ICES Database
ElectroMagnetic Field Literature
Search Engine
  

EMF Study
(Database last updated on Mar 27, 2024)

ID Number 2131
Study Type In Vivo
Model RF exposure (1500, 2450, 2856 and 4300 MHz) exposure to rats and analysis of protein expression and morphology in the brain and heart, transcriptome sequencing of RNA in brain tissue, spatial memory, cognition, EEG, neural cell apoptosis and sperm apoptosis.
Details

Wistar rats 9n = 25) were exposed to 2450 MHz RF at 14.1 W/kg (whole body average) for 5 minutes and evaluated for brain pathology at 6 hr, 1, 3, and 7 days post-exposure. The authors report a decrease in synapsin I protein at 3 days post exposure as determined by Western blot and a decrease in VAMP-2 and syntaxin binding from coimmunoprecipitation from synaptosome preparations of the cerebral cortex. VAMP-2 protein levels were decreased at 1 and 3 days, and syntaxin levels were decreased at 6 hr, 1 day, and 3 days post-exposure in both the cerebral cortex and hippocampus. VAMP-2 and syntaxin binding was increased at 1 day post-exposure in the hippocampus and then decreased at 3 days and increased again at 7 days post exposure. Synaptophysin protein levels were increased at all measured timepoints post-exposure. The authors conclude RF exposure can alter the nature of synaptic vesicle associated proteins. AUTHORS' ABSTRACT: Wang et al. 2013 (IEEE #5287): Purpose: To assess the impact of microwave exposure on learning and memory and to explore the underlying mechanisms. Materials and methods: 100 Wistar rats were exposed to a 2.856 GHz pulsed microwave field at average power densities of 0 mW/cm2, 5 mW/cm2, 10 mW/cm2 and 50 mW/cm2 for 6 min. The spatial memory was assessed by the Morris Water Maze (MWM) task. An in vivo study was conducted soon after microwave exposure to evaluate the changes of population spike (PS) amplitudes of long-term potentiation (LTP) in the medial perforant path (MPP)-dentate gyrus (DG) pathway. The structure of the hippocampus was observed by the light microscopy and the transmission electron microscopy (TEM) at 7 d after microwave exposure. Results: Our results showed that the rats exposed in 10 mW/cm2 and 50 mW/cm2 microwave displayed significant deficits in spatial learning and memory at 6 h, 1 d and 3 d after exposure. Decreased PS amplitudes were also found after 10 mW/cm2 and 50 mW/cm2 microwave exposure. In addition, varying degrees of degeneration of hippocampal neurons, decreased synaptic vesicles and blurred synaptic clefts were observed in the rats exposed in 10 mW/cm2 and 50 mW/cm2 microwave. Compared with the sham group, the rats exposed in 5 mW/cm2 microwave showed no difference in the above experiments. Conclusions: This study suggested that impairment of LTP induction and the damages of hippocampal structure, especially changes of synapses, might contribute to cognitive impairment after microwave exposure. AUTHORS' ABSTRACT: Qiao et al 2014 (IEEE #5719): Background: Abnormal release of neurotransmitters after microwave exposure can cause learning and memory deficits. This study investigated the mechanism of this effect by exploring the potential role of phosphorylated synapsin I (p-Syn I). Methods: Wistar rats, rat hippocampal synaptosomes, and differentiated (neuronal) PC12 cells were exposed to microwave radiation for 5 min at a mean power density of 30 mW/cm2. Sham group rats, synaptosomes, and cells were otherwise identically treated and acted as controls for all of the following post-exposure analyses. Spatial learning and memory in rats was assessed using the Morris Water Maze (MWM) navigation task. The protein expression and presynaptic distribution of p-Syn I and neurotransmitter transporters were examined via western blotting and immunoelectron microscopy, respectively. Levels amino acid neurotransmitter release from rat hippocampal synaptosomes and PC12 cells were measured using high performance liquid chromatograph (HPLC) at 6 hours after exposure, with or without synapsin I silencing via shRNA transfection. Results: In the rat experiments, there was a decrease in spatial memory performance after microwave exposure. The expression of p-Syn I (ser-553) was decreased at 3 days post-exposure and elevated at later time points. Vesicular GABA transporter (VGAT) was significantly elevated after exposure. The GABA release from synaptosomes was attenuated and p-Syn I (ser-553) and VGAT were both enriched in small clear synaptic vesicles, which abnormally assembled in the presynaptic terminal after exposure. In the PC12 cell experiments, the expression of p-Syn I (ser-553) and GABA release were both attenuated at 6 hours after exposure. Both microwave exposure and p-Syn I silencing reduced GABA release and maximal reduction was found for the combination of the two, indicating a synergetic effect. Conclusion: p-Syn I (ser-553) was found to play a key role in the impaired GABA release and cognitive dysfunction that was induced by microwave exposure. AUTHORS' ABSTRACT: Zuo et al. 2014 (IEEE #5732): To determine whether microwave (MW) radiation induces neural cell apoptosis, differentiated PC12 cells and Wistar rats were exposed to 2.856GHz for 5min and 15min, respectively, at an average power density of 30 mW/cm2. JC-1 and TUNEL staining detected significant apoptotic events, such as the loss of mitochondria membrane potential and DNA fragmentation, respectively. Transmission electron microscopy and Hoechst staining were used to observe chromatin ultrastructure and apoptotic body formation. Annexin V-FITC/PI double staining was used to quantify the level of apoptosis. The expressions of Bax, Bcl-2, cytochrome c, cleaved caspase-3 and PARP were examined by immunoblotting or immunocytochemistry. Caspase-3 activity was measured using an enzyme-linked immunosorbent assay. The results showed chromatin condensation and apoptotic body formation in neural cells 6h after microwave exposure. Moreover, the mitochondria membrane potential decreased, DNA fragmentation increased, leading to an increase in the apoptotic cell percentage. Furthermore, the ratio of Bax/Bcl-2, expression of cytochrome c, cleaved caspase-3 and PARP all increased. In conclusion, microwave radiation induced neural cell apoptosis via the classical mitochondria-dependent caspase-3 pathway. This study may provide the experimental basis for further investigation of the mechanism of the neurological effects induced by microwave radiation. AUTHORS' ABSTRACT: Li et al. 2015 (IEEE #4845): The increased use of microwaves raises concerns about its impact on health including cognitive function in which neurotransmitter system plays an important role. In this study, we focused on the serotonin system and evaluated the long term effects of chronic microwave radiation on cognition and correlated items. Wistar rats were exposed or sham exposed to 2.856 GHz microwaves with the average power density of 5, 10, 20 or 30 mW/cm2 respectively for 6 min three times a week up to 6 weeks. At different time points after the last exposure, spatial learning and memory function, morphology structure of the hippocampus, electroencephalogram (EEG) and neurotransmitter content (amino acid and monoamine) of rats were tested. Above results raised our interest in serotonin system. Tryptophan hydroxylase 1 (TPH1) and monoamine oxidase (MAO), two important rate-limiting enzymes in serotonin synthesis and metabolic process respectively, were detected. Expressions of serotonin receptors including 5-HT1A, 2A, 2C receptors were measured. We demonstrated that chronic exposure to microwave (2.856 GHz, with the average power density of 5, 10, 20 and 30 mW/cm2) could induce dose-dependent deficit of spatial learning and memory in rats accompanied with inhibition of brain electrical activity, the degeneration of hippocampus neurons, and the disturbance of neurotransmitters, among which the increase of 5-HT occurred as the main long-term change that the decrease of its metabolism partly contributed to. Besides, the variations of 5-HT1AR and 5-HT2CR expressions were also indicated. The results suggested that in the long-term way, chronic microwave exposure could induce cognitive deficit and 5-HT system may be involved in it. AUTHORS' ABSTRACT: Xiong et al. 2015 (IEEE (5929): Objective The aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment. Methods 48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated. Results Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined. Conclusion 30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity. AUTHORS' ABSTRACT: Liu et al. 2015 (IEEE #5945): To observe microwave induced dynamic pathological changes in the sinus nodes, wistar rats were exposed to 0, 5, 10, 50 mW/cm2 microwave. In 10 and 50 mW/cm2 groups, disorganized sinoatrial node cells, cell swelling, cytoplasmic condensation, nuclear pyknosis, and anachromasis, swollen, and empty mitochondria, and blurred and focally dissolved myofibrils could be detected from 1 to 28 d, while reduced parenchymal cells, increased collagen fibers, and extracellular matrix remodeling of interstitial cells were observed from 6 to 12 months. In conclusion, 10 and 50 mW/cm2 microwave could cause structural damages in the sinoatrial node and extracellular matrix remodeling in rats. AUTHORS' ABSTRACT: Wang et al. 2017 (IEEE 6828): OBJECTIVE: The long term effects of continuous microwave exposure cannot be ignored for the simulation of the real environment and increasing concerns about the negative cognitive effects of microwave exposure. METHODS: In this study, 220 male Wistar rats were exposed by a 2.856GHz radiation source with the average power density of 0, 2.5, 5 and 10mW/cm2 for 6min/day, 5days/week and up to 6weeks. The MWM task, the EEG analysis, the hippocampus structure observation and the western blot were applied until the 12months after microwave exposure to detect the spatial learning and memory abilities, the cortical electrical activity, changes of hippocampal structure and the NMDAR subunits expressions. RESULTS: Results found that the rats in the 10mW/cm2 group showed the decline of spatial learning and memory abilities and EEG disorders (the decrease of EEG frequencies, and increase of EEG amplitudes and delta wave powers). Moreover, changes of basic structure and ultrastructure of hippocampus also found in the 10 and 5mW/cm2 groups. The decrease of NR 2A, 2B and p-NR2B might contribute to the impairment of cognitive functions. CONCLUSIONS: Our findings suggested that the continuous microwave exposure could cause the dose-dependent long term impairment of spatial learning and memory, the abnormalities of EEG and the hippocampal structure injuries. The decrease of NMDAR key subunits and phosphorylation of NR 2B might contribute to the cognitive impairment. AUTHORS' ABSTRACT: Wu et al. 2017 (IEEE #6829): Microwave radiation could increase the expression of pro-inflammatory cytokines in rat Sertoli cells, which may impair spermatogenesis. However, the mechanisms that microwave radiation induces the cytokine expression in Sertoli cells remain to be clarified. The activation of TLRs by their ligands can trigger a common signalling pathway to upregulate inflammatory cytokines such as IL-1, IL-6, IL-12 and TNF-±. Microwave radiation can increase the expression of TLRs in lymphocytes. The purpose of this study was to determine the effect of microwave radiation on the TLRs in rat testis. We focus on the effect of TLR2-5 (which is expressed relatively highly) by microwave radiation. The results showed that the expression of TLR2-5 and the pro-inflammatory cytokines (IL-1², IL-6 and TNF-±) was increased both in mRNA and in protein. Furthermore, p-p38, p-ERK1/2, p-JNK and p-NF-ºB p65, the key factors of TLR signalling, were also elevated by microwave exposure. And the NF-ºB can be induced more dominantly. These results suggest that TLRs signalling can be activated by microwave radiation in testis, which may provide the molecular basis for the in-depth study. AUTHORS' ABSTRACT: Tan et al. 2017 (IEEE #6835): Many studies have revealed the cognitive decline induced by microwave radiation. However, the systematic study on dose-dependent, frequency-dependent and accumulative effects of microwave exposure at different frequencies was lacking. Here, we studied the relationship between the effects and the power and frequency of microwave and analyzed the accumulative effects of two different frequency microwaves with the same average power density. After microwave radiation, declines in spatial learning and memory and fluctuations of brain electric activities were found in the 10 mW/cm2 single frequency exposure groups and accumulative exposure groups. Meanwhile, morphological evidences in hippocampus also supported the cognitive dysfunction. Moreover, the decrease of Nissl contents in neurons indicated protein-based metabolic disorders in neurons. By detecting the key functional proteins of cholinergic transmitter metabolism, cytokines, energy metabolism and oxidative stress in the hippocampus, we found that microwave could lead to multiple metabolic disorders. Our results showed that microwave-induced cognitive decline was largely determined by its power rather than frequency. Injury effects were also found in accumulative exposure groups. We particularly concerned about the safety dose, injury effects and accumulative effects of microwaves, which might be very valuable in the future.The popularization of microwave raised concerns about its influence on health including cognitive function which is associated greatly with dendritic spines plasticity. SNK-SPAR is a molecular pathway for neuronal homeostatic plasticity during chronically elevated activity. In this study, Wistar rats were exposed to microwaves (30/mW/cm2 for 6/min, 3 times/week for 6/weeks). Spatial learning and memory function, distribution of dendritic spines, ultrastructure of the neurons and their dendritic spines in hippocampus as well as the related critical molecules of SNK-SPAR pathway were examined at different time points after microwave exposure. There was deficiency in spatial learning and memory in rats, loss of spines in granule cells and shrinkage of mature spines in pyramidal cells, accompanied with alteration of ultrastructure of hippocampus neurons. After exposure to 30/mW/cm2 microwave radiation, the up-regulated SNK induced decrease of SPAR and PSD-95, which was thought to cause the changes mentioned above. In conclusion, the microwave radiation led to shrinkage and even loss of dendritic spines in hippocampus by SNK-SPAR pathway, resulting in the cognitive impairments. AUTHORS' ABSTRACT: Zhi et al. 2018 (IEEE #7139):

Findings Effects
Status Completed With Publication
Principal Investigator Beijing Institute of Radiation Medicine, China
Funding Agency China National Natural Sc Found
Country CHINA
References
  • Wang, L et al. Synapse, (2009) 63:1010-1016
  • Wang, H et al. Int J Radiat Biol., (2013) 89:1100-1107
  • Qiao, S et al. PLOS ONE., (2014) 9(4): e95503.:-(9 pages)
  • Zuo, H et al. International Journal of Medical Sciences., (2014) 11:426-435
  • Li, HJ et al. Physiology & Behavior., (2015) 140:236-246
  • Xiong, L et al. Biomed Environ Sci., (2015) 28:13-24
  • Liu, YQ et al. Biomed Environ Sci, (2015) 28:72-75
  • Wang, H et al. Physiol Behav., (2017) :-
  • Wu, H et al. Andrologia., (2017) :-
  • Tan, S et al. Scientific Reports., (2017) 7:10781-
  • Zhi, WJ et al. Brain Res., (2018) 1679:134-143
  • Zhi, WJ et al. Mil Med Res., (2017) 4:29-(14 pages)
  • Zhao, L et al. Environmental Science and Pollution Research. , (2020) 27:40787-40794
  • Liu, Q et al. Reproductive Health., (2015) 12:Article number 65-
  • Lai, YF et al. Mil Med Res., (2021) 8:12-
  • Zhu, R et al. Scientific Reports., (2021) 11:10061-doi.org/10.1038/s41598-021-89348-4
  • Tan, S et al. Scientific Reports., (2021) 11:12348-doi.org/10.1038/s41598-021-91622-4
  • Yin, Y et al. J Immunol Res., (2021) 2021:3985697-
  • Li, H et al. Front Public Health. , (2022) 10:802386-
  • Zhao, L et al. Biomed. Environ. Sci., (2017) 30:323-332
  • Zhao, L et al. Int. J. Mol. Sci., (2022) 23:6949-
  • Xia, Z et al. ACS Chem. Neurosci., (2021) 12:2122-2132
  • Hao, Y et al. Physiol. Behav., (2018) 188:119-127
  • Zhao, L et al. Biomed. Environ. Sci., (2012) 25:182-188
  • Li, D et al. Oxid Med Cell Longev., (2022) :7145415-
  • Zhu, RQ et al. Biomed Environ Sci., (2022) 35:1079-1084
  • Wang, H et al. Environ Sci Pollut Res., (2022) :1-13
  • Zhao, L et al. Biomed Environ Sci., (2012) 25:182-188
  • Hao, YH et al. Mil Med Res., (2015) 2:4-
  • Hu, C et al. Front Public Health., (2021) 9:691880-
  • Comments

    Return