RESUMO
Many studies indicate that parental exposure to an electromagnetic field (EMF) can cause long-term toxicity to the health of the offspring. While concerns have been focused on maternal influence, much less is known regarding the effects of paternal factors. Electromagnetic pulse (EMP) is a special and widely used type of EMF. The present study was designed to investigate the effects of paternal EMP exposure on the reproductive endocrine function of the male rat offspring. Male Sprague Dawley rats were randomly exposed to EMP at 200 kV m-1 for 0, 100 or 400 pulses before mating. The adult male offspring were sacrificed and the structural changes of testes, levels of serum steroid hormones, sperm characteristics, reproductive behaviors, content of the reproductive endocrine-related neurotransmitter GABA and expression of the GABAA receptor were analyzed. The results showed that paternal exposure induced a decrease of testosterone (T), sperm quantity and acrosin activity in the male offspring (p < 0.05). It did not show significant changes in the structure of testes, sperm deformity frequency and reproductive behaviors compared with the sham-exposed group. The content of GABA and the protein and mRNA expression of the hypothalamic GABAA receptor protein increased in the EMP exposure group (p < 0.05). In conclusion, our study shows that under these experimental conditions EMP had a certain degree of influence on the reproductive endocrine function of the male rat offspring, and the hypothalamic GABAA receptor may be involved in the reproductive toxicity of the male offspring.
RESUMO
The increasing use of mobile phones by teenagers has raised concern about the cognitive effects of radiofrequency (RF) fields. In this study, we investigated the effects of 4-week exposure to a 1.8 GHz RF field on the emotional behavior and spatial memory of adolescent male mice. Anxiety-like behavior was evaluated by open field test (OFT) and elevated plus maze (EPM) test, while depression-like behavior was evaluated by sucrose preference test (SPT), tail suspension test (TST) and forced swim test (FST). The spatial learning and memory ability were evaluated by Morris water maze (MWM) experiments. The levels of amino acid neurotransmitters were determined by liquid chromatography-mass spectrometry (LC-MS). The histology of the brain was examined by hematoxylin-eosin (HE) staining. It was found that the depression-like behavior, spatial memory ability and histology of the brain did not change obviously after RF exposure. However, the anxiety-like behavior increased in mice, while, the levels of γ-aminobutyric acid (GABA) and aspartic acid (Asp) in cortex and hippocampus significantly decreased after RF exposure. These data suggested that RF exposure under these conditions do not affect the depression-like behavior, spatial memory and brain histology in adolescent male mice, but it may however increase the level of anxiety, and GABA and Asp were probably involved in this effect.
Assuntos
Ansiedade/etiologia , Comportamento Animal , Aprendizagem em Labirinto , Ondas de Rádio , Memória Espacial , Animais , Ácido Aspártico/metabolismo , Uso do Telefone Celular , Córtex Cerebral/metabolismo , Elevação dos Membros Posteriores , Hipocampo/metabolismo , Masculino , Camundongos Endogâmicos C57BL , Natação , Ácido gama-Aminobutírico/metabolismoRESUMO
Public concern is growing about the exposure to electromagnetic fields (EMF) and its effect on male reproductive health. Detrimental effect of EMF exposure on sex hormones, reproductive performance and sex-ratio was reported. The present study was designed to clarify whether paternal exposure to electromagnetic pulse (EMP) affects offspring sex ratio in mice. 50 male BALB/c mice aged 5-6 weeks were exposed to EMP daily for 2 weeks before mated with non-exposed females at 0d, 7d, 14d, 21d and 28d after exposure. Sex hormones including total testosterone, LH, FSH, and GnRH were detected using radioimmunoassay. The sex ratio was examined by PCR and agarose gel electrophoresis. The results of D0, D21 and D28 showed significant increases compared with sham-exposed groups. The serum testosterone increased significantly in D0, D14, D21, and D28 compared with sham-exposed groups (p<0.05). Overall, this study suggested that EMP exposure may lead to the disturbance of reproductive hormone levels and affect the offspring sex ratio.
Assuntos
Campos Eletromagnéticos , Razão de Masculinidade , Testosterona/sangue , Animais , Feminino , Hormônio Liberador de Gonadotropina/sangue , Hormônio Luteinizante/sangue , Masculino , Camundongos Endogâmicos BALB C , ReproduçãoRESUMO
The biological effects of electromagnetic pulse (EMP) on the brain have been focused on for years. It was reported that gelatinase played an important role in maintaining brain function through regulating permeability in the blood-brain barrier (BBB). To investigate the effects of EMP on gelatinase of BBB, an in vitro BBB model was established using primary cultured rat brain microvascular endothelial cells (BMVEC), astrocytes and half-contact culture of these cells in a transwell chamber. Cultured supernatant and cells were collected at different time points after exposure to EMP (peak intensity 400 kV/m, rise time 10 ns, pulse width 350 ns, 0.5 pps and 200 pulses). Protein levels of cellular gelatinase MMP-2 and MMP-9, and endogenous inhibitor TIMP-1 and TIMP-2 were detected by Western blot. The activity of gelatinase in culture supernatant was detected by gelatin zymography. It was found that compared with the sham-exposed group, the protein level of MMP-2 was significantly increased at 6 h (p < 0.05), and the protein level of its endogenous inhibitor TIMP-2 did not change after EMP exposure. In addition, the protein levels of MMP-9 and its endogenous inhibitor TIMP-1 did not change after EMP exposure. Gelatin zymography results showed that the activity of MMP-2 in the inner pool and the outer pool of the transwell chamber was significantly increased at 6 h after EMP exposure compared with that of the sham group. These results suggested that EMP exposure could affect the expression and activity of MMP-2 in the BBB model.
Assuntos
Barreira Hematoencefálica/enzimologia , Barreira Hematoencefálica/efeitos da radiação , Fenômenos Eletromagnéticos , Gelatinases/metabolismo , Animais , Barreira Hematoencefálica/metabolismo , Feminino , Regulação Enzimológica da Expressão Gênica/efeitos da radiação , Masculino , Ratos , Inibidor Tecidual de Metaloproteinase-1/metabolismo , Inibidor Tecidual de Metaloproteinase-2/metabolismoRESUMO
More studies that are focused on the bioeffects of radio-frequency (RF) electromagnetic radiation that is generated from the communication devices, but there were few reports with confirmed results about the bioeffects of RF radiation on reproductive cells. To explore the effects of 1950 MHz RF electromagnetic radiation (EMR) on mouse Leydig (TM3) cells. TM3 cells were irradiated or sham-irradiated continuously for 24 h by the specific absorption rate (SAR) 3 W/kg radiation. At 0, 1, 2, 3, 4, and 5 days after irradiation, cell proliferation was detected by cell counting kit-8 (CCK-8) method, cell cycle distribution, percentage of apoptosis, and cellular reactive oxygen species (ROS) were examined by flow cytometry, Testosterone level was measured using enzyme-linked immunosorbent assay (ELISA) assay, messenger ribonucleic acid (mRNA) expression level of steroidogenic acute regulatory protein (StAR) and P450scc in TM3 cells was detected by real-time polymerase chain reaction (PCR). After being irradiated for 24 h, cell proliferation obviously decreased and cell cycle distribution, secretion capacity of Testosterone, and P450scc mRNA level were reduced. While cell apoptosis, ROS, and StAR mRNA level did not change significantly. The current results indicated that 24 h of exposure at 1950 MHz 3 W/kg radiation could cause some adverse effects on TM3 cells proliferation and Testosterone secretion, further studies about the biological effects in the reproductive system that are induced by RF radiation are also needed.
Assuntos
Células Intersticiais do Testículo/efeitos da radiação , Ondas de Rádio/efeitos adversos , Testosterona/antagonistas & inibidores , Animais , Apoptose/efeitos da radiação , Ciclo Celular/efeitos da radiação , Linhagem Celular , Proliferação de Células/efeitos da radiação , Células Intersticiais do Testículo/metabolismo , Masculino , Camundongos , Fosfoproteínas/genética , Fosfoproteínas/metabolismo , RNA Mensageiro/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Testosterona/metabolismoRESUMO
OBJECTIVE: The objective was to observe damage of hippocampus in rats after exposure to infrasound, and to assess HSP70 expression in hippocampus. METHODS: SD rats in the experimental group were exposed to 140 dB (8 Hz) infrasound for 2 h per day for 3 days. The morphology of the hippocampus was examined by transmission electronic microscopic (TEM). Cell apoptosis was observed by TUNEL staining at 0 h, 24 h, 48 h, and 2 w after exposure. HSP70 expression was detected by immunohistochemistry (IHC) and Western blotting (WB). RESULTS: TEM showed that hippocampus was significantly damaged by exposure, and exhibited recovery 1 week after exposure. The TUNEL data showed that neuronal apoptosis after exposure was significantly higher than in the control rats at 24 h and 48 h, and the apoptotic cells decreased one week after exposure. IHC and WB showed HSP70 expression was significantly higher in the exposed rats, peaked at 24 h. CONCLUSION: Exposure to 140 dB (8 Hz) infrasound for 2 h per day for 3 days appeared to induce damage to the hippocampus of rats, based on changes in ultrastructure and increased cell apoptosis. However, recovery from the damage occurred overtime. HSP70 expression also increased after the exposure and decreased by 48.
Assuntos
Apoptose , Hipocampo/efeitos da radiação , Som/efeitos adversos , Animais , Western Blotting , Proteínas de Choque Térmico HSP70/genética , Proteínas de Choque Térmico HSP70/metabolismo , Imuno-Histoquímica , Marcação In Situ das Extremidades Cortadas , Masculino , Ratos , Ratos Sprague-DawleyRESUMO
A progressively expanded literature has been devoted in the past years to the noxious or beneficial effects of electromagnetic field (EMF) to Alzheimer׳s disease (AD). This study concerns the relationship between electromagnetic pulse (EMP) exposure and the occurrence of AD in rats and the underlying mechanisms, focusing on the role of oxidative stress (OS). 55 healthy male Sprague Dawley (SD) rats were used and received continuous exposure for 8 months. Morris water maze (MWM) test was conducted to test the ability of cognitive and memory. The level of OS was detected by superoxide dismutase (SOD) activity and glutathione (GSH) content. We found that long-term EMP exposure induced cognitive damage in rats. The content of ß-amyloid (Aß) protein in hippocampus was increased after long-term EMP exposure. OS of hippocampal neuron was detected. Western blotting and immunohistochemistry (IHC) assay showed that the content of Aß protein and its oligomers in EMP-exposed rats were higher than that of sham-exposed rats. The content of Beta Site App Cleaving Enzyme (BACE1) and microtubule-associated protein 1 light chain 3-II (LC3-II) in EMP-exposed rats hippocampus were also higher than that of sham-exposed rats. SOD activity and GSH content in EMP-exposed rats were lower than sham-exposed rats (p<0.05). Several mechanisms were proposed based on EMP exposure-induced OS, including increased amyloid precursor protein (APP) aberrant cleavage. Although further study is needed, the present results suggest that long-term EMP exposure is harmful to cognitive ability in rats and could induce AD-like pathological manifestation.
Assuntos
Doença de Alzheimer/metabolismo , Doença de Alzheimer/psicologia , Secretases da Proteína Precursora do Amiloide/efeitos da radiação , Peptídeos beta-Amiloides/efeitos da radiação , Precursor de Proteína beta-Amiloide/efeitos da radiação , Ácido Aspártico Endopeptidases/efeitos da radiação , Cognição/efeitos da radiação , Campos Eletromagnéticos , Estresse Oxidativo/efeitos da radiação , Secretases da Proteína Precursora do Amiloide/metabolismo , Peptídeos beta-Amiloides/metabolismo , Precursor de Proteína beta-Amiloide/metabolismo , Animais , Ácido Aspártico Endopeptidases/metabolismo , Cognição/fisiologia , Modelos Animais de Doenças , Hipocampo/metabolismo , Hipocampo/efeitos da radiação , Masculino , Aprendizagem em Labirinto/efeitos da radiação , Ratos , Ratos Sprague-DawleyRESUMO
Previously, we found that electromagnetic pulses (EMP) induced an increase in blood brain barrier permeability and the leakage of albumin from blood into brain tissue. Albumin is known to activate microglia cells. Thus, we hypothesised that microglia activation could occur in the brain after EMP exposure. To test this hypothesis, the morphology and secretory function of microglia cells, including the expression of OX-42 (a marker of microglia activation), and levels of TNF-α, IL-10, IL-1ß, and NO were determined in the rat cerebral cortex after EMP exposure. In addition, to examine the signalling pathway of EMP-induced microglia activation, protein and phosphorylated protein levels of p38, JNK and ERK were determined. It was found that the expression of OX-42increased significantly at 1, 6 and 12h (p<0.05) and recovered to the sham group level at 24h after EMP exposure. Levels of NO, TNF-α and IL-10 also changed significantly in vivo and in vitro after EMP exposure. The protein level of p38 and phosphorylated p38 increased significantly after EMP exposure (p<0.05) and recovered to sham levels at 12 and 24h, respectively. Protein and phosphorylated protein levels of ERK and JNK did not change. SB203580 (p38 inhibitor) partly prevented the change in NO, IL-10, IL-1ß, TNF-α levels induced by EMP exposure. Taken together, these results suggested that EMP exposure (200kV/m, 200 pulses) could activate microglia in rat brain and affect its secretory function both in vivo and in vitro, and the p38 pathway is involved in this process.
Assuntos
Córtex Cerebral/citologia , Campos Eletromagnéticos/efeitos adversos , Sistema de Sinalização das MAP Quinases , Microglia/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismo , Animais , Imidazóis/farmacologia , Interleucina-10/metabolismo , Interleucina-1beta/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Masculino , Microglia/efeitos dos fármacos , Óxido Nítrico/metabolismo , Cultura Primária de Células , Piridinas/farmacologia , Ratos , Fator de Necrose Tumoral alfa/metabolismoRESUMO
Power-line frequency electromagnetic field (PF-EMF) was reported as a human carcinogen by some epidemiological research, but the conclusion is lack of robust experiment evidence. To identify the effects of long-term PF-EMF exposure on cell behavior, Balb/c 3T3 cells in exponential growth phase were exposed or sham-exposed to 50 Hertz (Hz) PF-EMF at 2.3 mT for 2 hours (h) one day, 5 days every week. After 11 weeks exposure, cells were collected instantly. Cell morphology was observed under invert microscope and Giemsa staining, cell viability was detected by 3-(4, 5-dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide (MTT) assay, cell cycle and apoptosis was examined by flow cytometry, the protein level of Proliferating Cell Nuclear Antigen (PCNA) and CyclinD1 was detected by western blot, cell transformation was examined by soft agar clone assay and plate clone forming test, and cell migration ability was observed by scratch adhesion test. It was found that after PF-EMF exposure, cell morphology, apoptosis, cell migration ability and cell transformation didn't change. However, compared with sham group, cell viability obviously decreased and cell cycle distribution also changed after 11 weeks PF-EMF exposure. Meanwhile, the protein level of PCNA and CyclinD1 significantly decreased after PF-EMF exposure. These data suggested that although long-term 50Hz PF-EMF exposure under this experimental condition had no effects on apoptosis, cell migration ability and cell transformation, it could affect cell proliferation and cell cycle by down-regulation the expression of PCNA and CyclinD1 protein.
Assuntos
Fontes de Energia Elétrica , Campos Eletromagnéticos/efeitos adversos , Animais , Apoptose/efeitos da radiação , Células 3T3 BALB , Ciclo Celular/efeitos da radiação , Movimento Celular/efeitos da radiação , Proliferação de Células/efeitos da radiação , Sobrevivência Celular/efeitos da radiação , Regulação da Expressão Gênica/efeitos da radiação , Humanos , Camundongos , Ratos , Fatores de TempoRESUMO
Electromagnetic fields are considered to potentially affect embryonic development, but the mechanism is still unknown. In this study, human embryonic stem cell (hESC) line HUES-17 was applied to explore the mechanism of exposure on embryonic development to pulsed electromagnetic field (PEMF) for 400 pulses at different electric field intensities and the differentiation of HUES-17 cells was observed after PEMF exposure. The expression of alkaline phosphatase (AP), stage-specific embryonic antigen-3 (SSEA-3), SSEA-4 and the mRNA level and protein level of Oct4, Sox2 and Nanog in HUES-17 cells remained unchanged after PEMF exposure at the electric field intensities of 50, 100, 200 or 400 kV/m. Four hundred pulses PEMF exposure at the electric field intensities of 50, 100, 200 or 400 kV/m did not affect the differentiation of HUES-17 cells. The reason why electromagnetic fields affect embryonic development may be due to other mechanisms rather than affecting the differentiation of embryonic stem cells.
Assuntos
Campos Eletromagnéticos , Células-Tronco Embrionárias/citologia , Células-Tronco Embrionárias/metabolismo , Fosfatase Alcalina/metabolismo , Antígenos Glicosídicos Associados a Tumores/metabolismo , Diferenciação Celular/fisiologia , Linhagem Celular , Proteínas de Homeodomínio/genética , Proteínas de Homeodomínio/metabolismo , Humanos , Proteína Homeobox Nanog , Fator 3 de Transcrição de Octâmero/genética , Fator 3 de Transcrição de Octâmero/metabolismo , Fatores de Transcrição SOXB1/genética , Fatores de Transcrição SOXB1/metabolismo , Antígenos Embrionários Estágio-Específicos/metabolismoRESUMO
Electromagnetic pulse (EMP) causes central nervous system damage and neurobehavioral disorders, and sevoflurane protects the brain from ischemic injury. We investigated the effects of sevoflurane on EMP-induced brain injury. Rats were exposed to EMP and immediately treated with sevoflurane. The protective effects of sevoflurane were assessed by Nissl staining, Fluoro-Jade C staining and electron microscopy. The neurobehavioral effects were assessed using the open-field test and the Morris water maze. Finally, primary cerebral cortical neurons were exposed to EMP and incubated with different concentration of sevoflurane. The cellular viability, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity and malondialdehyde (MDA) level were assayed. TUNEL staining was performed, and the expression of apoptotic markers was determined. The cerebral cortexes of EMP-exposed rats presented neuronal abnormalities. Sevoflurane alleviated these effects, as well as the learning and memory deficits caused by EMP exposure. In vitro, cell viability was reduced and LDH release was increased after EMP exposure; treatment with sevoflurane ameliorated these effects. Additionally, sevoflurane increased SOD activity, decreased MDA levels and alleviated neuronal apoptosis by regulating the expression of cleaved caspase-3, Bax and Bcl-2. These findings demonstrate that Sevoflurane conferred neuroprotective effects against EMP radiation-induced brain damage by inhibiting neuronal oxidative stress and apoptosis.
Assuntos
Apoptose/efeitos dos fármacos , Lesões Encefálicas/patologia , Campos Eletromagnéticos , Éteres Metílicos/farmacologia , Neurônios/patologia , Fármacos Neuroprotetores/farmacologia , Estresse Oxidativo/efeitos dos fármacos , Animais , Comportamento Animal/efeitos dos fármacos , Lesões Encefálicas/complicações , Lesões Encefálicas/tratamento farmacológico , Caspase 3/metabolismo , Sobrevivência Celular/efeitos dos fármacos , Córtex Cerebral/patologia , Cognição/efeitos dos fármacos , L-Lactato Desidrogenase/metabolismo , Masculino , Malondialdeído/metabolismo , Éteres Metílicos/uso terapêutico , Degeneração Neural/complicações , Degeneração Neural/tratamento farmacológico , Degeneração Neural/patologia , Neurônios/efeitos dos fármacos , Neurônios/enzimologia , Neurônios/ultraestrutura , Ratos Sprague-Dawley , Sevoflurano , Superóxido Dismutase/metabolismo , Proteína X Associada a bcl-2/metabolismoRESUMO
Upregulation of translationally controlled tumor protein (TCTP) has been reported in a variety of malignant tumors. However, the impact of TCTP in glioma remains unclear. The objective of this study was to investigate the expression and prognostic value of TCTP in glioma patients. Western blot analysis was used to characterize the expression patterns of TCTP in 45 glioma and 22 normal brain tissues. Immunohistochemistry on a tissue microarray containing 127 cases of glioma was performed to analyze the association between TCTP expression and clinicopathological features. Compared with normal brain tissues, TCTP expression was significantly higher in glioma tissues (p <0.001). In addition, high TCTP expression in glioma was significantly associated with advanced pathological grade (p = 0.018). Kaplan-Meier analysis showed that patients with glioma and higher TCTP expression tend to have shorter overall survival time (p <0.001). In multivariate analysis, TCTP expression was proved to be an independent prognostic factor for patients with glioma (p <0.001). In conclusion, this study confirmed the overexpression of TCTP and its association with tumor progression in glioma. It also provided the first evidence that TCTP expression in glioma was an independent prognostic factor of patients, which might be a potential diagnostic and therapeutic target of glioma.
Assuntos
Biomarcadores Tumorais/metabolismo , Neoplasias Encefálicas/metabolismo , Glioma/metabolismo , Adulto , Western Blotting , Neoplasias Encefálicas/patologia , Neoplasias Encefálicas/cirurgia , Progressão da Doença , Feminino , Glioma/patologia , Glioma/cirurgia , Humanos , Imuno-Histoquímica , Estimativa de Kaplan-Meier , Masculino , Pessoa de Meia-Idade , Análise Multivariada , Gradação de Tumores , Prognóstico , Análise Serial de Tecidos , Resultado do Tratamento , Proteína Tumoral 1 Controlada por TraduçãoRESUMO
The blood-retinal barrier (BRB) is critical for maintaining retina homeostasis and low permeability. In this study, we evaluated the effects of electromagnetic pulse (EMP) exposure on the permeability of BRB, alterations of tight junction (TJ) proteins of BRB and if any, involvement of mitogen-activated protein kinase (MAPK) pathway. Male Sprague-Dawley (SD) rats and RF/6A cells which were pretreated with or without MAPKs inhibitors were sham exposed or exposed to EMP at 200kV/m for 200 pulses. The alteration of BRB permeability was examined through fluorescence microscope and quantitatively assessed using Evans blue (EB) and endogenous albumin as tracers. The expressions of TJ proteins and some signaling molecules of MAPK pathway were measured by Western blots. The observations were that EMP exposure resulted in increased BRB permeability concurrent with the decreased expressions of occludin and claudin-5, which were correlated with the increased expressions of phospho-p38, phospho-JNK and phospho-ERK and could be blocked when pretreated with p38 MAPK inhibitor. Thus, the results suggested that the alterations of occludin and claudin-5 may play an important role in the disruption of TJs, which may lead to the transient breakdown of BRB after EMP exposure with the involvement of p38 MAPK pathway through phosphorylation of signaling molecules.
Assuntos
Barreira Hematorretiniana/efeitos da radiação , Campos Eletromagnéticos/efeitos adversos , Sistema de Sinalização das MAP Quinases/efeitos da radiação , Junções Íntimas/efeitos da radiação , Animais , Barreira Hematorretiniana/metabolismo , Células Cultivadas , Claudina-5/metabolismo , Claudina-5/efeitos da radiação , Inibidores Enzimáticos/farmacologia , Azul Evans/metabolismo , Sistema de Sinalização das MAP Quinases/fisiologia , Masculino , Microscopia de Fluorescência , Ocludina/metabolismo , Ocludina/efeitos da radiação , Permeabilidade/efeitos da radiação , Fosforilação , Ratos , Ratos Sprague-Dawley , Junções Íntimas/metabolismo , Fatores de TempoRESUMO
OBJECTIVE: To investigate the effect of long-term power frequency electromagnetic field (50 Hz) exposure on the proliferation and apoptosis of human lens epithelial cells (SRA01/04 cells). METHODS: SRA01/04 cells in the exponential growth phase were exposed or sham-exposed to power frequency electromagnetic field (50 Hz, 2.3 mT) for 2 hours per day, 5 days every week. After 11 weeks of exposure, the cells were collected; the cell morphology was observed under a microscope, the cell viability was measured by MTT assay, the cell cycle and apoptosis were examined by flow cytometry, and the protein expression levels of cyclin D and proliferating cell nuclear antigen (PCNA) were determined by western blot. RESULTS: Compared with the sham-exposed SRA01/04 cells, most exposed cells became rounded and more stereoscopic, and heterochromatin gathered near the nuclear membrane in some exposed cells. The MTT assay showed that the viability of exposed cells was significantly increased compared with that of the sham-exposed cells (P < 0.05). Long-term power frequency electromagnetic field exposure led to significantly increased number of cells in S phase (P < 0.05), and the proliferation index was significantly higher in the exposed cells than in the sham-exposed cells (P < 0.05). There was no significant difference in apoptotic rate between the exposed cells and sham-exposed cells (P > 0.05). The exposed cells had significantly higher protein expression levels of cyclin D and PCNA than the sham-exposed cells (P < 0.05). CONCLUSION: Long-term power frequency electromagnetic field exposure can promote cellular proliferation and change cell cycle in SRA01/04 cells, but it has no marked effect on the apoptosis of SRA01/04 cells.
Assuntos
Apoptose , Proliferação de Células , Campos Eletromagnéticos/efeitos adversos , Células Epiteliais/citologia , Linhagem Celular , Ciclina D1/metabolismo , Exposição Ambiental/efeitos adversos , Humanos , Cristalino/citologia , Antígeno Nuclear de Célula em Proliferação/metabolismoRESUMO
There is an increasing public concern regarding potential health impacts from electromagnetic radiation exposure. Embryonic development is sensitive to the external environment, and limb development is vital for life quality. To determine the effects of electromagnetic pulse (EMP) on polydactyly of mouse fetuses, pregnant mice were sham-exposed or exposed to EMP (400 kV/m with 400 pulses) from Days 7 to 10 of pregnancy (Day 0 = day of detection of vaginal plug). As a positive control, mice were treated with 5-bromodeoxyuridine on Days 9 and 10. On Days 11 or 18, the fetuses were isolated. Compared with the sham-exposed group, the group exposed to EMP had increased rates of polydactyly fetuses (5.1% vs. 0.6%, P < 0.05) and abnormal gene expression (22.2% vs. 2.8%, P < 0.05). Ectopic expression of Fgf4 was detected in the apical ectodermal ridge, whereas overexpression and ectopic expression of Shh were detected in the zone of polarizing activity of limbs in the EMP-exposed group and in the positive control group. However, expression of Gli3 decreased in mesenchyme cells in those two groups. The percentages of programmed cell death of limbs in EMP-exposed and positive control group were decreased (3.57% and 2.94%, respectively, P < 0.05, compared with 7.76% in sham-exposed group). In conclusion, polydactyly induced by EMP was accompanied by abnormal expression of the above-mentioned genes and decreased percentage of programmed cell death during limb development.
Assuntos
Radiação Eletromagnética , Polidactilia/etiologia , Animais , Apoptose , Extremidades/embriologia , Feminino , Feto/embriologia , Feto/metabolismo , Feto/efeitos da radiação , Fator 4 de Crescimento de Fibroblastos/genética , Expressão Gênica , Idade Gestacional , Proteínas Hedgehog/genética , Fatores de Transcrição Kruppel-Like/genética , Camundongos , Proteínas do Tecido Nervoso/genética , Polidactilia/embriologia , Polidactilia/epidemiologia , Gravidez , Proteína Gli3 com Dedos de ZincoRESUMO
BACKGROUND AND AIMS: With the developing and widely used electromagnetic field (EMF) technology, more and more studies are focusing on the relationship between EMF and Alzheimer's disease (AD). Electromagnetic pulse (EMP) is one type of widely used EMF. This study aimed to clarify whether EMP exposure could induce cognitive and memory impairment, thus finding a possible relationship between EMP and AD. METHODS: Forty healthy male Sprague Dawley rats were randomly divided into four groups. Animals, respectively, received 100, 1000, and 10,000 pulses EMP (field strength 50 kV/m, repetition rate 100 Hz) exposure and sham exposure when 2 months old. Monthly Morris water maze (MWM) was used to test the changes of cognitive and memory ability. Superoxide dismutase (SOD) activity and glutathione (GSH) content were used as oxidative stress indexes. Expressions of some types of Alzheimer's disease-related proteins were also detected. RESULTS: After exposure, EMP exposure caused clear cognitive and memory impairment compared with sham exposure group (p <0.05). Determination of oxidation indexes showed decreased SOD activity and GSH content in exposure groups compared with sham group. Immunohistochemical (IHC) staining showed increased beta amyloid protein (Aß) in EMP exposure groups compared with sham group. Western blot experiments showed increased expressions of Aß oligomer and beta amyloid protein precursor (APP) in EMP exposure groups. Increased expression of microtubule-associated protein 1 light chain 3-II (LC3-II) was also found. CONCLUSIONS: The present results showed that EMP exposure can cause long-term impairment in impaired cognition and memory of rats, resulting in AD-like symptoms. This may be induced by enhancing oxidative stress and is related to autophagy dysfunction.
Assuntos
Precursor de Proteína beta-Amiloide/biossíntese , Campos Eletromagnéticos/efeitos adversos , Regulação para Cima , Doença de Alzheimer/etiologia , Doença de Alzheimer/metabolismo , Doença de Alzheimer/fisiopatologia , Peptídeos beta-Amiloides/biossíntese , Peptídeos beta-Amiloides/metabolismo , Precursor de Proteína beta-Amiloide/metabolismo , Animais , Autofagia , Transtornos Cognitivos/enzimologia , Transtornos Cognitivos/etiologia , Transtornos Cognitivos/metabolismo , Transtornos Cognitivos/fisiopatologia , Glutationa/metabolismo , Masculino , Aprendizagem em Labirinto , Memória , Transtornos da Memória/enzimologia , Transtornos da Memória/etiologia , Transtornos da Memória/metabolismo , Transtornos da Memória/fisiopatologia , Proteínas Associadas aos Microtúbulos/metabolismo , Estresse Oxidativo , Ratos , Ratos Sprague-Dawley , Superóxido Dismutase/metabolismoRESUMO
The aim of this study was to investigate the association between keratin 17 (K17) expression and the clinicopathological features of patients with epithelial ovarian cancer (EOC). K17 expression was detected by real-time quantitative RT-PCR in EOC and adjacent noncancerous tissues. In addition, K17 expression was analyzed by immunohistochemistry in 104 clinicopathologically characterized EOC cases. The expression levels of K17 mRNA and protein in EOC tissues were both significantly higher than those in noncancerous tissues. In addition, positive expression of K17 correlated with the clinical stage (p=0.001). Furthermore, Kaplan-Meier survival analysis showed that a high expression level of K17 resulted in a significantly poor prognosis of EOC patients. Multivariate analysis revealed that EOC expression level was an independent prognostic parameter for the overall survival rate of EOC patients. Our data are the first to suggest that increased K17 expression in EOC is significantly associated with aggressive progression and poor prognosis. K17 may be an important molecular marker for predicting the carcinogenesis, progression, and prognosis of EOC.
Assuntos
Biomarcadores Tumorais/genética , Cistadenocarcinoma Seroso/genética , Perfilação da Expressão Gênica , Queratina-17/genética , Neoplasias Ovarianas/genética , Ovário/metabolismo , Biomarcadores Tumorais/metabolismo , Estudos de Casos e Controles , Cistadenocarcinoma Seroso/metabolismo , Cistadenocarcinoma Seroso/mortalidade , Feminino , Seguimentos , Humanos , Técnicas Imunoenzimáticas , Queratina-17/metabolismo , Pessoa de Meia-Idade , Gradação de Tumores , Estadiamento de Neoplasias , Análise de Sequência com Séries de Oligonucleotídeos , Neoplasias Ovarianas/metabolismo , Neoplasias Ovarianas/mortalidade , Prognóstico , RNA Mensageiro/genética , Reação em Cadeia da Polimerase em Tempo Real , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Taxa de SobrevidaRESUMO
OBJECTIVE: To study the effect of electromagnetic pulse (EMP) exposure on permeability of in vitro blood-brain-barrier (BBB) model. METHODS: An in vitro BBB model, established by co-culturing brain microvascular endothelial cells (BMVEC) and astroglial cells (AC) isolated from rat brain, was exposed to EMP at 100 kV/m and 400 kV/m, respectively. Permeability of the model was assayed by measuring the transendothelial electrical resistance (TEER) and the horseradish peroxidase (HRP) transmission at different time points. Levels of BBB tight junction-related proteins were measured at 0, 1, 2, 4, 8, 12, 16, 20, 24 h after EMP exposure by Western blotting. RESULTS: The TEER level was lower in BBB model group than in control group at 12 h after EMP, exposure which returned to its normal level at 24 h. The 24 h recovery process was triphasic and biphasic respectively after EMP exposure at 100 kV/m and 400 kV/m. Following exposure to 400 kV/m EMP, the HRP permeability increased at 1-12 h and returned to its normal level at 24 h. Western blotting showed that the claudin-5 and ZO-1 protein levels were changed after EMP exposure. CONCLUSION: EMP exposure at 100 kV/m and 400 kV/m can increase the permeability of in vitro BBB model and BBB tight junction-related proteins such as ZO-1 and claudin-5 may change EMP-induced BBB permeability.
Assuntos
Barreira Hematoencefálica/efeitos da radiação , Permeabilidade Capilar/efeitos da radiação , Campos Eletromagnéticos/efeitos adversos , Animais , Células Cultivadas , Feminino , Ratos , Ratos Sprague-DawleyRESUMO
OBJECTIVE: To study the effects of electromagnetic pulse (EMP) exposure on the morphological change and excretion functions of mouse microglia (BV-2) cells and possible mechanism. METHODS: BV-2 cells were divided into two groups: the group exposed to EMP at 200 kV/m for 200 pulses and sham exposure group. At 1, 6, 12 and 24 hour after exposure the cells and culture supernatant were collected. Cellular morphological change was observed under invert microscope, the levels of TNF-α, IL-1ß and IL-10 in culture supernatant were determined by enzyme-linked immunosorbent assay (ELISA), nitric oxide (NO) and reactive oxygen species (ROS) were detected by nitrate reductase method and DCFH-DA probe, respectively. The protein and phosphorylation levels of ERK, JNK and p38 were measured by Western Blot method. After the cells pre-treated with the inhibitor of p38 (SB203580) were exposed to EMP, the levels of NO and ROS in culture supernatant were detected. RESULTS: It was found that the large ameboid shape appeared in some microglia cells exposed to EMP for 1, 6 and 12 h. Moreover, the number of microglia cells with ameboid shape increased significantly at 1 h, 6 h and 12 h after EMP exposure compared with sham group (P < 0.05). The levels of cytokines, such as TNF-α, IL-1ß and IL-10, in culture supernatant did not change obviously after EMP exposure. The levels of NO and ROS increased significantly at 1h after EMP exposure, reached the peak at 6 h, began to recover at 12 h and recovered to sham group level at 24 h (P < 0.05). Western blot results showed that the protein and protein phosphorylation levels of ERK and JNK did not change significantly after EMP exposure, however, the protein and protein phosphorylation levels of p38 increased obviously at 1 h and 6 h after EMP exposure, compared with sham group (P < 0.05). In addition, the pretreatment of p38 inhibitor (SB203580) significantly decreased NO and ROS production induced by EMP. CONCLUSION: EMP exposure may activate microglia cells and promote the production of NO and ROS in mouse microglia cells, and p38 pathway is involved in this process.
Assuntos
Campos Eletromagnéticos , Microglia/citologia , Microglia/metabolismo , Animais , Linhagem Celular , Citocinas/metabolismo , Camundongos , Óxido Nítrico/metabolismo , Espécies Reativas de Oxigênio/metabolismo , Proteínas Quinases p38 Ativadas por Mitógeno/metabolismoRESUMO
OBJECTIVE: To study the effects of electromagnetic pulses (EMP) on pathological changes and apoptosis of spleen lymphocytes in mice. METHODS: The male BALB/c mice (18 â¼ 22 g) were sham-exposed or exposed to EMP at 200 kV/m for 400 pulses a day for 7 days. On the 1st, 3rd, 7th, 14th 28th days after exposure the mice were killed. The weight of mice, the pathological change and the weight of mouse spleens were observed, the spleen indexes were calculated. The lymphocytes extracted from spleens were counted. The apoptosis and cell cycle of the lymphocyte were detected by flow cytometry, and the migration of the lymphocyte was measured by transwell assay. RESULTS: No pathological changes were found on the first day after exposure. However, the expanded sinusoid and the changed structure of spleen corpuscle on the 3rd day after exposure were observed. There was no difference of spleen indexes between the sham group and the exposure group on the 1st and 14th day after exposure. On the 3rd and 7th days after exposure, the spleen indexes of exposure group were significantly higher than those of sham-exposure group (P < 0.05). On the 28th day after exposure, the spleen indexes of exposure group was significantly lower than those of sham-exposure group (P < 0.05). The number of spleen lymphocytes on the 3rd and 7th days after exposure in exposure group increased significantly, compared with sham-exposure group (P < 0.05). But there were no differences of apoptotic cells and cellular cycle between the exposure group and sham-exposure group (P > 0.05). The ability of migration of the exposure group was significantly higher than that of sham-exposure group (P < 0.05). than the sham group (P < 0.05). CONCLUSION: The spleen of the male mouse is one of the target organs of EMP. After exposure to EMP, the number of spleen lymphocytes increased. But there were no differences of cell apoptotic cells and cell cycle between the sham group and the exposure group, due to the enhanced migration of lymphocytes induced by EMP.