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首页> 外文期刊>Frontiers in Public Health >Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies
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Extremely Low-Frequency Magnetic Fields and Redox-Responsive Pathways Linked to Cancer Drug Resistance: Insights from Co-Exposure-Based In Vitro Studies

机译：与癌症耐药相关的极低频磁场和氧化还原反应途径：基于共同暴露的体外研究的见解

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摘要

Electrical devices currently used in clinical practice and common household equipments generate extremely low-frequency magnetic fields (ELF-MF) that were classified by the International Agency for Research on Cancer as “possible carcinogenic.” Assuming that ELF-MF plays a role in the carcinogenic process without inducing direct genomic alterations, ELF-MF may be involved in the promotion or progression of cancers. In particular, ELF-MF-induced responses are suspected to activate redox-responsive intracellular signaling or detoxification scavenging systems. In fact, improved protection against oxidative stress and redox-active xenobiotics is thought to provide critical proliferative and survival advantage in tumors. On this basis, an ever-growing research activity worldwide is attempting to establish whether tumor cells may develop multidrug resistance through the activation of essential cytoprotective networks in the presence of ELF fields, and how this might trigger relevant changes in tumor phenotype. This review builds a framework around how the activity of redox-responsive mediators may be controlled by co-exposure to ELF-MF and reactive oxygen species-generating agents in tumor and cancer cells, in order to clarify whether and how such potential molecular targets could help to minimize or neutralize the functional interaction between ELF-MF and malignancies.
机译：当前在临床实践中使用的电气设备和普通家用设备会产生极低频磁场（ELF-MF），该磁场被国际癌症研究机构归类为“可能致癌物质”。假设ELF-MF在致癌过程中起作用而不诱导直接的基因组改变，则ELF-MF可能参与了癌症的促进或发展。特别是，怀疑ELF-MF诱导的反应可激活氧化还原反应性细胞内信号传导或排毒清除系统。实际上，人们认为增强的抗氧化应激和氧化还原活性异种生物的保护作用在肿瘤中具有关键的增殖和生存优势。在此基础上，世界范围内一项日益增长的研究活动正在试图确定在存在ELF场的情况下肿瘤细胞是否可以通过激活必需的细胞保护网络来发展多药耐药性，以及这如何引发肿瘤表型的相关变化。这篇综述建立了一个框架，围绕如何通过共同暴露于肿瘤和癌细胞中的ELF-MF和活性氧物种生成剂来控制氧化还原反应介体的活性，以阐明这种潜在的分子靶标能否以及如何帮助最小化或中和ELF-MF与恶性肿瘤之间的功能相互作用。

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