Shortwave radiation-induced reproductive organ damage in male rats by enhanced expression of molecules associated with the calpain/Cdk5 pathway and oxidative stress.

Shortwave radiation has been reported to have harmful effects on several organs in humans and animals. However, the biological effects of 27 MHz shortwave on the reproductive system are not clear. In this study, we investigated the effects of shortwave whole-body exposure at a frequency of 27 MHz on structural and functional changes in the testis. Male Wistar rats were exposed to 27 MHz continuous shortwaves at average power densities of 0, 5, 10, or 30 mW/cm2 for 6 min. The levels of insulin-like factor 3 (INSL3) and anti-sperm antibodies (AsAb) in the peripheral serum, sperm motility, sperm malformation rate, and testicular tissue structure of rats were analyzed. Furthermore, the activity of superoxide dismutase (SOD), catalase (CAT), malondialdehyde (MDA) content, calpain, and Cdk5 expression were analyzed at 1, 7, 14, and 28 days after exposure. We observed that the rats after radiation had decreased serum INSL3 levels (p < 0.01), increased AsAb levels (p < 0.05), decreased percentage of class A+B sperm (p < 0.01 or p < 0.05), increased sperm malformation (p < 0.01 or p < 0.05), injured testicular tissue structure, decreased SOD and CAT activities (p < 0.01 or p < 0.05), increased MDA content (p < 0.01), and testicular tissue expressions of calpain1, calpain2, and Cdk5 were increased (p < 0.01 or p < 0.05). In conclusion, Shortwave radiation caused functional and structural damage to the reproductive organs of male rats. Furthermore, oxidative stress and key molecules in the calpain/Cdk5 pathway are likely involved in this process.

Shortwave radiation has been used in communications, medical and military applications, and its damaging effects on several organs of the human body have been reported in the literature. However, the biological effects of shortwave radiation on the male reproductive system are unknown. The present study, by constructing an animal model of short-wave radiation and analyzing the experimental results, revealed that shortwave radiation could cause functional and structural damage to the reproductive organs of male rats, and that oxidative stress and key molecules in the calpain/Cdk5 pathway might be involved in this process. It will provide organizational data for further studies on the mechanisms of male reproductive damage by shortwave radiation.

Microwave-Induced Structural and Functional Injury of Hippocampal and PC12 Cells Is Accompanied by Abnormal Changes in the NMDAR-PSD95-CaMKII Pathway.

Recent studies have highlighted the important role of the postsynaptic NMDAR-PSD95-CaMKII pathway for synaptic transmission and related neuronal injury. Here, we tested changes in the components of this pathway upon microwave-induced neuronal structure and function impairments. Ultrastructural and functional changes were induced in hippocampal neurons of rats and in PC12 cells exposed to microwave radiation. We detected abnormal protein and mRNA expression, as well as posttranslational modifications in the NMDAR-PSD95-CaMKII pathway and its associated components, such as synapsin I, following microwave radiation exposure of rats and PC12 cells. Thus, microwave radiation may induce neuronal injury via changes in the molecular organization of postsynaptic density and modulation of the biochemical cascade that potentiates synaptic transmission.

The protective role of interleukin-11 against neutron radiation injury in mouse intestines via MEK/ERK and PI3K/Akt dependent pathways.

BACKGROUND: Neutron irradiation (IR) has been proven to cause more serious damage than gamma IR. Preventing and curing neutron IR damage remains an urgent issue. AIMS: The objective of this study was to investigate the radioprotective effects of IL-11 against neutron IR-induced damage in small intestine of mice. METHODS: Mice were exposed to 3-Gy neutron IR whole body and then treated with 500 µg/kg interleukin-11 (IL-11) intraperitoneally every day. Mice were observed at various time-points over 1-5 days after IR. IEC-6 cells were exposed to 4 Gy neutron IR, and 100 ng/mL rhIL-11 was added to culture medium. Cell proliferation activity was estimated by MTT assay and rates of apoptosis were estimated by flow cytometry. RESULTS: IL-11 slightly alleviated the incidence of diarrhea in the mice and promoted intestinal epithelia regeneration. In the in vitro study, neutron IR activated extracellular signal-regulated kinase (ERK)1/2 phosphorylation in intestinal epithelial cells constitutively, which was initially suppressed and then activated later by IL-11. The MEK-specific inhibitor U0126 could antagonize the positive effect of IL-11 on cell growth. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway activation was suppressed after neutron IR, but could be triggered by IL-11 to protect the cells. The PI3K inhibitor LY294002 suppressed the positive effect of IL-11 on cell growth, and antagonized the protective effect of IL-11 against cell death after neutron IR. CONCLUSION: IL-11 increases cell proliferation after neutron IR in MEK and PI3K-dependent signaling pathways, but protects cells against death only in the PI3K-dependent signaling pathway.

Neural cell apoptosis induced by microwave exposure through mitochondria-dependent caspase-3 pathway.

To determine whether microwave (MW) radiation induces neural cell apoptosis, differentiated PC12 cells and Wistar rats were exposed to 2.856 GHz for 5 min and 15 min, 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.

L-arginine attenuates Streptococcus uberis-induced inflammation by decreasing miR155 level.

L-arginine, as an essential substance of the immune system, plays a vital role in innate immunity. MiR155, a multi-functional microRNA, has gained importance as a regulator of homeostasis in immune cells. However, the immunoregulatory mechanism between L-arginine and miR155 in bacterial infections is unknown. Here, we investigated the potential role of miR155 in inflammation and the molecular regulatory mechanisms of L-arginine in Streptococcus uberis (S. uberis) infections. And we observed that miR155 was up-regulated after infection, accompanying the depletion of L-arginine, leading to metabolic disorders of amino acids and severe tissue damage. Mechanically, the upregulated miR155 mediated by the p65 protein played a pro-inflammatory role by suppressing the suppressor of cytokine signaling 6 (SOCS6)-mediated p65 ubiquitination and degradation. This culminated in a violently inflammatory response and tissue damage. Interestingly, a significant anti-inflammatory effect was revealed in L-arginine supplementation by reducing miR155 production via inhibiting p65. This work firstly uncovers the pro-inflammatory role of miR155 and an anti-inflammatory mechanism of L-arginine in S.uberis infection with a mouse mastitis model. Collectively, we provide new insights and strategies for the prevention and control of this important pathogen, which is of great significance for ensuring human food health and safety.

Rhabdomyolysis-induced acute kidney injury under hypoxia and deprivation of food and water.

BACKGROUND: To investigate the renal pathophysiologyin rhabdomyolysis-induced acute kidney injury (AKI) in rats under hypoxia and deprivation of food and water (HDFW), thus broadening the knowledge about rhabdomyolysis-induced AKI in massive earthquake. METHODS: Male Wistar rats weighing 200-230g were randomized into control, rhabdomyolysis (R), HDFW and rhabdomyolysis in combination with HDFW (R/HDFW) group. Experimental rhabdomyolysis rat model was established through clamping hind limb muscles, HDFW model rats were kept in 10% hypoxic chamber unavailable to food and water. At 1, 3, 5, 7, 9, 11d after treatment, serum creatinine (Scr) level, renal index, renal structural changes and cell apoptosis were analyzed. RESULTS: After R, HDFW, R/HDFW treatment, the animals showed significantly higher Scr levels than the control group. Renal index in R and R/HDFW groups elevated remarkably compared with that in control and HDFW group. The results of histopathology, ultra-structure and apoptosis assay suggested that rhabdomyolysis caused renal tubular injury, HDFW treatment resulted in renal vascular dilation, tissue congestion and tubular cell damage. In addition, more severe renal lesion appeared in R/HDFW. CONCLUSIONS: We conclude that the association of experimental rhabdomyolysis with HDFW results in a different functional and histological pattern. The rhabdomyolysis-HDFW combination causes more severe renal injury.

Microarray analysis of altered gene expression and the role of ATF3 in HK-2 cells treated with hemin.

OBJECTIVE: To identify gene expression changes and the role of activating transcription factor 3 (ATF3) in hemin toxicity in renal tubular epithelial cells, then elucidate molecular mechanisms of hemin toxicity on renal tubular epithelial cells. METHODS: An oligo array comprising 35,035 genes was used to compare differential gene expression in hemin-treated and non-treated HK-2 cells (human renal proximal tubular epithelial cells), and the role of ATF3 in hemin toxicity was assessed using siRNA technique. RESULTS: A total of 128 mRNAs were at least twofold up-regulated and 101 mRNAs were at least twofold down-regulated after hemin treatment. Expression levels of ATF3, heat shock protein 70, c-fos, and c-jun were remarkably increased. Hemin also suppressed nuclear factor-kappa B inhibitor α, ß-2 adrenergic receptor, and interleukin-6 mRNA amounts more than twofold. We further demonstrated the protective role of ATF3 in hemin cytotoxicity. CONCLUSIONS: The data suggest that hemin caused multiple changes of gene expression in HK-2 cells, and ATF3 protects against hemin cytotoxicity.

Application of 1H-NMR-based metabolomics for detecting injury induced by long-term microwave exposure in Wistar rats' urine.

There has been growing public concern regarding exposure to microwave fields as a potential human health hazard. This study aimed to identify sensitive biochemical indexes for the detection of injury induced by microwave exposure. Male Wistar rats were exposed to microwaves for 6 min per day, 5 days per week over a period of 1 month at an average power density of 5 mW/cm(2) (specific absorption rate of 2.1 W/kg). Urine specimens were collected over 24 h in metabolic cages at 7 days, 21 days, 2 months, and 6 months after exposure. (1)H NMR spectroscopy data were analyzed using multivariate statistical techniques. Urine metabolic profiles of rats after long-term microwave exposure were significantly differentiated from those of sham-treated controls using principal component analysis or partial least squares discriminant analysis. Significant differences in low molecular weight metabolites (acetate, succinate, citrate, ketoglutarate, glucose, taurine, phenylalanine, tyrosine, and hippurate) were identified in the 5 mW/cm(2) microwave exposure group compared with the sham-treated controls at 7 days, 21 days, and 2 months. Metabolites returned to normal levels by 6 months after exposure. These data indicated that these metabolites were related to the perturbations of energy metabolism particularly in the tricarboxylic acid cycle, and the metabolism of amino acids, monoamines, and choline in urine represent potential indexes for the detection of injury induced by long-term microwave exposure.

Effects of perceived teacher support on motivation and engagement amongst Chinese college students: Need satisfaction as the mediator.

College students' motivation and engagement are regarded as essential factors to promote their academic development and wellbeing. However, motivation and engagement among college students appear to decline after they enter the university. Guided by the framework of self-determination theory, this study attempted to explore a motivational model of how three dimensions of perceived teacher support (autonomy, structure, and involvement) related to student motivation and class engagement, using need satisfaction as a mediator. Drew on a survey of the perceptions of 705 Chinese university students, the results showed that besides structure, both autonomy support and involvement positively related to students' need satisfaction. Further, need satisfaction was positively associated with autonomous motivation, controlled motivation, and class engagement and negatively linked with amotivation. Yet, only autonomous motivation was positively predicted for class engagement. Need satisfaction and the chain from need satisfaction to autonomous motivation were found to be the significant mediators. The practical implications of educational practices are discussed.

Reduction of ROS-HIF1α-driven glycolysis by taurine alleviates Streptococcus uberis infection.

Antibiotic-resistant strains of Streptococcus uberis (S. uberis) frequently cause clinical mastitis in dairy cows resulting in enormous economic losses. The regulation of immunometabolism is a promising strategy for controlling this bacterial infection. To investigate whether taurine alleviates S. uberis infection by the regulation of host glycolysis via HIF1α, the murine mammary epithelial cell line (EpH4-Ev) and C57BL/6J mice were challenged with S. uberis. Our data indicate that HIF1α-driven glycolysis promotes inflammation and damage in response to the S. uberis challenge. The activation of HIF1α is dependent on mTOR-mediated ROS production. These results were confirmed in vivo. Taurine, an intracellular metabolite present in most animal tissues, has been shown to effectively modulate HIF1α-triggered metabolic reprogramming and contributes to a reduction of inflammation, which reduces mammary tissue damage and prevents mammary gland dysfunction in S. uberis-induced mastitis. These data provide a novel putative prophylactic and therapeutic strategy for amelioration of dairy cow mastitis and bacterial inflammation.

Taurine inhibits Streptococcus uberis-induced NADPH oxidase-dependent neutrophil extracellular traps via TAK1/MAPK signaling pathways.

Neutrophil extracellular traps (NETs) are produced by neutrophil activation and usually have both anti-infective and pro-damage effects. Streptococcus uberis (S. uberis), one of the common causative organisms of mastitis, can lead to the production of NETs. Taurine, a free amino acid abundant in the organism, has been shown to have immunomodulatory effects. In this study, we investigated the molecular mechanisms of S. uberis-induced NETs formation and the regulatory role of taurine. The results showed that NETs had a disruptive effect on mammary epithelial cells and barriers, but do not significantly inhibit the proliferation of S. uberis. S. uberis induced NADPH oxidase-dependent NETs. TLR2-mediated activation of the MAPK signaling pathway was involved in this process. Taurine could inhibit the activation of MAPK signaling pathway and NADPH oxidase by modulating the activity of TAK1, thereby inhibiting the production of ROS and NETs. The effects of taurine on NADPH oxidase and NETs in S. uberis infection were also demonstrated in vivo. These results suggest that taurine can protect mammary epithelial cells and barriers from damage by reducing S. uberis-induced NETs. These data provide new insights and strategies for the prevention and control of mastitis.

Hsp72-Based Effect and Mechanism of Microwave Radiation-Induced Cardiac Injury in Rats.

The purpose of this study was to determine the role of heat shock protein 72 (Hsp72) changes in cardiac injury caused by microwave radiation, aimed at providing novel insights into the mechanism of this damage. A digital thermometer was used to measure the rectal temperature of the rats' pre- and post-radiation. On the 1st, 7th, 14th, and 28th days post-radiation, the changes in electrocardiogram (ECG) were analyzed by a multi-channel physiological recorder. The myocardial enzyme activities and ion concentrations were detected by an automatic biochemical analyzer. Additionally, the levels of myocardial injury markers were established by the enzyme-linked immunosorbent assay (ELISA), and those of hormones were measured by radioimmunoassay. The structure and ultrastructure of the myocardial tissue were observed using an optical microscope and transmission electron microscopy (TEM). The expression of Hsp72 was measured by Western blot and immunofluorescence analyses. Post-exposure, the rectal temperature in the R-group increased significantly, ECG was disordered, and the concentrations of ions were decreased. Furthermore, the activities of myocardial enzymes were changed, and the contents of myocardial injury markers and hormones were increased. We observed damage to the structure and ultrastructure and significantly increased expression of Hsp72. As a whole, the results indicated that S-wave microwave radiation at 30 mW/cm2 for 35 min resulted in damage to the cardiac functionality organigram, caused by a combination of the thermal and nonthermal effects.

[Long-term microwave radiation affects male reproduction in rats].

OBJECTIVE: To investigate the effect of long-term microwave radiation on male reproduction in rats. METHODS: 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. RESULTS: 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). CONCLUSION: Long-term microwave radiation may cause injury to male reproduction, which is positively correlated with the radiation dose, and has an obvious late effect.

[The protective effects of Aduola Fuzhenglin on the heart injury induced by microwave exposure in rats].

OBJECTIVE: To study the protective effects of AduoLa Fuzhenglin(ADL) on the heart injury induced by microwave exposure in rats. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Recombinant human hepassocin stimulates proliferation of hepatocytes in vivo and improves survival in rats with fulminant hepatic failure.

BACKGROUND: Human hepassocin (HPS) was originally detected by subtractive and differential cDNA cloning as a liver-specific gene that was markedly upregulated during liver regeneration. Previous studies suggested that HPS showed mitogenic activity on isolated hepatocytes in vitro. However, its in vivo functions remained largely unknown. Therefore, the function of recombinant human HPS during liver regeneration and chemically induced liver injury was investigated. METHODS: The proliferation of primary hepatocytes was examined by [(3)H]thymidine incorporation and immunohistological staining of proliferating cell nuclear antigen (PCNA). RNA interference was performed to knock down the endogenous expression of HPS. The proliferation of L02 cells was examined by MTS assay. The phosphorylation of ERK1/2 (extracellular signal-regulated kinase 1/2) was investigated by western blotting analysis. Assessment of liver injury (histology, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels) and of apoptosis, by TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling) assay, was performed. RESULTS: Purified recombinant human HPS showed specific mitogenic activity on primary hepatocytes and normal liver cell lines in a mitogen-activated protein kinase (MAPK)-dependent manner and stimulated the proliferation of hepatocytes in rats with 70% partial hepatectomy. Administration of HPS to rats after d-galactose and carbon tetrachloride (CCl(4)) treatment protected against liver injury (minimal liver necrosis, depressed ALT and AST levels, and decreased lethality), reduced apoptosis and enhanced proliferation. Knock-down of endogenous HPS in vivo enhanced the liver injury induced by d-galactose by increasing the apoptosis and elevating ALT and AST levels. CONCLUSIONS: HPS is a hepatic growth factor which can accelerate hepatocyte proliferation in vivo and protect against liver injury. These data point to the potential interest of HPS in the treatment of fulminant hepatic failure.

Abnormal Expression of Connexin43 in Cardiac Injury Induced by S-Band and X-Band Microwave Exposure in Rats.

Although the effects of microwave exposure on the heart have gradually become the focus of domestic and foreign scholars, the biological effects caused by different doses and different frequency bands of exposure are still unclear. In this study, we will investigate the damaging effect of S-band and X-band microwave composite exposure on cardiac structure and function, as well as the pathophysiological significance of Cx43 in cardiac conduction dysfunction after exposure. We used S- and X-band radiation sources with the average power density of 5 and 10 mW/cm2 to expose Wistar rats to single or composite exposure. At the 6th hour, on the 7th, 14th, and 28th days after exposure, ECG was used to detect the electrical conduction of the heart, and the myocardial enzyme was measured by the automatic biochemical analyzer. We selected the observation time points and groups with severe damage to observe the changes of myocardial structure and ultrastructure with an optical microscope and TEM; and to detect the expression and distribution of Cx43 by western blotting and immunohistochemistry. After exposure, the heart rate increased, the P wave amplitude decreased, and the R wave amplitude increased; the content of the myocardial enzyme in serum increased; the structure and ultrastructure of cardiac tissue were damaged. The damage was dose-dependent and frequency-dependent. The expression of Cx43 in myocardial tissue decreased, and distribution was abnormal. Taken together, these findings suggested that the mechanism of abnormal electrical conduction in the heart of rats by S- and X-band microwave exposure might be related to the decreased expression and disordered distribution of Cx43 after microwave exposure.

Effects of 1.5 and 4.3 GHz microwave radiation on cognitive function and hippocampal tissue structure in Wistar rats.

Previous studies have shown that single-frequency microwave radiation can lead to cognitive decline in rats. However, few studies have focused on the combined effects of irradiation with different frequencies of microwaves. Our research aimed to investigate the effects of 1.5 GHz and 4.3 GHz microwave radiation, singly and in combination, on cognitive function and hippocampal tissue structure in rats. A total of 140 male Wistar rats were randomly divided into 4 groups: the S group (sham radiation group), L10 group (10 mW/cm2 1.5 GHz group), C10 group (10 mW/cm2 4.3 GHz band group) and LC10 group (10 mW/cm2 1.5 and 4.3 GHz multi-frequency radiation group). For 1-28 days after microwave radiation, we analyzed the average escape latency for the Morris water maze task, electroencephalograms, change in hippocampal tissue structure and ultrastructure, content of the Nissl body in the hippocampus, and activities of lactate dehydrogenase and succinate dehydrogenase. Compared to the S group, all exposure groups showed varying degrees of learning and memory decline and hippocampal structural damage. The results showed that 1.5 GHz and 4.3 GHz microwave radiation was able to induce cognitive impairment and hippocampal tissue damage in rats and combined radiation with both frequencies caused more serious injuries, but none of these damaging effects varied with microwave frequency.

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

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.

[Microwave radiation decreases the expressions of occludin and JAM-1 in rats].

OBJECTIVE: 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. METHODS: 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. RESULTS: 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. CONCLUSION: 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.

Abnormality of synaptic vesicular associated proteins in cerebral cortex and hippocampus after microwave exposure.

Studies were performed to determine the effects of microwave on synaptic vesicles and the expression of synaptic vesicular associated proteins including synapsin I, VAMP-2, syntaxin, and synaptophysin. 25 Wistar rats were exposed to microwave which the average power density was 30 mW/cm(2), and whole body average specific absorption rate was 14.1 W/kg for 5 min. Synaptosome preparations in the cerebral cortex and hippocampus were obtained by isotonic Percoll/sucrose discontinuous gradients at 6 h, 1, 3, and 7 days after radiation. The expression of synaptic vesicular associated proteins was measured using Western blots and image analysis. The interaction between VAMP-2 and syntaxin was examined by coimmunoprecipitation analysis. Synapsin I in the cerebral cortex were decreased at 3 days (P < 0.01) after radiation and in the hippocampus increased at 1 day (P < 0.01), decreased at 3 days (P < 0.01), increased again at 7 days (P < 0.01) after exposure, compared with the sham-treated controls. Synaptophysin were increased in 1-7 days (P < 0.01) after exposure in the cerebral cortex and hippocampus. VAMP-2 were decreased at 1 and 3 days (P < 0.01) and syntaxin were decreased in 6 h to 3 days (P < 0.01) after radiation in the cerebral cortex and hippocampus. The interactions between VAMP-2 and syntaxin were decreased at 3-7 days (P < 0.01) after radiation in the cerebral cortex and hippocampus, compared with the sham-treated controls. These results suggest that 30 mW/cm(2) (SAR 14.1 W/kg) microwave radiation can result in the perturbation of the synaptic vesicles associated proteins: synapsin I, synaptophysin, VAMP-2, and syntaxin. The perturbation could induce the deposit of synaptic vesicle, which might be relative to the dysfunction of the synaptic transmission, even the cognition deficit.