Immune Responses to Multi-Frequencies of 1.5 GHz and 4.3 GHz Microwave Exposure in Rats: Transcriptomic and Proteomic Analysis

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

The Biological Effects of Compound Microwave Exposure with 2.8 GHz and 9.3 GHz on Immune System: Transcriptomic and Proteomic Analysis

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

Role of Cx43 in iPSC-CM Damage Induced by Microwave Radiation

The heart is one of the major organs affected by microwave radiation, and these effects have been extensively studied. Previous studies have shown that microwave-radiation-induced heart injury might be related to the abnormal expression and distribution of Cx43. In order to make the research model closer to humans, we used iPSC-CMs as the cell injury model to investigate the biological effect and mechanism of iPSC-CM injury after microwave radiation. To model the damage, iPSC-CMs were separated into four groups and exposed to single or composite S-band (2.856 GHz) and X-band (9.375 GHz) microwave radiation sources with an average power density of 30 mW/cm2. After that, FCM was used to detect cell activity, and ELISA was used to detect the contents of myocardial enzymes and injury markers in the culture medium, and it was discovered that cell activity decreased and the contents increased after radiation. TEM and SEM showed that the ultrastructure of the cell membrane, mitochondria, and ID was damaged. Mitochondrial function was aberrant, and glycolytic capacity decreased after exposure. The electrical conduction function of iPSC-CM was abnormal; the conduction velocity was decreased, and the pulsation amplitude was reduced. Wb, qRT-PCR, and IF detections showed that the expression of Cx43 was decreased and the distribution of Cx43 at the gap junction was disordered. Single or composite exposure to S- and X-band microwave radiation caused damage to the structure and function of iPSC-CMs, primarily affecting the cell membrane, mitochondria, and ID. The composite exposure group was more severely harmed than the single exposure group. These abnormalities in structure and function were related to the decreased expression and disordered distribution of Cx43

Physiological and Psychological Stress of Microwave Radiation-Induced Cardiac Injury in Rats

Electromagnetic waves are widely used in both military and civilian fields, which could cause long-term and high-power exposure to certain populations and may pose a health hazard. The aim of this study was to simulate the long-term and high-power working environment of workers using special electromagnetic radiation occupations to clarify the radiation-induced stress response and cardiac damage and thus gain insights into the mechanisms of injuries caused by electromagnetic radiation. In this study, the combination of microwave and stress was an innovative point, aiming to broaden the research direction with regard to the effect and mechanism of cardiac injury caused by radiation. The myocardial structure was observed by optical and transmission electron microscope, mitochondrial function was detected by flow cytometry, oxidative-stress markers were detected by microplate reader, serum stress hormone was detected by radioimmunoassay, and heart rate variability (HRV) was analyzed by multichannel-physiological recorder. The rats were weighed and subjected to an open field experiment. Western blot (WB) and immunofluorescence (IF) were used to detect the expressions and distributions of JNK (c-Jun N-terminal kinase), p-JNK (phosphorylated c-Jun N-terminal kinase), HSF1 (heat shock factor), and NFATc4 (nuclear factor of activated T-cell 4). This study found that radiation could lead to the disorganization, fragmentation, and dissolution of myocardial fibers, severe mitochondrial cavitation, mitochondrial dysfunction, oxidative-stress injury in myocardium, increase to stress hormone in serum, significant changes in HRV, and a slow gain in weight. The open field experiment indicated that the rats experienced anxiety and depression and had decreased exercise capacity after radiation. The expressions of JNK, p-JNK, HSF1, and NFATc4 in myocardial tissue were all increased. The above results suggested that 30 mW/cm2 of S-band microwave radiation for 35 min could cause both physiological and psychological stress damage in rats; the damage was related to the activation of the JNK pathway, which provided new ideas for research on protection from radiation

Acute effects of 2.856 GHz and 1.5 GHz microwaves on spatial memory abilities and CREB-related pathways

Abstract This study aimed to evaluate the acute effects of 2.856 GHz and 1.5 GHz microwaves on spatial memory and cAMP response element binding (CREB)-related pathways. A total of 120 male Wistar rats were divided into four groups: a control group (C); 2.856 GHz microwave exposure group (S group); 1.5 GHz microwave exposure group (L group); and 2.856 and 1.5 GHz cumulative exposure group (SL group). Decreases in spatial memory abilities, changes in EEG, structural injuries, and the downregulation of phosphorylated-Ak strain transforming (p-AKT), phosphorylated-calcium/calmodulin-dependent protein kinase II (p-CaMKII), phosphorylated extracellular signal regulated kinase (p-ERK) and p-CREB was observed 6 h after microwave exposure. Significant differences in the expression of p-CaMKII were found between the S and L groups. The power amplitudes of the EEG waves (θ, δ), levels of structural injuries and the expression of p-AKT, p-CaMK II, p-CREB, and p-ERK1/2 were significantly different in the S and L groups compared to the SL group. Interaction effects between the 2.856 and 1.5 GHz microwaves were found in the EEG and p-CREB changes. Our findings indicated that 2.856 GHz and 1.5 GHz microwave exposure induced a decline in spatial memory, which might be related to p-AKT, p-CaMK II, p-CREB and p-ERK1/2

The compound Chinese medicine "Kang Fu Ling" protects against high power microwave-induced myocardial injury.

BACKGROUND: The prevention and treatment of Microwave-caused cardiovascular injury remains elusive. This study investigated the cardiovascular protective effects of compound Chinese medicine "Kang Fu Ling" (KFL) against high power microwave (HPM)-induced myocardial injury and the role of the mitochondrial permeability transition pore (mPTP) opening in KFL protection. METHODS: Male Wistar rats (100) were divided into 5 equal groups: no treatment, radiation only, or radiation followed by treatment with KFL at 0.75, 1.5, or 3 g/kg/day. Electrocardiography was used to Electrophysiological examination. Histological and ultrastructural changes in heart tissue and isolated mitochondria were observed by light microscope and electron microscopy. mPTP opening and mitochondrial membrane potential were detected by confocal laser scanning microscopy and fluorescence analysis. Connexin-43 (Cx-43) and endothelial nitric oxide synthase (eNOS) were detected by immunohistochemistry. The expression of voltage-dependent anion channel (VDAC) was detected by western blotting. RESULTS: At 7 days after radiation, rats without KFL treatment showed a significantly lower heart rate (P<0.01) than untreated controls and a J point shift. Myocyte swelling and rearrangement were evident. Mitochondria exhibited rupture, and decreased fluorescence intensity, suggesting opening of mPTP and a consequent reduction in mitochondrial membrane potential. After treatment with 1.5 g/kg/day KFL for 7 d, the heart rate increased significantly (P<0.01), and the J point shift was reduced flavorfully (P<0.05) compared to untreated, irradiated rats; myocytes and mitochondria were of normal morphology. The fluorescence intensities of dye-treated mitochondria were also increased, suggesting inhibition of mPTP opening and preservation of the mitochondrial membrane potential. The microwave-induced decrease of Cx-43 and VDAC protein expression was significantly reversed. CONCLUSION: Microwave radiation can cause electrophysiological, histological and ultrastructural changes in the heart. KFL at 1.5 g/kg/day had the greatest protective effect on these cardiovascular events. mPTP plays an important role in the protective effects of KFL against microwave-radiation-induced myocardial injury

Progress and Prospects of Emerging Potassium–Sulfur Batteries

The potassium–sulfur battery (K–S battery) as an innovative battery technology is a promising candidate for large-scale applications, due to its high energy density and the low cost of both K and S. The development of the K–S technology is, however, inhibited by its low reversible capacity and the safety issues related to the K metal anode. Here, the review starts by discussing the mechanism of the redox reactions for the K–S batteries and emphasizes the challenges for this battery system based on its current research status. Furthermore, the current improvement strategies for the K–S system in terms of the sulfur cathode, electrolyte, separator, and K metal anode are summarized. Finally, future perspectives on the development of the K–S system are proposed

Lipid Peroxides Mediated Ferroptosis in Electromagnetic Pulse-Induced Hippocampal Neuronal Damage via Inhibition of GSH/GPX4 Axis

Electromagnetic pulse (EMP) radiation was reported to be harmful to hippocampal neurons. However, the mechanism underlying EMP-induced neuronal damage remains unclear. In this paper, for the first time, we attempted to investigate the involvement of ferroptosis in EMP-induced neuronal damage and its underlying mechanism. In vivo studies were conducted with a rat model to examine the association of ferroptosis and EMP-induced hippocampal neuronal damage. Moreover, in vitro studies were conducted with HT22 neurons to investigate the underlying mechanism of EMP-induced neuronal ferroptosis. In vivo results showed that EMP could induce learning and memory impairment of rats, ferroptotic morphological damages to mitochondria, accumulation of malonaldehyde (MDA) and iron, overexpression of prostaglandin-endoperoxide synthase 2 (PTGS2) mRNA, and downregulation of GPX4 protein in rat hippocampus. In vitro results showed that EMP could induce neuronal death, MDA accumulation, iron overload, PTGS2 overexpression, and GPX4 downregulation in HT22 neurons. These adverse effects could be reversed by either lipid peroxides scavenger ferrostatin-1 or overexpression of GPX4. These results suggest that EMP radiation can induce ferroptosis in hippocampal neurons via a vicious cycle of lipid peroxides accumulation and GSH/GPX4 axis downregulation. Lipid peroxides and the GSH/GPX4 axis provide potential effective intervention targets to EMP-induced hippocampal neuronal damage