Ionizing radiation (IR)-induced alterations in glucose metabolism are closely associated with radioresistance, yet the underlying mechanisms remain incompletely understood. Here, we identify a post-translational modification axis in which IR induces general control non-repressible protein 5 (GCN5/KAT2A)-mediated crotonylation of acetyl-CoA acetyltransferase 1 (ACAT1) at lysine 181 (K181), thereby enhancing ACAT1 activity and promoting increased acetylation of pyruvate dehydrogenase E1 subunit alpha (PDHA1) along with its phosphorylation at S293.These changes led to inhibition of PDHA1, impaired pyruvate metabolism, and increased lactate accumulation. Functional studies demonstrated that ACAT1 K181R (a decrotonylation-mimicking mutant) increased radiosensitivity and significantly attenuated IR-induced lactate production. Collectively, these findings reveal an unrecognized mechanism by which radiotherapy reprograms cellular metabolism through the GCN5-ACAT1-PDHA1 axis, linking ACAT1 crotonylation to altered pyruvate metabolism, enhanced lactate production, and subsequent radioresistance. These findings suggest that targeting ACAT1 K181 crotonylation represents a potential therapeutic strategy to improve tumor radiosensitivity.

Objective To explore the neuroprotective effects of nicotinamide riboside against microwave radiation-induced brain injury in mice.Methods Mice were subjected to whole-body uniform microwave radiation(at a central frequency of 2.856 GHz,and average power density of 20 mW/cm² for 30 min).After radiation,the mice received intraperitoneal injections of nicotinamide riboside chloride at doses of 250,500,or 1000 mg/(kg·d).Behavioral performance was assessed using the open field test(OFT)and elevated plus maze(EPM).Histopathological changes in the cortex(CTX),hippocampus(HPC),and hypothalamus(HT)were detected via hematoxylin-eosin(HE)staining.Levels of such pro-inflammatory cytokines as tumor necrosis factor-α(TNF-α)and interleukin-6(IL-6)in the CTX,HPC,and HT were measured using enzyme-linked immunosorbent assay(ELISA).Proteomic analysis was performed to assess changes in protein expressions in the CTX.Results After microwave exposure,the exploratory behavior of mice was reduced,and the entries into the central zone and open arms were decreased(P<0.05).Neuronal injuries were increased,and the levels of TNF-α and IL-6 were elevated(P<0.05).Proteomic analysis indicated that differentially expressed proteins were mostly enriched through oxidative phosphorylation related pathways.NR interventions significantly ameliorated these alterations,as evidenced by increased exploratory behavior,reduced neuronal injury,decreased inflammatory cytokine levels(P<0.05),and the reversal of expressions of dysregulated proteins,including zinc finger AN1-type domain-containing protein 5(Zfand5).Conclusion NR can alleviate brain injury and associated behavioral and neuroinflammatory alterations in mice induced by microwave radiation,which might involve the zfands and other key molecules.

Terahertz (THz) waves, with frequencies between those of microwaves and infrared light, can excite nonlinear resonance and affect cellular function. However, the effects and underlying mechanism of terahertz radiation on neurons and rodent behaviour are still unclear. Here, we constructed THz radiation exposure models in the perirhinal cortex (PRH) of male mice. First, we measured the power and depth of penetration of the 0.152 THz photons cranially above the PRH. We demonstrated that the visual recognition memory of mice was improved after THz wave irradiation, which was similar to the effect of light activation of glutamatergic neurons in the PRH. In addition, THz wave exposure increased the number of c-Fos+ neurons, synchronous electrical activity, synaptic plasticity and glutamatergic neuronal excitability in the PRH. Moreover, the expression of molecules involved in glutamate transmission, such as VAMP2, EAAT, CaMKII and PSD95, increased along with enhanced NMDAR and AMPAR activity. Our findings revealed that THz waves could improve recognition memory via the activation of excitatory neurons and accelerated glutamate metabolism in the PRH, suggesting that THz photon stimulation might be developed as a noninvasive neuromodulation technique to promote cognitive function.

Cardiovascular and cerebrovascular diseases are serious threats to human health and impose a significant burden on individuals and society. As the two critical and complex organs with the highest metabolic demands, the brain and the heart form an interactive relationship through metabolic networks. As a core prerequisite for maintaining the normal physiological functions of the body, metabolic homeostasis is also a crucial foundation for ensuring the brain-heart synergy. When the human metabolism is in a stable state, the energy supply and material exchange of the brain and the heart can accurately match demand, the neural signal transmission is smooth, and the myocardial contraction is strong and regular-thus ensuring the coordinated and unified functions of these two vital organs. However, once metabolic homeostasis is disrupted, problems such as energy metabolism disorders will arise, which will then become a core inducing mechanism for cardiovascular and cerebrovascular comorbidities. This article presents a review of the research progress on the potential mechanisms of brain-heart interactions based on metabolic regulation from three aspects: neurometabolic, endocrino-metabolic and immune-metabolic regulation, the impact of cardiac function on brain metabolism, and the bidirectional regulation of brain-heart metabolism.

Discovering effective anti-inflammatory peptides targeting the NF-κB pathway is a critical research priority. Herein, a docking study was carried out to screen 25 original linear peptides. Next, 44 novel stapled peptides via the all-hydrocarbon cross-linking strategy were designed and synthesized. 75%-80% stapled peptides displayed reduced cytotoxicity and improved anti-inflammatory activity over the original peptides in vitro. Compared with Dex, s-12s significantly inhibited the expression of proinflammatory mediators in vitro and in vivo. Notably, s-12s also protected mice from LPS-induced mortality and acute organ injury. Mechanistically, s-12s reduced LPS-induced activation of the NF-κB pathway. Moreover, surface plasmon resonance and MD simulations have determined the possibility of NF-κB as a target for s-12s. Therefore, s-12s could be used as a promising therapeutic candidate for inflammatory disorders. Meanwhile, these results have proven that the all-hydrocarbon stapling of anti-inflammatory peptides was a feasible approach for the future development of anti-inflammatory therapeutics.

With the widespread application of microwave technology in communication and medical fields, concerns regarding its biosafety, particularly the effects on the central nervous system, have increased. The brain is considered a sensitive target organ for microwave radiation; however, the molecular mechanisms underlying microwave-induced cognitive impairment remain unclear. The purpose of this study was to evaluate the effects of 4.3 GHz microwave radiation at different power densities on spatial learning and memory in mice, and to identify key molecular changes in the hippocampus associated with cognitive impairment. Mice (male, C57BL/6N) were exposed to 4.3 GHz microwave radiation at power densities of 10 or 30 mW/cm2 for 30 min. Spatial learning and memory abilities were assessed using the Morris water maze (MWM). The hippocampal structure was assessed by HE staining at multiple time points following microwave exposure. Integrated RNA-sequencing (RNA-seq) and 4D-data-independent acquisition (4D-DIA) analyses of the hippocampus were performed at 6 h after microwave exposure, and differentially expressed molecules were selected and validated by quantitative polymerase chain reaction (qPCR) and parallel reaction monitoring (PRM). The 4.3 GHz microwave exposure significantly prolonged escape latency in the MWM, indicating impaired spatial learning or navigation ability. Histological examination revealed transient neuronal damage in the hippocampal CA1 and CA3 regions. Multi-omics analysis and subsequent validation revealed molecular alterations. Following microwave radiation, the expression of synaptic plasticity-related genes Arc and Ebf3 was significantly upregulated. At the protein level, significant downregulation was observed for Protein sidekick-2 and IQGAP1, while WNK3 was significantly upregulated. In summary, 4.3 GHz microwave exposure impaired spatial learning or navigation ability, accompanied by structural damage in the hippocampus and molecular alterations in synaptic plasticity-related pathways. Arc, Ebf3, Protein sidekick-2, WNK3, and IQGAP1 might serve as candidate molecules for understanding and mitigating microwave-induced cognitive deficits.

Objective To investigate the dynamic changes in cardiac structure and function at different time points within one week following high-power microwave exposure in rats in order to provide data for formulating protective strategies and elucidating the mechanisms of microwave-induced cardiac injury.Methods Male Wistar rats were exposed to high-power microwave radiation in the S-band(2.856 GHz)at an average power density of 50 mW/cm²for 30 min.At 1,3,and 7 days post-radiation,cardiac electrophysiological function,macroscopic morphology,and microscopic structure were assessed using serum biochemical analysis(the cardiac enzyme profile,injury markers,and ion concentrations),electrocardiography(ECG),echocardiography,hematoxylin-eosin(HE)staining,and transmission electron microscopy.Results Rectal temperatures significantly increased in rats after microwave irradiation.Biochemical results of the serum showed significant increases in levels of aspartate aminotransferase,lactate dehydrogenase,and creatine kinase at 1 and 7 days post-microwave exposure.Peak changes in fatty acid-binding protein,cardiac troponin T,N-terminal pro-B-type natriuretic peptide,and serum calcium and potassium ion concentrations occurred at 3 days post-exposure,indicating maximal injury at this time point.ECG revealed decreased heart rate,prolonged R-R intervals,and shortened corrected QT intervals at 1 day post-irradiation.Three days after exposure,heart rate increased and P-wave amplitude was elevated,but all parameters largely returned to control levels by day 7.Echocardiography suggested significant thickening of the interventricular septum and left ventricular wall,along with increased left ventricular mass starting at 3 days post-irradiation.These structural alterations persisted until day 7.Histopathological and ultrastructural observations confirmed that myocardial injury peaked at 3 days post-radiation,characterized by inflammatory cell infiltration,myofibrillar disarray,mitochondrial swelling and vacuolation,and disruption of sarcomere structure.These lesions were mitigated by day 7,but complete recovery did not occur.Conclusion 2.856 GHz high-power microwave radiation induces acute cardiac injury in rats,manifested as myocardial enzyme leakage,ion homeostasis imbalance,abnormal electrical activity,and tissue structural remodeling.The effect of injury occurs in a time-dependent manner and peaks at 3 days post-radiation.By day 7,there is partial recovery,yet residual structural abnormalities persist.

This study explores the potential protective effects and mechanisms of astragaloside (AST) on microwave radiation-induced cardiac injury. Rats and H9c2 cells were irradiated with S-band microwave to induce in vivo and in vitro cardiac injury models. In irradiated rats, experiments such as electrophysiological examination, serum biochemical analysis, hematoxylin and eosin (H&E) staining, transmission electron microscopy (TEM), western blot, and immunohistochemical staining were performed after AST were administrated for 7 and/or 14 days. In irradiated H9c2 cells that were pretreated with 1-Azakenpaullone (glycogen synthase kinase-3b inhibitor) or AST, experiments such as TEM, cell counting kit-8 assay, western blot, tetramethylrhodamine methylester staining, and determination of reactive oxygen species (ROS), adenosine triphosphate (ATP) and mitochondrial membrane potential (MMP) were performed. In vivo results showed that at 7 days after exposure, microwave radiation- induced severe cardiac injury (as evidenced by abnormal electrocardiograms and cardiac tissue structure, increased serum myocardial enzyme activities and Ca21 concentration) and lower level of phosphorylation of glycogen synthase kinase-3b (p-GSK-3bSer9).All these changes were reversed after AST treatment. The results of in vitro experiments showed that microwave radiation induced a lower level of p-GSK-3bSer9, more mitochondrial permeability transition pore (mPTP) opening and more serious mitochondrial dysfunction (characterized by increased intracellular ROS production, decreased intracellular ATP synthesis and MMP decline) in H9c2 cells. All these changes were reversed by 1-Azakenpaullone and AST pretreatment. The findings suggest that AST could shield against microwave radiation-induced cardiac injury by promoting the phosphorylation of GSK-3bSer9, thereby inhibiting mPTP opening and restoring mitochondrial function. This study offers valuable insights into potential therapeutic strategies for mitigating the adverse effects of microwave radiation on cardiac health. (c) 2025 by Radiation Research Society

Background: Terahertz (THz) waves, lying between millimeter waves and infrared light, may interact with biomolecules due to their unique energy characteristics. However, whether THz waves are neurally regulated remains controversial, and the underlying mechanism is elusive. Methods: Mouse brain slices were exposed to 1.94 THz waves for 1 h. Synaptic plasticity was evaluated via transmission electron microscopy (TEM), long-term potentiation (LTP), and neuronal class III β-tubulin (Tuj1) and synaptophysin (SYN) expression. Immunofluorescence (IF) and electrophysiology were used to identify neurons sensitive to THz waves. The calcium activity of excitatory neurons, glutamate receptor currents, and glutamate neuron marker expression was also assessed using calcium imaging, a patch clamp, and Western blotting (WB). Optogenetics and chemogenetics were used to determine the role of excitatory neurons in synaptic plasticity impairment after THz wave exposure. NMDA receptor 2B (GluN2B) was overexpressed in the ventral hippocampal CA1 (vCA1) by a lentivirus to clarify the role of GluN2B in THz wave-induced synaptic plasticity impairment. Results: Exposure to 1.94 THz waves increased postsynaptic density (PSD) thickness and reduced the field excitatory postsynaptic potential (fEPSP) slope and Tuj1 and SYN expression. THz waves diminished vCA1 glutamatergic neuron activity and excitability, neural electrical activity, and glutamate transporter function. THz waves reduced N-methyl-D-aspartate receptor (NMDAR) current amplitudes and NMDAR subunit expression. Activating vCA1 glutamatergic neurons through optogenetics and chemogenetics mitigated THz wave-induced synaptic plasticity impairment. GluN2B subunit overexpression improved synaptic plasticity marker expression, synaptic ultrastructure, and the fEPSP slope. Conclusions: Exposure to 1.94 THz waves decreased synaptic plasticity, glutamatergic neuron excitability, and glutamatergic synaptic transmission in the vCA1. Glutamatergic neuron activation and GluN2B overexpression alleviated THz wave-induced synaptic plasticity impairment; thus, neuromodulation could be a promising therapeutic strategy to mitigate the adverse effects of THz radiation.

Background: Previous studies have suggested that electromagnetic pulse (EMP) can induce openings in the blood–brain barrier (BBB). However, the temporal variation and spatial distribution of BBB permeability after EMP radiation are difficult to assess using conventional histopathological approaches. Dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) is a valuable tool for the in vivo evaluation of BBB permeability. The main purpose of this study was to investigate the temporal variation and spatial distribution of BBB permeability after EMP radiation in rats using DCE-MRI. Methods: The dose of EMP was estimated through simulations utilizing a digital rat model comprising 16 distinct brain regions. Then, the changes in BBB permeability of the different rat brain regions at different time points (3 h and 24 h) after EMP radiation were evaluated using quantitative DCE-MRI. Furthermore, the spatial difference in BBB permeability was assessed 3 h after exposure. Finally, the dose–effect relationship between the electric field strength and the BBB permeability was also investigated. Results: The results demonstrated that the changes in the values of volume transfer constant (ΔKtrans) significantly increased in several rat brain regions at 3 h after 400 kV/m EMP radiation. These changes vanished 24 h after exposure. Meanwhile, no significant spatial differences in BBB permeability were observed after EMP radiation. Moreover, Pearson’s correlation analysis showed that there was a significant positive linear relationship between BBB permeability and the electric field strength within an external electric field strength range of 0 to 400 kV/m at 3 h after EMP radiation. Conclusions: EMP radiation can induce a reversible increase in BBB permeability in rats. Moreover, no significant differences in BBB permeability were found across different brain regions. Additionally, the degree of BBB permeability was positively correlated with the regional electric field strength of EMP radiation within an external electric field strength range of 0 to 400 kV/m at 3 h after EMP radiation. These results indicate the promising potential of employing EMP for transient openings in the BBB, which could facilitate clinical pharmacological interventions via drug delivery into the brain.

OBJECTIVE:With the widespread utilization of S band (2 GHz ∼ 4 GHz) microwave (MW) in communication, its potential health risks have drawn significant attention. The purpose of this study was to investigate the impacts of acute 2.856 GHz MW exposure on recognition memory, its corresponding functional brain network, and the relationships between them in rats. METHODS:Novel object recognition (NOR) tests were conducted to examine the influence of 50 mW/cm2 acute 2.856 GHz MW on rat's recognition memory. Subsequently, resting state functional magnetic resonance imaging (rs-fMRI) was implemented to investigate the changes in the topological characteristics, long-range functional connectivity (FC), local FC assessed by regional homogeneity (ReHo), and fractional amplitude of low frequency fluctuation (fALFF) of rats' brain network related to recognition memory. Furthermore, the relationships between recognition memory and the potentially changed functional characteristics were investigated. RESULTS:Our findings revealed that the acute MW exposure induced recognition memory decline in rats. Though no significant alterations were detected in topological properties, long-range FCs, and fALFF within the brain network related to recognition memory, the local FCs of bilateral perirhinal cortex and right hippocampus in rats exhibited marginally significant increases following the MW exposure. Moreover, in the Sham group, the local FC of the left perirhinal cortex demonstrated a significantly positive linear correlation with recognition memory ability (p = 0.0193, r = 0.7182). However, this linear relationship was disrupted after the MW exposure. CONCLUSION:In conclusion, acute 2.856 GHz MW exposure can induce recognition memory impairments in rats. There is a positive linear relationship between recognition memory and the local FC of the left perirhinal cortex in normal rats. However, this relationship is disrupted after MW exposure, potentially due to maladaptive reorganization or failure of compensation within the brain region.

Terahertz (THz) waves, a novel type of radiation with quantum and electronic properties, have attracted increasing attention for their effects on the nervous system. Spatial working memory, a critical component of higher cognitive function, is coordinated by brain regions such as the infralimbic cortex (IL) region of the medial prefrontal cortex and the ventral cornu ammonis 1 (vCA1) of hippocampus. However, the regulatory effects of THz waves on spatial working memory and the underlying mechanisms remain unclear. In this study, the effects of 0.152 THz waves on glutamatergic neuronal activity and spatial working memory and the related mechanisms were investigated in cell, brain slice, and mouse models. Cellular experiments revealed that THz waves exposure for 60 min significantly increased the intrinsic excitability of primary hippocampal neurons, enhanced glutamatergic neuron activity, and upregulated the expression of molecules involved in glutamate metabolism. In brain slice experiments, THz waves markedly elevated neuronal activity, promoted synaptic plasticity, and increased glutamatergic synaptic transmission within the IL and vCA1 regions. Molecular dynamics simulations found that THz waves could inhibit the ion transport function of glutamate receptors. Moreover, Y-maze tests demonstrated that mice exposed to THz waves exhibited significantly improved spatial working memory. Multiomics analyses indicated that THz waves could induce changes in chromatin accessibility and increase the proportion of excitatory neurons. These findings suggested that exposure to 0.152 THz waves increased glutamatergic neuronal activity, promoted synaptic plasticity, and improved spatial working memory, potentially through modifications in chromatin accessibility and excitatory neuron proportions.

The mechanisms underlying the negative health effects of microwave exposure on male reproduction remain unclear. Thus, this study aimed to explore the role and regulatory mechanisms of ferroptosis in microwave-induced reproductive damage. The exposure of male C57 mice to 2.856 GHz of microwave radiation at 0, 10 and 20 mW/cm² for 30 min decreased sperm motility, induced morphological changes, damaged testicular tissue and mitochondrial morphology, increased malondialdehyde (MDA) contents and decreased the GSH/GSSG ratio. Simultaneously, the Fe²⁺ levels increased and SLC7A11 and GPX4 protein expressions decreased, causing oxidative stress. After 30 min of mouse spermatocyte (GC-2) irradiation, the cell viability of the Fer-1 inhibitor group and the GSH/GSSG ratio increased, while the reactive oxygen species, MDA and ferrous iron contents decreased. Furthermore, the depolarisation of membrane potential improved. Western blotting revealed that Nrf2, Keap1, SLC7A11, GPX4 and HO-1 expressions were down-regulated by microwave exposure and significantly up-regulated following the addition of the Fer-1 inhibitor. The results confirmed that the Nrf2 signalling pathway can regulate ferroptosis of oxidative stress. This study demonstrates that microwave exposure affects mouse reproductive function by enhancing oxidative stress, inducing ferroptosis by inhibiting the Nrf2 signalling pathway and reducing SLC7A11 and GPX4 protein expressions.

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 study aims to explore the new mechanism of human induced pluripotent stem cell-derived myocardial cells (iPSC-CMs) damage caused by microwave exposure, focusing on the changes in inflammatory factors, and to clarify the association between the dynamic sensing network and electrophysiological disorders. In this study, iPSC-CMs were exposed to 60 W/kg S-band microwaves for 30 min. The damage effects and mechanisms were investigated 1 h, 3 h, and 6 h after radiation. Using techniques such as flow cytometry, transmission electron microscopy, calcium transient, Olink proteomics, and immunofluorescence, the activity, ultrastructure, calcium signal changes, and expression of inflammatory factors of iPSC-CMs after microwave radiation were detected. Results: After microwave radiation, the activity of iPSC-CMs significantly decreased, the mitochondrial cristae were broken, the Ca2 + activation time and activation speed were abnormal, the amplitude of calcium transient changed significantly, and the action potential repolarization was abnormal. The dynamic changes of inflammatory factors were as follows: 1 h after microwave radiation, IL-6 drove acute inflammatory response, 3 h when the NF-κB pathway integrated inflammatory signals through IL-8, and 6 h after, CXCL11 dominated the repair program, and VEGFA expression rebounded to synergistically promote generation. Microwave radiation activated the classical NF-κB pathway and regulated the inflammatory balance. This study found that microwave radiation caused structural and functional damage to iPSC-CMs, and the temporal inflammatory regulation is a new mechanism of injury.

The effect of electromagnetic exposure on health is becoming increasingly important as it affects many aspects of human life and health. However, the effects in environmental electromagnetic fields on the male reproductive system were still controversial, and the impacts of long-term microwave exposure on testicular tissue remain poorly defined. This study exposed rats to 30 mW/cm2 of microwave radiation (2.856 GHz) for six weeks and revealed that long-term microwave exposure damaged the testis structures, sperm motility, and morphology, affected hormone levels, energy metabolism, and induced oxidative stress. Assays for bulk RNA, metabonomics, single-cell RNA, and transposase-accessible chromatin with high-throughput sequencing were performed to analyze the transcriptional and metabolic atlas of testicular damage after microwave radiation. Differentially expressed genes were enriched in oxidative stress and energy metabolism pathways. Furthermore, ten subgroups were identified with scRNA-seq, including five developmental phases of germ cells, and radiation-associated changes in cell composition, especially stuck in round spermatids, were observed. Radiation significantly upregulated the expression of Atp6v1e2 in round spermatids and enriched the expression of many transcription factors by disturbing the accessibility profile of chromatin. This study provides effective insights into the long-term impacts of microwave radiation on male reproduction.

Terahertz (THz) waves,also known as T-rays,encompass frequencies ranging from 0.1 to 10 THz and possess unique properties that render them applicable in various biomedical domains,particularly in neurobiology[1]. Synaptic transmission,the process through which signals propagate between neurons at synapses,is pivotal for brain function and information processing.

From the severe acute respiratory syndrome coronavirus in 2003 to the severe acute respiratory syndrome coronavirus 2 in 2019, coronavirus has seriously threatened human health. Electromagnetic waves not only own high penetration and low pollution but also can physically resonate with the virus. Several studies have demonstrated that electromagnetic waves can inactivate viruses efficiently. However, there is still a lack of systemic studies to analyze the potential factors closely associated with the effectiveness of inactivation, such as pH, temperature, and so on. In this study, we evaluated the inactivation ability of a 2.8 GHz microwave (MW) on MHV-A59, a substitute virus for coronavirus. Moreover, the influences of environmental pH and temperature on inactivation abilities were also discussed. The results showed that the viral morphology was destroyed, and the infectivity of MHV-A59 was significantly decreased after exposure to a 2.8 GHz MW at a density of 100 mW/cm2. Furthermore, alteration of pH 8 could produce synergistic effects with MW on virus inactivation. And, it was also proved that MWs could inactivate viruses better at room temperature than that under lower environmental temperatures. These results suggested that electromagnetic wave has great promise to become an effective tool to eliminate coronavirus.

Researches have shown that microwave radiation could cause oxidative stress injury in male reproductive system, and blueberry anthocyanins had excellent oxidation resistance. Our study aimed to investigate the protective effect of blueberry anthocyanins (100, 200 and 400 mg/kg/d) on testicular tissue damage in Wistar rats exposed to 2.856 GHz microwave and the optimal dose. We found that blueberry anthocyanins could ameliorate the decrease of sperm motility and sex hormone levels and testicular tissue structure damage caused by microwave radiation, increase SIRT1 expression and decrease FoxO1 expression, increase GSH/GSSG, SOD and inhibit MDA. The LDH, SDH and ATP synthase were increased, and Caspase-3 expression was decreased, and the high-dose of blueberry anthocyanins (400 mg/kg/d) had the best protective effect. These results suggested that blueberry anthocyanins could inhibit oxidative stress injury induced by 2.856 GHz microwave radiation in rat testicular tissue by regulating SIRT1/FoxO1 pathway, enhance energy metabolism and reduce cell apoptosis.