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长期暴露于 835MHz 的射频电磁辐射会导致小鼠皮质神经元的过度活跃、自噬和脱髓鞘。

Long-term exposure to 835 MHz RF-EMF induces hyperactivity, autophagy and demyelination in the cortical neurons of mice.

机构信息

Department of Pharmacology, College of Medicine, Dankook University, Cheonan-si, Chungnam, Republic of Korea.

Center for Electron Microscopy Research, Korea Basic Science Institute, Ochang, Chung-Buk, Republic of Korea.

出版信息

Sci Rep. 2017 Jan 20;7:41129. doi: 10.1038/srep41129.

DOI:10.1038/srep41129
PMID:28106136
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5247706/
Abstract

Radiofrequency electromagnetic field (RF-EMF) is used globally in conjunction with mobile communications. There are public concerns of the perceived deleterious biological consequences of RF-EMF exposure. This study assessed neuronal effects of RF-EMF on the cerebral cortex of the mouse brain as a proxy for cranial exposure during mobile phone use. C57BL/6 mice were exposed to 835 MHz RF-EMF at a specific absorption rate (SAR) of 4.0 W/kg for 5 hours/day during 12 weeks. The aim was to examine activation of autophagy pathway in the cerebral cortex, a brain region that is located relatively externally. Induction of autophagy genes and production of proteins including LC3B-II and Beclin1 were increased and accumulation of autolysosome was observed in neuronal cell bodies. However, proapoptotic factor Bax was down-regulted in the cerebral cortex. Importantly, we found that RF-EMF exposure led to myelin sheath damage and mice displayed hyperactivity-like behaviour. The data suggest that autophagy may act as a protective pathway for the neuronal cell bodies in the cerebral cortex during radiofrequency exposure. The observations that neuronal cell bodies remained structurally stable but demyelination was induced in cortical neurons following prolonged RF-EMF suggests a potential cause of neurological or neurobehavioural disorders.

摘要

射频电磁场(RF-EMF)在全球范围内与移动通信结合使用。公众对射频电磁场暴露的有害生物后果存在担忧。本研究评估了 RF-EMF 对小鼠大脑皮质的神经元效应,作为手机使用期间颅部暴露的替代指标。C57BL/6 小鼠在 12 周内每天暴露于 835MHz 的射频电磁场中,SAR 为 4.0W/kg,持续 5 小时。目的是研究大脑皮质中自噬途径的激活情况,大脑皮质位于相对外部的位置。自噬基因的诱导和包括 LC3B-II 和 Beclin1 在内的蛋白质的产生增加,并且在神经元细胞体中观察到自噬溶酶体的积累。然而,大脑皮质中的促凋亡因子 Bax 被下调。重要的是,我们发现 RF-EMF 暴露导致髓鞘损伤,并且小鼠表现出多动样行为。这些数据表明,自噬可能在射频暴露期间作为大脑皮质神经元细胞体的保护途径。观察到神经元细胞体在结构上保持稳定,但在长时间 RF-EMF 暴露后皮质神经元中诱导了脱髓鞘,这提示了神经或神经行为障碍的潜在原因。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/ce66b5d0dfd9/srep41129-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/81efa96e725f/srep41129-f1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/6c91b4f02491/srep41129-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/ce66b5d0dfd9/srep41129-f6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/81efa96e725f/srep41129-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/9fd25e29e54a/srep41129-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/61a4e2940c08/srep41129-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/10bd888de647/srep41129-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/6c91b4f02491/srep41129-f5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c26b/5247706/ce66b5d0dfd9/srep41129-f6.jpg

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