure can cause both acute and chronic effects that are mediated by increased free radical levels: (1) Direct activation of, for example macrophages (or other cells) by short-term exposure to EMF leads to phagocytosis (or other cell specific responses) and consequently, free radical production. This pathway may be utilized to positively influence certain aspects of the immune response, and could be useful for specific therapeutic applications. (2) EMF-induced macrophage (cell) activation includes direct stimulation of free radical production. (3) An increase in the lifetime of free radicals by EMF leads to persistently elevated free radical concentrations. In general, reactions in which radicals are involved become more frequent, increasing the possibility of DNA damage. (4) Long-term EMF exposure leads to a chronically increased level of free radicals, subsequently causing an inhibition of the effects of the pineal gland hormone melatonin. Taken together, these EMF induced reactions could lead to a higher incidence of DNA damage and therefore, to an increased risk of tumour development. While the effects on melatonin and the extension of the lifetime of radicals can explain the link between EMF exposure and the incidence of for example leukaemia, the two additional mechanisms described here specifically for mouse macrophages, can explain the possible correlation between immune cell system stimulation and EMF exposure. Copyright 2004 Wiley-Liss, Inc.
机译：当前正在激烈讨论电磁场（EMF）暴露是否会对人体健康造成影响。这包括暴露于在电磁频谱的极低频（ELF）范围内发射的结构和设备，以及来自使用频谱的射频部分的通信设备的发射。尽管对具体健康影响的含义还不清楚，但人们经常注意到这种接触的生物效应。这些领域与生物之间的基本相互作用机制是未知的。尽管实验数据没有说服力，但已经提出了许多假设。各种细胞成分，过程和系统可能会受到EMF暴露的影响。由于EMF不可能直接诱导DNA损伤，因此大多数研究都检查了EMF对细胞膜水平，一般和特定基因表达以及信号转导途径的影响。另外，已经进行了关于细胞增殖，细胞周期调节，细胞分化，代谢和细胞的各种生理特性的大量研究。尽管50/60 Hz EMF不会直接导致遗传毒性作用，但可能由于暴露于EMF而改变的某些细胞过程会间接影响DNA结构，从而引起链断裂和其他染色体畸变。本文的目的是提出一个可能的初始细胞事件的假设，该事件可能受暴露于ELF EMF的影响，该事件与暴露后观察到的多种效应相适应。基于广泛的文献综述，我们建议ELF EMF暴露能够通过增加自由基的水平来进行这种活化。这样的一般激活与所观察到的效应的多种性质相容。自由基是自然过程（如线粒体代谢）的中间体，并且也是吞噬作用的关键特征。通过电离辐射或佛波酯处理可诱导自由基释放，两者均导致基因组不稳定。 EMF可能是一种诱导细胞“激活状态”（例如吞噬作用）的刺激，然后增强了自由基的释放，进而导致了遗传毒性事件。我们设想，EMF暴露可引起自由基水平升高介导的急性和慢性影响：（1）短期暴露于EMF会直接激活例如巨噬细胞（或其他细胞）导致吞噬作用（或其他细胞）具体的反应），因此产生自由基。该途径可用于积极影响免疫应答的某些方面，并且可用于特定的治疗应用。 （2）EMF诱导的巨噬细胞（细胞）活化包括直接刺激自由基产生。 （3）EMF延长了自由基的寿命，导致自由基浓度持续升高。通常，涉及自由基的反应变得更加频繁，从而增加了DNA损伤的可能性。 （4）长期暴露于EMF会导致自由基水平长期升高，从而导致松果体激素褪黑激素的抑制作用。综上所述，这些EMF诱导的反应可能导致DNA损伤的发生率更高，因此增加了发生肿瘤的风险。虽然对褪黑激素的影响和自由基寿命的延长可以解释EMF暴露与例如白血病的发生率之间的联系，但此处针对小鼠巨噬细胞特别描述的两种其他机制可以解释免疫细胞系统刺激与EMF暴露。版权所有2004 Wiley-Liss，Inc.

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