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细胞对极低频磁场和热的反应:热休克蛋白共同参与的证据?

Cellular Response to ELF-MF and Heat: Evidence for a Common Involvement of Heat Shock Proteins?

作者信息

Zeni Olga, Simkó Myrtill, Scarfi Maria Rosaria, Mattsson Mats-Olof

机构信息

Institute for Electromagnetic Sensing of the Environment (IREA), National Research Council, Naples, Italy.

SciProof International AB, Östersund, Sweden.

出版信息

Front Public Health. 2017 Oct 18;5:280. doi: 10.3389/fpubh.2017.00280. eCollection 2017.

Abstract

It has been shown that magnetic fields in the extremely low frequency range (ELF-MF) can act as a stressor in various or systems, at flux density levels below those inducing excitation of nerve and muscle cells, which are setting the limits used by most generally accepted exposure guidelines, such as the ones published by the International Commission on Non-Ionizing Radiation Protection. In response to a variety of physiological and environmental factors, including heat, cells activate an ancient signaling pathway leading to the transient expression of heat shock proteins (HSPs), which exhibit sophisticated protection mechanisms. A number of studies suggest that also ELF-MF exposure can activate the cellular stress response and cause increased HSPs expression, both on the mRNA and the protein levels. In this review, we provide some of the presently available data on cellular responses, especially regarding HSP expression, due to single and combined exposure to ELF-MF and heat, with the aim to compare the induced effects and to detect possible common modes of action. Some evidence suggest that MF and heat can act as costressors inducing a kind of thermotolerance in cell cultures and in organisms. The MF exposure might produce a potentiated or synergistic biological response such as an increase in HSPs expression, in combination with a well-defined stress, and in turn exert beneficial effects during certain circumstances.

摘要

研究表明,极低频磁场(ELF-MF)在低于诱导神经和肌肉细胞兴奋的磁通密度水平时,可作为各种组织或系统中的应激源,而这些磁通密度水平设定了大多数公认的暴露指南(如国际非电离辐射防护委员会发布的指南)所使用的限制。作为对包括热在内的各种生理和环境因素的响应,细胞会激活一条古老的信号通路,导致热休克蛋白(HSPs)的瞬时表达,这些热休克蛋白具有复杂的保护机制。多项研究表明,暴露于ELF-MF也可激活细胞应激反应,并导致mRNA和蛋白质水平上HSPs表达增加。在本综述中,我们提供了一些目前可用的关于细胞反应的数据,特别是关于HSP表达的数据,这些数据涉及单独和联合暴露于ELF-MF及热的情况,目的是比较诱导效应并检测可能的共同作用模式。一些证据表明,磁场和热可作为共应激源,在细胞培养物和生物体中诱导一种热耐受性。磁场暴露可能会与明确的应激相结合,产生增强或协同的生物学反应,如HSPs表达增加,进而在某些情况下发挥有益作用。

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