The anxieties and concerns about health hazards caused by microwave has been growing recently. Previous studies have reported microwave induced structural and functional injuries to brain. However, the biological effects caused by compound microwave were largely unexplored. In this study, we investigated the biological effects on rat’s hippocampus after sequentially exposure to 2.8 GHz and 9.3 GHz at average power density of 10 mW/cm2. Morris water maze (MWM) navigation tests showed that microwave exposure significantly extended the average escape latency (AEL) at 1d and 3d after exposure, suggesting reduced learning and memory ability. Importantly, compound microwave produced strongest responses at 3 d after exposure. Moreover, microwave also could induce abnormal electroencephalogram (EEG), such as increasing the power of θ wave and δ wave, suggesting brain damage or dysfunction. Histopathological analysis suggested that microwave resulted in obvious structural injuries in hippocampus at 7 d after exposure, and most serious injuries were observed in compound microwave exposed rats. Moreover, disorder of mitochondria and reduced Nissl bodies in hippocampus might contribute to the decrease of cognitive function. However, both the cognitive function and hippocampal structure restored to normal at 28 d after exposure, which might be attributed to self-recovery mechanisms. Gene ontology (GO) and Protein-protein interaction (PPI) analyses of differential expressed genes (DEGs) in peripheral blood suggested that Htt and Bdnf might be potential indicators to predict microwave. In conclusion, compound microwave of 2.8 GHz and 9.3 GHz could elicit reversible structural injuries to hippocampus, which could decrease the cognitive function of rats.

The brain is complex and metabolically active, and the detection of metabolites plays an important role in brain development and diseases. Currently, there is a lack of research on the metabolic spectrum changes in learning and memory impairment, and hippocampal damage induced by microwave radiation from the metabolic perspective. Aiming to provide sensitive indicators for microwave radiation-induced brain damage and establish a foundation for understanding its injury mechanisms, this study employed non-targeted metabolomics to investigate metabolic fluctuations and key metabolic pathway alterations in rats’ hippocampal tissue after microwave radiation. The memory and spatial exploration abilities of rats decreased after radiation. The postsynaptic densities were thickened in the MW group. The cholesterol sulfate, SM(d16:1/24:1(15Z)), and linoelaidylcarnitine were significantly increased after radiation, whereas etrahydrocorticosterone, L-phenylalanine, and histamine were significantly decreased after radiation. These metabolites were enriched in signaling pathways related to the inflammatory mediator regulation of transient receptor potential (TRP) channels, neuroactive ligand–receptor interaction, steroid hormone biosynthesis, and phenylalanine, tyrosine, and tryptophan biosynthesis. These findings indicate that microwave radiation causes spatial learning and memory dysfunction in rats and structural damage to hippocampal tissue.

To investigate the dynamic changes in hippocampal metabolism after microwave radiation using liquid chromatography in tandem with mass spectrometry/mass spectrometry (LC–MS/MS) and to identify potential biomarkers. Wistar rats were randomly assigned to a sham group and a microwave radiation group. The rats in the microwave radiation group were exposed to 2.856 GHz for 15 min for three times, with 5 min intervals. The rats in the sham group were not exposed. Transmission electron microscope revealed blurring of the synaptic cleft and postsynaptic dense thickening in hippocampal neurons after microwave radiation. Metabolomic analysis revealed 38, 24, and 39 differentially abundant metabolites at 3, 7, and 14 days after radiation, respectively, and the abundance of 9 metabolites, such as argininosuccinic acid, was continuously decreased. After microwave radiation, the abundance of metabolites such as argininosuccinic acid was successively decreased, indicating that these metabolites could be potential biomarkers for hippocampal tissue injury.

Microwave ablation can produce immune activation due to thermal effects. However, the nonthermal effects of microwaves on the immune system are still largely unexplored. In this study, we sequentially exposed rats to 1.5 GHz microwave for 6 min and 2.8 GHz microwave for 6 min at an average power density of 5, 10, and 30 mW/cm2. The structure of the thymus, spleen, and mesenteric lymph node were observed, and we showed that multifrequency microwave exposure caused tissue injuries, such as congestion and nuclear fragmentation in lymphocytes. Ultrastructural injuries, including mitochondrial swelling, mitochondrial cristae rupture, and mitochondrial cavitation, were observed, especially in the 30 mW/cm2 microwave-exposed group. Generally, multifrequency microwaves decreased white blood cells, as well as lymphocytes, monocytes, and neutrophils, in peripheral blood, from 7 d to 28 d after exposure. Microwaves with an average density of 30 mW/cm2 produced much more significant inhibitory effects on immune cells. Moreover, multifrequency microwaves at 10 and 30 mW/cm2, but not 5 mW/cm2, reduced the serum levels of several cytokines, such as interleukin-1 alpha (IL-1α), IL-1β, interferon γ (IFN-γ) and tumor necrosis factor α (TNF-α), at 7 d and 14 d after exposure. We also found similar alterations in immunoglobulins (Igs), IgG, and IgM in serum. However, no obvious changes in complement proteins were detected. In conclusion, multifrequency microwave exposure of 1.5 GHz and 2.8 GHz caused both structural injuries of immune tissues and functional impairment in immune cells. Therefore, it will be necessary to develop an effective strategy to protect people from multifrequency microwave-induced immune suppression.

With the rapidly increasing application of microwave technologies, the anxiety and speculation about microwave induced potential health hazards has been attracting more and more attention. In our daily life, people are exposed to complex environments with multi-frequency microwaves, especially L band and C band microwaves, which are commonly used in communications. In this study, we exposed rats to 1.5 GHz (L10), 4.3 GHz (C10) or multi-frequency (LC10) microwaves at an average power density of 10 mW/cm2. Both single and multi-frequency microwaves induced slight pathological changes in the thymus and spleen. Additionally, the white blood cells (WBCs) and lymphocytes in peripheral blood were decreased at 6 h and 7 d after exposure, suggesting immune suppressive responses were induced. Among lymphocytes, the B lymphocytes were increased while the T lymphocytes were decreased at 7 d after exposure in the C10 and LC10 groups, but not in the L10 group. Moreover, multi-frequency microwaves regulated the B and T lymphocytes more strongly than the C band microwave. The results of transcriptomics and proteomics showed that both single and multi-frequency microwaves regulated numerous genes associated with immune regulation and cellular metabolism in peripheral blood and in the spleen. However, multi-frequency microwaves altered the expression of many more genes and proteins. Moreover, multi-frequency microwaves down-regulated T lymphocytes’ development, differentiation and activation-associated genes, while they up-regulated B lymphocytes’ activation-related genes. In conclusion, multi-frequency microwaves of 1.5 GHz and 4.3 GHz produced immune suppressive responses via regulating immune regulation and cellular metabolism-associated genes. Our findings provide meaningful information for exploring potential mechanisms underlying multi-frequency induced immune suppression.

It is well-known that microwaves produce both thermal and nonthermal effects. Microwave ablation can produce thermal effects to activate the body’s immune system and has been widely used in cancer therapy. However, the nonthermal effects of microwaves on the immune system are still largely unexplored. In the present study, we exposed rats to multifrequency microwaves of 2.8 GHz and 9.3 GHz with an average power density of 10 mW/cm2, which are widely used in our daily life, to investigate the biological effects on the immune system and its potential mechanisms. Both single-frequency microwaves and multifrequency microwaves caused obvious pathological alterations in the thymus and spleen at seven days after exposure, while multifrequency microwaves produced more pronounced injuries. Unexpectedly, multifrequency microwave exposure increased the number of both leukocytes and lymphocytes in the peripheral blood and upregulated the proportion of B lymphocytes among the total lymphocytes, indicating activation of the immune response. Our data also showed that the cytokines associated with the proliferation and activation of B lymphocytes, including interleukin (IL)-1α, IL-1β and IL-4, were elevated at six hours after exposure, which might contribute to the increase in B lymphocytes at seven days after exposure. Moreover, multifrequency microwave exposure upregulated the mRNA and protein expression of B cell activation-associated genes in peripheral blood. In addition to immune-associated genes, multifrequency microwaves mainly affected the expression of genes related to DNA duplication, cellular metabolism and signal transduction in the peripheral blood and spleen. In conclusion, multifrequency microwaves with 2.8 GHz and 9.3 GHz caused reversible injuries of the thymus and spleen but activated immune cells in the peripheral blood by upregulating mRNA and protein expression, as well as cytokine release. These results not only uncovered the biological effects of multifrequency microwave on the immune system, but also provide critical clues to explore the potential mechanisms.

目的 探讨2.8 GHz微波辐射对大鼠空间记忆、工作记忆、识别记忆能力及脑组织结构的影响,为深入研究微波辐射致脑损伤的特征与机制提供依据.方法 采用30mW/cm2的2.8 GHz微波辐射雄性Wistar大鼠,辐射时间为15 min.于辐射后6 h～4 d,采用Morris水迷宫检测大鼠学习和空间记忆能力,并于辐射后5～10d,采用Morris水迷宫反转实验检测大鼠空间工作记忆能力.于辐射后1 h和1 d,采用新物体识别实验检测大鼠识别记忆能力.于辐射后3d和7 d,采用苏木素伊红染色和光镜观察海马组织结构改变.结果 ①Morris水迷宫空间探索实验结果显示,辐射组大鼠原平台所在象限停留时间占比显著低于假辐射组(P＜0.05),两组大鼠穿越平台区域次数无显著差异(P＞0.05);在水迷宫定位航行实验中,两组大鼠平均逃避潜伏期均无显著差异(P＞0.05).Morris水迷宫定位航行反转实验结果显示,两组大鼠平均逃避潜伏期均无显著差异(P＞0.05),在空间探索反转实验中,两组大鼠在穿越平台区域次数与原平台时间占比上均无显著差异(P＞0.05).②新物体识别结果显示,于辐射后1 h,辐射组大鼠辨别指数显著低于假辐射组(P＜0.05).辐射后24 h,两组大鼠辨别指数无显著差异(P＞0.05).③海马组织结构观察发现,辐射后3d,假辐射组海马组织结构正常,辐射组大鼠海马组织齿状回区神经元核固缩、深染,呈梭形改变;辐射后7 d损伤呈恢复趋势.结论 30 mW/cm2的2.8 GHz微波辐射可引起大鼠空间记忆和识别记忆能力障碍,海马组织特别是齿状回区结构损伤可能是其致伤的结构基础.

目的 探索微波复合暴露对小鼠免疫功能的影响,为微波复合暴露对免疫功能损伤机制和防治靶点研究提供依据.方法 将30只SPF级雄性C57BL/6N小鼠随机分为假辐射组、低剂量复合组(比吸收率为3 W/kg)和高剂量复合组(比吸收率为15 W/kg).采用X和S波段微波复合照射,于辐射后6 h和7 d,分别采集小鼠外周血,采用全自动血细胞计数仪检测外周血细胞计数,流式细胞仪分析小鼠外周血淋巴细胞亚群,酶联免疫吸附法检测血清免疫球蛋白IgG、IgM和IgA浓度,多功能液相芯片分析平台检测小鼠血清细胞因子IL-2、IL-4和TNF-α 浓度.结果 与假辐射组相比,辐射后6 h,低剂量和高剂量复合组白细胞(WBC)和淋巴细胞(LYMPH)计数显著增加(P<0.05或P<0.01);外周血CD19+B淋巴细胞与CD3+T淋巴细胞比值显著增加(P<0.05),CD4+T淋巴细胞与CD8+T淋巴细胞比值均显著升高(P<0.01).与假辐射组相比,辐射后6 h,低剂量复合组血清IgG、IgM和IgA浓度均显著增加(P<0.01或P<0.05),高剂量复合组血清IgG和IgM浓度明显增加(P<0.01或P<0.05);辐射后7 d,低剂量和高剂量复合组血清IgA浓度均显著降低(P<0.01).辐射后6 h,低剂量和高剂量复合组血清IL-2、IL-4和TNF-α 浓度显著下降(P<0.05或P<0.01);辐射后7 d,与假辐射组和低剂量复合组相比,高剂量复合组IL-2浓度显著下降(P<0.05或P<0.01).结论 微波复合暴露可导致小鼠细胞免疫功能紊乱;体液免疫呈现先激活后抑制现象;辐射后6 h外周血LYMPH计数、血清IgG浓度、IL-2、IL-4和TNF-α 浓度等指标改变与辐射剂量呈正相关.