Dose-dependent Cardiac Dysfunction and Structural Damage in Rats after Shortwave Radiation / 生物医学与环境科学（英文）

Objective@#To detect the effects of shortwave radiation on dose-dependent cardiac structure and function in rats after radiation and to elucidate the mechanism of shortwave radiation induced cardiac injury to identify sensitive indicators and prophylactic treatment.@*Methods@#One hundred Wistar rats were either exposed to 27 MHz continuous shortwave at a power density of 5, 10, and 30 mW/cm for 6 min or undergone sham exposure for the control (the rats had to be placed in the exposure system with the same schedules as the exposed animals, but with an inactive antenna). The Ca , glutamic oxaloacetic transaminase (AST), creatine kinase (CK) and lactate dehydrogenase (LDH) content in the peripheral serum of the rats were detected by an automatic blood biochemical analyser. The electrocardiogram (ECG) of standard lead II was recorded by a multi-channel physiological recording and analysis system. The cardiac structure of rats was observed by light and electron microscopy.@*Results@#The results showed that the 5, 10, and 30 mW/cm shortwave radiation caused a significant increased in the levels of Ca , AST, CK, and LDH in the peripheral serum of rats. The cardiac structure was damaged by radiation and showed a disordered arrangement of myocardial fibres, the cavitation and swelling of myocardial mitochondria. These injuries were most significant 7 d after radiation and were not restored until 28 d after radiation.@*Conclusion@#Shortwave radiation of 5, 10, and 30 mW/cm can damage rat cardiac function, including damage to the tissue structure and ultrastructure, especially at the level of the myocardial fibres and mitochondria. Shortwave radiation at 5, 10, and 30 mW/cm induced damage to rat heart function and structure with a dose-effect relationship, i.e., the greater the radiation dose was, the more significant the damage was.

Behavioral Abnormality along with NMDAR-related CREB Suppression in Rat Hippocampus after Shortwave Exposure / 生物医学与环境科学（英文）

OBJECTIVE@#To estimate the detrimental effects of shortwave exposure on rat hippocampal structure and function and explore the underlying mechanisms.@*METHODS@#One hundred Wistar rats were randomly divided into four groups (25 rats per group) and exposed to 27 MHz continuous shortwave at a power density of 5, 10, or 30 mW/cm2 for 6 min once only or underwent sham exposure for the control. The spatial learning and memory, electroencephalogram (EEG), hippocampal structure and Nissl bodies were analysed. Furthermore, the expressions of N-methyl-D-aspartate receptor (NMDAR) subunits (NR1, NR2A, and NR2B), cAMP responsive element-binding protein (CREB) and phosphorylated CREB (p-CREB) in hippocampal tissue were analysed on 1, 7, and 14 days after exposure.@*RESULTS@#The rats in the 10 and 30 mW/cm2 groups had poor learning and memory, disrupted EEG oscillations, and injured hippocampal structures, including hippocampal neurons degeneration, mitochondria cavitation and blood capillaries swelling. The Nissl body content was also reduced in the exposure groups. Moreover, the hippocampal tissue in the 30 mW/cm2 group had increased expressions of NR2A and NR2B and decreased levels of CREB and p-CREB.@*CONCLUSION@#Shortwave exposure (27 MHz, with an average power density of 10 and 30 mW/cm2) impaired rats' spatial learning and memory and caused a series of dose-dependent pathophysiological changes. Moreover, NMDAR-related CREB pathway suppression might be involved in shortwave-induced structural and functional impairments in the rat hippocampus.

Real-time Microwave Exposure Induces Calcium Efflux in Primary Hippocampal Neurons and Primary Cardiomyocytes / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To detect the effects of microwave on calcium levels in primary hippocampal neurons and primary cardiomyocytes by the real-time microwave exposure combined with laser scanning confocal microscopy.</p><p><b>METHODS</b>The primary hippocampal neurons and primary cardiomyocytes were cultured and labeled with probes, including Fluo-4 AM, Mag-Fluo-AM, and Rhod-2, to reflect the levels of whole calcium [Ca2+], endoplasmic reticulum calcium [Ca2+]ER, and mitochondrial calcium [Ca2+]MIT, respectively. Then, the cells were exposed to a pulsed microwave of 2.856 GHz with specific absorption rate (SAR) values of 0, 4, and 40 W/kg for 6 min to observe the changes in calcium levels.</p><p><b>RESULTS</b>The results showed that the 4 and 40 W/kg microwave radiation caused a significant decrease in the levels of [Ca2+], [Ca2+]ER, and [Ca2+]MIT in primary hippocampal neurons. In the primary cardiomyocytes, only the 40 W/kg microwave radiation caused the decrease in the levels of [Ca2+], [Ca2+]ER, and [Ca2+]MIT. Primary hippocampal neurons were more sensitive to microwave exposure than primary cardiomyocytes. The mitochondria were more sensitive to microwave exposure than the endoplasmic reticulum.</p><p><b>CONCLUSION</b>The calcium efflux was occurred during microwave exposure in primary hippocampal neurons and primary cardiomyocytes. Additionally, neurons and mitochondria were sensitive cells and organelle respectively.</p>

Real-time Assessment of Cytosolic, Mitochondrial, and Nuclear Calcium Levels Change in Rat Pheochromocytoma Cells during Pulsed Microwave Exposure Using a Genetically Encoded Calcium Indicator / 生物医学与环境科学（英文）

Little information is available about the effects of exposure to pulsed microwaves on neuronal Ca2+ signaling under non-thermal conditions. In this study, rat pheochromocytoma (PC12) cells were exposed to pulsed microwaves for 6 min at a specific absorption rate (SAR) of 4 W/kg to assess possible real-time effects. During microwave exposure, free calcium dynamics in the cytosol, mitochondria, and nucleus of cells were monitored by time-lapse microfluorimetry using a genetically encoded calcium indicator (ratiometric-pericam, ratiometric-pericam-mt, and ratiometric-pericam-nu). We established a waveguide-based real-time microwave exposure system under accurately controlled environmental and dosimetric conditions and found no significant changes in the cytosolic, mitochondrial, or nuclear calcium levels in PC12 cells. These findings suggest that no dynamic changes occurred in [Ca2+]c, [Ca2+]m, or [Ca2+]n of PC12 cells at the non-thermal level.

Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To investigate microwave-induced morphological and functional injury of natural killer (NK) cells and uncover their mechanisms.</p><p><b>METHODS</b>NK-92 cells were exposed to 10, 30, and 50 mW/cm2 microwaves for 5 min. Ultrastructural changes, cellular apoptosis and cell cycle regulation were detected at 1 h and 24 h after exposure. Cytotoxic activity was assayed at 1 h after exposure, while perforin and NKG2D expression were detected at 1 h, 6 h, and 12 h after exposure. To clarify the mechanisms, phosphorylated ERK (p-ERK) was detected at 1 h after exposure. Moreover, microwave-induced cellular apoptosis and cell cycle regulation were analyzed after blockade of ERK signaling by using U0126.</p><p><b>RESULTS</b>Microwave-induced morphological and ultrastructural injury, dose-dependent apoptosis (P < 0.001) and cell cycle arrest (P < 0.001) were detected at 1 h after microwave exposure. Moreover, significant apoptosis was still detected at 24 h after 50 mW/cm2 microwave exposure (P < 0.01). In the 30 mW/cm2 microwave exposure model, microwaves impaired the cytotoxic activity of NK-92 cells at 1 h and down regulated perforin protein both at 1 h and 6 h after exposure (P < 0.05). Furthermore, p-ERK was down regulated at 1 h after exposure (P < 0.05), while ERK blockade significantly promoted microwave-induced apoptosis (P < 0.05) and downregulation of perforin (P < 0.01).</p><p><b>CONCLUSION</b>Microwave dose-dependently induced morphological and functional injury in NK-92 cells, possibly through ERK-mediated regulation of apoptosis and perforin expression.</p>

Effects of long-term microwave irradiation on NMDAR, BDNF and related molecular expression in their signal pathways in rat hippocampus / 军事医学

Objective To evaluate the effect of long-term microwave radiation on the expression of N-methyl-D-aspartate receptor(NMDAR),brain derived neurotrophic factor(BDNF) and related molecules in signal pathways in the hippocampus of rats.Methods Fifty male Wistar rats were exposed to microwave radiation at an average power density of 0,5,10,20 and 30 mW/cm2for 6 min/time,3 times/week,and for 6 weeks,which were sacrificed and the hippocampus was quickly removed at 14 d and 28 d after exposure.The changes in NMDAR (NR1,NR2A,NR2B),postsynaptic density protein(PSD)-95,cortactin,BDNF and tyrosine kinase receptor B (TrkB) in hippocampal neurons of each group were detected by Western blotting and image analysis techniques.Results Compared with the control group,the expressions of related proteins did not change significantly after microwave irradiation of 5 mW/cm2 at each time point.After 20 mW/cm2 microwave radiation,the expression of NR1 was increased at 14 and 28 d (P ＜0.05),the expression of NR2A was increased at 28 d (P ＜ 0.05),but the expression of NR2B was decreased at 14 and 28 d (P ＜ 0.05).At a average power density of 30 mW/cm2,the expressions of NR1,NR2A and PSD-95 and the expression of NR2B were decreased at 14 and 28 d(P ＜0.05),and cortactin,BDNF and TrkB were increased at 14 d after irradiation (P ＜ 0.05).Conclusion The effect of different dosages of long-term microwave radiation on the proteins of NMDAR and its signal pathway related molecules is different.Microwave radiation may affect the NMDAR of postsynaptic information transmission through the BDNF-TrkB signaling pathways,which might play an important role in the impediment of learning and memory function caused by microwave radiation.

1H-MRS and its application in study of microwave induced impairment of learning and memory: a review / 军事医学

The brain is the center of neurological functions.Learning and memory are the most basic and significant neurological functions.Previous studies demonstrated that microwave radiation could induce impairment of learning and memory.Proton magnetic resonance spectroscopy (1H-MRS) is a non-invasive and in vivo technique that can measure and analyze neurochemicals and their related metabolites,which can facilitate the investigation of the mechanism by which microwave radiation induces learning and memory impairment.In this paper,we reviewed the studies on microwave radiation induced learning and memory impairment,1H-MRS technique and its applications in learning and memory research,and the applications of 1 H-MRS in studies on learning and memory impairment induced by microwave radiation.

Heijiangdan ointment relieves oxidative stress from radiation dermatitis induced by (60)Co γ-ray in mice / 中国结合医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of Heijiangdan Ointment ( HJD) on oxidative stress in (60)Co γ-ray radiation-induced dermatitis in mice.</p><p><b>METHODS</b>Female Wistar mice with grade 4 radiation dermatitis induced by (60)Co γ-rays were randomly divided into four groups (n=12 per group); the HJD-treated, recombinant human epidermal growth factor (rhEGF)-treated, Trolox-treated, and untreated groups, along with a negative control group. On the 11th and 21st days after treatment, 6 mice in each group were chosen for evaluation. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), and lactate dehydrogenase (LDH) were detected using spectrophotometric methods. The fibroblast mitochondria were observed by transmission electron microscopy (TEM). The expressions of fibroblast growth factor 2 (FGF-2) and transforming growth factor β1 (TGF-β1) were analyzed by western blot.</p><p><b>RESULTS</b>Compared with the untreated group, the levels of SOD, MDA and LDH, on the 11th and 21st days after treatment showed significant difference (P<0.05). TEM analysis indicated that fibroblast mitochondria in the untreated group exhibited swelling and the cristae appeared fractured, while in the HJD group, the swelling of mitochondria was limited and the rough endoplasmic reticulum appeared more relaxed. The expressions of FGF-2 and TGF-β1 increased in the untreated group compared with the negative control group (P<0.05). After treatment, the expression of FGF-2, rhEGF and Trolox in the HJD group were significantly increased compared with the untreated group (P<0.05), or compared with the negative control group (P<0.05). The expression of TGF-β1 showed significant difference between untreated and negative control groups (P<0.05). HJD and Trolox increased the level of TGF-β1 and the difference was marked as compared with the untreated and negative control groups (P<0.05).</p><p><b>CONCLUSION</b>HJD relieves oxidative stress-induced injury, increases the antioxidant activity, mitigates the fibroblast mitochondrial damage, up-regulates the expression of growth factor, and promotes mitochondrial repair in mice.</p>

Pathological changes in the sinoatrial node tissues of rats caused by pulsed microwave exposure / 生物医学与环境科学（英文）

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.

Microwave exposure impairs synaptic plasticity in the rat hippocampus and PC12 cells through over-activation of the NMDA receptor signaling pathway / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>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.</p><p><b>METHODS</b>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.</p><p><b>RESULTS</b>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.</p><p><b>CONCLUSION</b>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.</p>

AduoLa Fuzhenglin down-regulates microwave-induced expression of β1-adrenergic receptor and muscarinic type 2 acetylcholine receptor in myocardial cells of rats / 生物医学与环境科学（英文）

This paper is aimed to study the effect of ADL on expression of β1-AR and M2-AchR in myocardial cells of rats exposed to microwave radiation. Immunohistochemistry, Western blot and image analysis were used to detect the expression of β1-AR and M2-AchR in myocardial cells at 7 and 14 d after microwave exposure. The results show that the expression level was higher in microwave exposure group and 0.75 g/(kg•d) ADL group than in sham operation group and significantly lower in 1.5 and 3.0 g/(kg•d) ADL groups than in microwave group. So we have a conclusion that the expression of β1-AR and M2-AchR is down-regulated in myocardial cells of rats exposed to microwave radiation. ADL can protect rats against microwave-induced heart tissue injury.

Microwave radiation induces injury to GC-2spd cells / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the impact of microwave radiation on GC-2spd cells.</p><p><b>METHODS</b>We exposed cultured GC-2spd cells to microwave radiation at the average power densities of 0, 10 and 30 mW/cm2 for 15 minutes and, from I to 24 hours after the exposure, we observed the changes in cell proliferation, histology and ultrastructure, cell apoptosis, and cAMP content by MTIT, light microscopy, electron microscopy, flow cytometry and ELISA.</p><p><b>RESULTS</b>Compared with the control group, the GC-2spd cells showed a significant decrease in proliferation ability at 1 -24 hours after 10 and 30 mW/cm2 microwave radiation, except at 12 hours after 30 mW/cm2 radiation (P <0.05 or P <0.01), with reduced length and number of cell enation and increased intra cytoplasm vacuoles. The rate of cell apoptosis (%) was significantly increased in the 10 and 30 mW/cm2 groups at 6 hours (4.56 +/- 2.09 vs 14.59 +/- 1.09 and 8.48 +/- 1.73, P <0.05 or P <0.01) , with agglutination and margin translocation of chromatins and obvious dilation of endo cytoplasmic reticula. The cAMP content (nmol/g) in the GC-2spd cells was remarkably reduced in the 10 and 30 mW/cm2 groups at 6 and 24 hours (2.77 +/-0.24 vs 1.65+/- 0. 17 and 1.96+/-0.10, 3.02 +/-0.47 vs 2.13 +/-0.33 and 1.69 +/-0.27, P <0.05 or P <0.01).</p><p><b>CONCLUSION</b>Microwave radiation at 10 and 30 mW/cm2 may cause injury to GC-2spd cells, which is manifested by decreased content of intracellular cAMP, reduced activity of cell proliferation, and increased rate of cell apoptosis.</p>

Changes in Ca(2+)concentration and caspase-3 expression and their relationship in Raji cells exposed to electromagnetic radiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the effects of electromagnetic pulse (EMP), S-band high power microwave (S-HPM), and X-band high power microwave (X-HPM) on the Ca(2+) concentration and caspase-3 expression in Raji cells and the relationship between Ca(2+) concentration and caspase-3 expression, and to investigate the regulatory mechanism of electromagnetic radiation damage.</p><p><b>METHODS</b>Raji cells were cultured conventionally. Some cells were irradiated by EMP, S-HPM, and X-HPM in the logarithmic growth phase for 6 hours and then collected; others received sham irradiation as a control. The Ca(2+) concentration in the cells was measured by laser scanning confocal microscope; the caspase-3 expression in the cells was evaluated by Western blot.</p><p><b>RESULTS</b>Compared with the control group (Ca(2+) fluorescence intensity = 43.08 ± 2.08; caspase-3 expression level = 0.444 ± 0.13), the EMP,S-HPM, and X-HPM groups had significantly increased Ca(2+) concentrations, with Ca(2+) fluorescence intensities of 69.56 ± 1.71, 50.06 ± 1.89, and 70.68 ± 1.59, respectively (P < 0.01), and had upregulated caspase-3 expression, with expression levels of 0.964 ± 0.12, 0.586 ± 0.16, and 0.970 ± 0.07, respectively (P < 0.01). Each of the EMP and X-HPM groups had significantly higher Ca(2+) fluorescence intensity and caspase-3 expression level than the S-HPM group (P < 0.01), but there were no significant differences between the EMP and X-HPM groups. The linear regression analysis showed that the caspase-3 expression was upregulated as the Ca(2+) concentration increased, with a positive correlation between them (P < 0.01).</p><p><b>CONCLUSION</b>EMP, S-HPM, and X-HPM cause damage probably by increasing the Ca(2+) concentration in cells and in turn inducing caspase-3 overexpression.</p>

Relationship between cognition function and hippocampus structure after long-term microwave exposure / 生物医学与环境科学（英文）

<p><b>OBJECTIVE</b>To analyze the effects of long-term microwave exposure on hippocampal structure and function in the rat.</p><p><b>METHODS</b>Experiments were performed on 184 male Wistar rats (three exposure groups and a sham group). Microwaves were applied daily for 6 min over 1 month at average power densities of 2.5, 5, and 10 mW/cm2. Learning and memory abilities were assessed by Morris water maze. High performance liquid chromatography was used to detect neurotransmitter concentrations in the hippocampus. Hippocampal structures were observed by histopathological analysis.</p><p><b>RESULTS</b>Following long-term microwave exposure there was a significant decrease in learning and memory activity in the 7 d, 14 d, and 1 m in all three microwave exposure groups. Neurotransmitter concentrations of four amino acids (glutamate, aspartic acid, glycine, and gamma-aminobutyric acid) in hippocampus were increased in the 2.5 and 5 mW/cm2 groups and decreased in the 10 mW/cm2 group. There was evidence of neuronal degeneration and enlarged perivascular spaces in the hippocampus in the microwave exposure groups. Further, mitochondria became swollen and cristae were disordered. The rough endoplasmic reticulum exhibited sacculated distension and there was a decrease in the quantity of synaptic vesicles.</p><p><b>CONCLUSION</b>These data suggest that the hippocampus can be injured by long-term microwave exposure, which might result in impairment of cognitive function due to neurotransmitter disruption.</p>

The protective effects of Aduola Fuzhenglin on the heart injury induced by microwave exposure in rats / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To study the protective effects of AduoLa Fuzhenglin(ADL) on the heart injury induced by microwave exposure in rats.</p><p><b>METHODS</b>One hundred forty male Wistar rats were divided randomly into 5 groups: control, microwave radiation, 0.75 g x kg(-1) d(-1) ADL, 1.50 g x kg(-1) d(-1) ADL and 3.00 g x kg(-1) d(-1) ADL pretreatment groups. Rats in three ADL pretreatment groups were administrated by ADL per day for 2w then exposed to 30 mW/cm2 microwaves for 15 min. The left ventricle blood of rats was obtained at 7 d and 14 d after exposure to microwaves, and the blood Ca2+, AST and CK were detected with Coulter automatic biochemical analyzer, then the histological changes and ultrastructure of heart were observed under light and electron microscopes.</p><p><b>RESULTS</b>At 7 d and 14 d after exposure to microwaves, the blood Ca2+, AST and CK concentrations significantly increased (P<0.05 or P<0.01) as compared with controls; Heart muscle fibers showed wavilness, endotheliocyte karyopyknosis, anachromasis; The mitochondria swelling and cavitation, intercalary dies blurred in radiation groups. The changes in 0.75 g x kg(-1) d(-1) ADL pretreatment group were similar to the radiation group, but in 1.50 g x kg(-1)d(-1) and 3.00 g x kg(-1) d(-1) ADL pretreatment groups, above indexes of rats significantly reduced as compared with microwaves group (P<0.05); also the blood Ca2+, AST, CK contents were significantly lower than those in microwave group (P<0.05); The heart showed a tendency to improve.</p><p><b>CONCLUSION</b>Microwave radiation (30 mW/cm2) can cause the blood Ca2+, AST and CK turbulence, and heart injury in the histology and ultrastructure; ADL at the dosages of 1.50 g x kg(-1) d(-1) and 3.00 g x kg(-1) d(-1) has a protective effects on the heart injury induced by microwave in rats.</p>

Long-term microwave radiation affects male reproduction in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the effect of long-term microwave radiation on male reproduction in rats.</p><p><b>METHODS</b>A total of 100 male Wistar rats were exposed to microwave radiation with average power density of 0, 2.5, 5 and 10 mW/cm2 for 4 weeks, 5 times a week and 6 minutes per time. Changes in serum testosterone, testicular index, histology and ultrastructure, and the percentage of teratospermia in the epididymis were observed dynamically at 6 h, 7 d, 14 d, 28 d and 60 d after the exposure.</p><p><b>RESULTS</b>There was a significant decrease in serum testosterone concentration at 28 d after microwave radiation at 2.5, 5 and 10 mW/cm2 ([10.20 +/- 4.31] ng/ml, [5.56 +/- 3.47] ng/ml and [7.53 +/- 4.54] ng/ml) and at 60 d at 10 mW/cm2 ( [15.95 +/- 9.54] ng/ml), as compared with the control group ([23.35 +/- 8.06] ng/ml and [31.40 +/- 9.56] ng/ml) (P < 0.05 or P < 0.01). No significant changes were found in the testis index at 6 h -60 d after microwave radiation at the three doses, but different degrees of degeneration, necrosis and shedding of spermatogenic cells, thinning of spermatogenic epithelia, and decrease or deletion of spermatozoa were observed, and more obvious at 28 d and 60 d. Swelling and cavitation of mitochondria in all spermatogenic cells, agglutination and margin translocation of nuclear chromatin in the spermatogonial and Leydig cells were seen at 7 d and 60 d after 5 mW/cm2 microwave radiation. The rate of teratospermia of the epididymis was increased, more obviously at 7 d after 2.5, 5 mW/cm2, 60 d after 5 mW/cm2, and 7 d, 28 d and 60 d after 10 mW/cm2 microwave radiation (P < 0.05 or P < 0.01).</p><p><b>CONCLUSION</b>Long-term microwave radiation may cause injury to male reproduction, which is positively correlated with the radiation dose, and has an obvious late effect.</p>

Microwave radiation decreases the expressions of occludin and JAM-1 in rats / 中华男科学杂志

<p><b>OBJECTIVE</b>To explore the changes in the expressions of the tight junction related protein occludin and junctional adhesion molecule-1 (JAM-1) of the blood-testis barrier and their significance in rats after microwave radiation.</p><p><b>METHODS</b>Eighty male Wistar rats were exposed to microwave radiation with average power density of 0, 10, 30 and 100 mW/cm2 for five minutes, and dynamic changes in the expressions of testicular occludin and JAM-1 were observed by Western blot and image analysis at 6 h, 1 d, 3 d, 7 d and 14 d after the radiation.</p><p><b>RESULTS</b>There was a significant down-regulation in the expression of the occludin protein at 3 - 7 d, 6 h - 7 d and 6 h - 14 d (P < 0. 05), as well as in that of JAM-1 at 3 - 7 d, 1 - 7 d and 1-14 d (P < 0.05) after exposure to 10, 30 and 100 mW/cm2 microwave radiation.</p><p><b>CONCLUSION</b>The decreased protein expressions of occludin and JAM-1 may play an important role in the microwave radiation induced-damage to the blood-testis barrier.</p>

A aquaporin 4 expression and effects in rat hippocampus after microwave radiation / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To investigate the expression of aquaporin 4 (AQP4) after microwave exposure and the correlation with the brain injury by radiation.</p><p><b>METHODS</b>70 male rats were exposed to microwave whose average power density was 0, 10, 30 and 100 mW/cm(2) respectively. Rats were sacrificed at 6 h, 1 d, 3 d and 7 d after exposure. Immunohistochemistry and Western blot were used to detect the expression of AQP4 in protein level in rat hippocampus, and the expression of AQP4 in gene level was measured by in situ hybridization and RT-PCR.</p><p><b>RESULTS</b>The expression of AQP4 in rat hippocampus was abnormal after 10, 30, 100 mW/cm(2) microwave exposure. The protein level showed increased at first and then recovered at 10 and 30 mW/cm(2) groups, while increased progressively in 100 mW/cm(2) group within 14 d (P < 0.01). The gene expression of AQP4 was increased (0.51 +/- 0.02) at the beginning (6 h) and then regained after 10 mW/cm(2) microwave exposure, while in 30 and 100 mW/cm(2) groups, it rose to the peak at 7 d (0.46 +/- 0.02 and 0.43 +/- 0.08) and didn't get back (P = 0.004; P = 0.012).</p><p><b>CONCLUSION</b>Microwave radiation can increase the expression of AQP4 in rat hippocampus. The change might participate in the process of increasing permeability of blood-brain barrier and lead to the brain edema after microwave radiation.</p>

Effect of microwave radiation on primary cultured Sertoli cells / 中华劳动卫生职业病杂志

<p><b>OBJECTIVE</b>To explore whether microwave radiation may cause injury of primary cultured Sertoli cells.</p><p><b>METHODS</b>The model of primary cultured Sertoli cells in vitro was established, which was radiated by microwave with average power density 0, 30 and 100 mW/cm(2) for five minutes. The changes of cell cycle, apoptosis and death, and intracellular Ca2+ concentration in the Sertoli cells were measured at sixth hours through Annexin V-PI double labeling and Fluo-3-AM labeling, flow cytometry combined with laser scanning confocal microscopy after microwave exposure.</p><p><b>RESULTS</b>The numbers of Sertoli cells were obviously reduced in G0-G1 and G2-M phase (62.57% +/- 3.22% and 8.25% +/- 1.75%) and increased in S phase (29.17% +/- 4.87%) compared with the control groups (79.18% +/- 0.24%, 11.17% +/- 0.50% and 9.64% +/- 0.62%) (P < 0.05 or P < 0.01), but the changes of rate of apoptosis and death and intracellular Ca2+ concentration showed no difference at 6 h after exposure to 30 mW/cm(2) microwave. There was a significant increase in the Sertoli cell counts of G0-G1 phase (87.69% +/- 1.32%), and decrease in the Sertoli cell counts of G2-M and S phase (7.41% +/- 0.60% and 4.87% +/- 0.91%) (P < 0.01). There was also a significant increase in intracellular Ca2+ concentration and rate of apoptosis and death (P < 0.05 or P < 0.01) at 6 h after exposure to 100 mW/cm(2) microwave.</p><p><b>CONCLUSION</b>100 mW/cm(2) microwave radiation may cause growth inhibition and increase of apoptosis and death in the primary cultured Sertoli cells. The increase of intracellular Ca2+ concentration is one of the injury mechanisms.</p>

Effects of electromagnetic radiation on RAF/MEK/ERK signaling pathway in rats hippocampus / 中国应用生理学杂志

<p><b>AIM</b>To study the development of changes for signaling molecules related to Raf/MEK/ERK pathway in hippocampus of rats after electromagnetic radiation, and investigate the mechanisms of radiation injury.</p><p><b>METHODS</b>Rats were exposed to X-HPM, S-HPM and EMP radiation source respectively, and animal model of electromagnetic radiation was established. Western blot was used to detect the expression of Raf-1, phosphorylated Raf-1 and phospholylated ERK.</p><p><b>RESULTS</b>The expression of Raf-1 down-regulated during 6 h-14 d after radiation, most significantly at 7 d, and recovered at 28 d. There was no significant difference between the radiation groups. The expression of phosphorylated Raf-1 and phosphorylated ERK both up-regulated at 6 h and 7 d after radiation, more significantly at 6 h, and the two microwave groups were more serious for phosphorylated ERK. During 6 h-14 d after S-HPM radiation, the expression of phosphorylated Raf-1 increased continuously, but phosphorylated ERK changed wavily, 6 h and 7 d were expression peak.</p><p><b>CONCLUSION</b>Raf/MEK/ERK signaling pathway participates in the hippocampus injury induced by electromagnetic radiation. The excessive activation of ERK pathway may result in the apoptosis and death of neurons, which is the important mechanism of recognition disfunction caused by electromagnetic radiation.</p>