20-Hydroxyecdysone Improves Neuronal Differentiation of Adult Hippocampal Neural Stem Cells in High Power Microwave Radiation-Exposed Rats.

Objective: The hippocampus is thought to be a vulnerable target of microwave exposure. The aim of the present study was to investigate whether 20-hydroxyecdysone (20E) acted as a fate regulator of adult rat hippocampal neural stem cells (NSCs). Furthermore, we investigated if 20E attenuated high power microwave (HMP) radiation-induced learning and memory deficits. Methods: Sixty male Sprague-Dawley rats were randomly divided into three groups: normal controls, radiation treated, and radiation+20E treated. Rats in the radiation and radiation+20E treatment groups were exposed to HPM radiation from a microwave emission system. The learning and memory abilities of the rats were assessed using the Morris water maze test. Primary adult rat hippocampal NSCs were isolated in vitro and cultured to evaluate their proliferation and differentiation. In addition, hematoxylin & eosin staining, western blotting, and immunofluorescence were used to detect changes in the rat brain and the proliferation and differentiation of the adult rat hippocampal NSCs after HPM radiation exposure. Results: The results showed that 20E induced neuronal differentiation of adult hippocampal NSCs from HPM radiation-exposed rats via the Wnt3a/ß-catenin signaling pathway in vitro. Furthermore, 20E facilitated neurogenesis in the subgranular zone of the rat brain following HPM radiation exposure. Administration of 20E attenuated learning and memory deficits in HPM radiation-exposed rats and frizzled-related protein (FRZB) reduced the 20E-induced nuclear translocation of ß-catenin, while FRZB treatment also reversed 20E-induced neuronal differentiation of NSCs in vitro. Conclusion: These results suggested that 20E was a fate regulator of adult rat hippocampal NSCs, where it played a role in attenuating HPM radiation-induced learning and memory deficits.

[Methane Production Potential and Methanogenic Pathways in Paddy Soils Under Different Rice-based Cropping Systems].

Differences inmethane (CH4) production potential in paddy soils under different rice-based cropping systems and especially in the methanogenic pathways (mainly acetate fermentation and CO2/H2 reduction) remain unclear. Anaerobic incubations of soil with or without fluoromethane (CH3F) inhibitor (2% and 0%) were conducted. With the soils from three typical paddy ecosystems (rice-wheat rotation, RW; rice-fallow, RF; double-rice, DR) in China, the cumulative concentration of CH4 production, CH4 production potential, dissolved organic carbon (DOC) content, and acetic acid content were determined. Meanwhile, the relative contribution of acetate-dependent methanogenesis (fac) was quantified using the stable carbon isotope method. The results showed that the CH4 production potential was 7.18 µg·(g·d)-1 in RF, which was significantly lower than that in RW[10.33 µg·(g·d)-1]and DR[13.42 µg·(g·d)-1] (P<0.05). Correlation analysis showed that CH4 production potential was significantly negatively correlated with soil cation exchange capacity and pH (P<0.01); the addition of CH3F significantly inhibited CH4 production (P<0.05). The content of DOC and acetic acid in DR were 255 mg·kg-1 and 7.34 mg·kg-1, respectively, which were 17%-51% and 22%-23% higher than those in RW and RF, respectively. The δ13CH4 and δ13CO2 values were affected greatly by different rice-based cropping systems, and the highest δ13CH4 value was -43.89‰ in RF, which was more positive than that of RW and DR by 11.06‰ and 8.33‰, respectively (P<0.05). By contrast, the lowest value of δ13CO2 was observed in RF, which was more negative than that of RW (7.63‰) and DR (5.14‰) (P<0.05). The α(CO2/CH4) values of RW and RF were 1.057 and 1.058, respectively, which were significantly lower than 1.062 in DR (P<0.05). The fac values of RF ranged from 84% to 98%, being 34%-38% and 20%-23% higher than those of RW and DR, respectively (P<0.05).

Application of thermal alkaline hydrolysis technology to improve the loading and in-vitro release of gallic acid in UiO-66.

The purpose of this study was to treat UiO-66 (University of Oslo 66) under suitable thermal alkaline hydrolysis condition to realize the loading of gallic acid. UiO-66-SH (UiO-66-separated-heating) was obtained by separated heating UiO-66 and 0.2 M KOH aqueous solution to 120 ℃ before mixing for 3 h. The material was in an amorphous state, maintained the octahedron structure and size of UiO-66. UiO-66-SH has better porosity and specific surface area than UiO-66, and had good thermal stability until heated to 1000 ℃. Furthermore, UiO-66-SH had very little influence of the cellular activity of human normal heptical cell line, demonstrating its good biocompatibility. The prepared UiO-66-SH could successfully adsorb gallic acid and control the release of gallic acid in simulated gastric fluid (∼58% vs. âˆ¼ 88% of free gallic acid). This study will be conducive to preparation of appropriate carrier used to load with polyphenolic compounds such as gallic acid.

[Response of Yield, CH4, and N2O Emissions from Paddy Fields to Long-term Elevated CO2 Concentrations].

Elevated atmospheric CO2 concentrations([CO2]e) are the main driving force of global climate change, which directly and indirectly affect carbon and nitrogen cycling in the paddy ecosystems. Therefore, understanding the response of rice yield and greenhouse gas emissions to long-term(more than 10 years)[CO2]e from paddy fields is of great significance for food security and future climate change assessment. In this study, strongly and weakly responsive cultivars were used as the experimental materials. Based on a free-air CO2 enrichment(FACE) platform continuously run for 14 years, two treatments of different[CO2] were set:a control(i.e., normal[CO2] and[CO2]a) and a 200 µmol·mol-1 higher than[CO2]a condition, ([CO2]e). CH4 and N2O emissions from the rice paddy fields were monitored in situ by static transparent chamber-gas chromatography, and grain yields were also obtained. The results showed that compared with the[CO2]a treatment, long-term[CO2]e increased grain yields of the strongly and weakly responsive cultivars by 29%-31%(P<0.05) and 12%-14%(P>0.05), and CH4 emissions of the strongly and weakly responsive cultivars were reduced by 21%-59% and 11%-54%, respectively. Furthermore, N2O emissions from the strongly and weakly responsive cultivars were significantly reduced by 70%(P<0.05) and 40%(P<0.05), respectively. The short- and long-term responses of grain yields and CH4 emissions from rice paddy fields to[CO2]e were significantly different. Specifically, with the increase in the duration of[CO2]e, the increases in rice yields and CH4 emissions significantly decreased, while the N2O emissions showed no significant changes. Therefore, under long-term[CO2]e conditions, the strongly responsive cultivar has a high potential to reduce greenhouse gas emission and increase grain yields.

[Effect of Elevated CO2 on N2O Emissions from Different Rice Cultivars in Rice Fields].

Using the free air CO2 enrichment (FACE) platform, an in-situ field experiment was conducted to explore the impacts of elevated CO2 mole fraction (x[CO2]) on N2O emissions from strongly and weakly responsive rice cultivars. Under elevated x[CO2], grain yield of the strongly responsive rice cultivars increased significantly, by more than 30%, whereas the weakly responsive cultivars showed a growth rate of 10%-15%. The four treatments comprised A-W (normal x[CO2]+weakly responsive cultivar), F-W (elevated x[CO2]+weakly responsive cultivar), A-S (normal x[CO2]+strongly responsive cultivar), and F-S (elevated x[CO2]+strongly responsive cultivar). Compared to the normal x[CO2] treatments (A-S and A-W), when the strongly and weakly responsive cultivars were exposed to elevated x[CO2](F-S and F-W), N2O emissions decreased by 52.54% (P<0.05) and 38.40% (P<0.05), rice yield increased by 22.96% (P<0.05) and 12.11% (P>0.05), and N2O emission intensity decreased by 61.68% (P<0.05) and 45.13% (P<0.05), respectively. Moreover, N2O emissions of all treatments were significantly positively correlated with NH4+-N content (P<0.05), whereas not correlated with NO2--N content. Soil temperature is an important factor affecting the N2O emissions of the strongly responsive cultivar in rice fields under elevated x[CO2] conditions. Through comprehensive consideration of climate conditions, in the future, priority should be given to planting the strongly responsive cultivar, ensuring high rice yield and significant reduction in N2O emissions.

[The Chinese medicine nutrient diet intervention prevent against the neurologic damage induce by EMF irradiation in rat hippocampus].

OBJECTIVE: To observe the neurologic damage in rat hippocampus after electromagnetic field (EMF) acute or chronic irradiation and research the protective effects of Chinese medicine diet (CMD) which comprised ferulic acid, ginsenoside, astragalus polysaccharide and rhodiola sachalinensis. METHODS: Eighty rats were divided into ten groups (n = 8): normal diet with shame irradiation group (NS), normal diet with chronic irradiation group (NCI), three groups of normal diet with acute irradiation after 3 h, 24 h, 72 h (NAI), Chinese medicine diet with shame irradiation group (CS), Chinese medicine diet with chronic irradiation group (CCI), three groups of Chinese medicine diet with acute irradiation after 3 h, 24 h, 72 h (CAI). The chronic EMF irradiation were performed by electromagnetic wave at 15 W/cm2 for 20 min everyday for 8 weeks continuously. The acute EMF irradiation were performed by electromagnetic wave at 65 W/cm2 for 20 min after feeding with CMD for 8 weeks. The learning and memory were evaluated by Morris water maze before/after electromagnetic wave irradiation. The apoptotic cells in hippocampus was detected by Tunel staining. The peroxidation damage of EMF and the protective effect of CMD intervention were assayed by measuring superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px) and reactive oxygen species (ROS). RESULTS: The acute and chronic EMF irradiation disturbed the ability of learning and memory significantly (P < 0.05), CMD intervention markedly antagonized this effect. The apoptotic cells in hippocampus increased evidently after EMF irradiation (P < 0.05), but CMD intervention reduced the apoptotic cells. The acute and chronic EMF irradiation induced the oxidative stress by down-regulating SOD activity, GSH-Px activity, ROS inhibiting and up-regulating the content of MDA obviously (P < 0.05), and CMD intervention reduced peroxidation damage significantly (P < 0.05). CONCLUSION: The acute and chronic EMF irradiation could initiate neurologic damage in hippocampus. CMD intervention has protective effect on the impaired learning and memory, the neuron apoptosis, the peroxidation damage induced by EMF irradiation. CMD intervention plays a significant protective role in antagonizing neurologic damage in the later stage of acute irradiation and chronic irradiation.

Luminol-K3Fe(CN)6 chemiluminescence system for the determination of glipizide.

A rapid and sensitive flow-injection chemiluminescence (CL) method for the determination of glipizide was developed on the basis of finding that glipizide can enhance the CL intensity of the luminol-K3Fe(CN)6 system. In optimum condition, the increased CL intensity was directly proportional to the concentration of glipizide in the range from 4.0×10-8 g/mL to 1.0×10-6 g/mL and the detection limit was 1.0×10-8 g/mL glipizide. The relative standard deviation (RSD) of the developed method was 2.1% with 11 repeated measurements of 1.0×10-7 g/mL glipizide. The developed method has been successfully applied to the analysis of glipizide in its pharmaceutical preparations.

[The injury effects of microwave exposure on visual performance and retinal ganglion cells (RGCs) in rats].

OBJECTIVE: To investigate the injury effects of microwave on the visual performance and the apoptosis of retinal ganglion cells (RGCs) in rats and the relationship between the impaired visual performance and RGCs apoptosis induced by microwave. METHODS: The visual performance of rats was observed by Electroretinogram (ERG) and Flash visual evoked potentials (F-VEP). The apoptosis of RGCs in vivo and in vitro was detected by TUNEL assay and Hoechst staining. RESULTS: Microwave exposure had no influence on ERG-a wave. The amplitude of ERG-b wave decreased significantly on the 3rd day and 7th day after microwave exposure (P < 0.01).The latency of ERG-b wave shortened significantly only at 3rd day after microwave exposure (P < 0.01). The latency of F-VEP extended markedly on the 3rd day after exposure (P < 0.05) and recovered on the 7th day after microwave exposure. The amplitude of F-VEP decreased significantly in exposure group, as compared with sham-exposure group, on the 3rd day and 7th day after microwave exposure (P < 0.05). After microwave exposure for 12 h, the apoptotic rate of RGCs in rat increased from 2.85% to 6.73%, and on the 7th day after exposure, the apoptotic rate of RGCs remained 8.93% (P < 0.05). The apoptotic rate of cultured RGCs increased from 8.42% to 13.91% at 6 hour (P < 0.05) and to 24.14% at 24 hour (P < 0.01) after microwave exposure (P < 0.05 or P < 0.01). CONCLUSION: Microwave exposure can injure the visual performance of rats, and the apoptosis of RGCs induced microwave may be one of the main pathological mechanisms.

Exposure to 2.45 GHz electromagnetic fields elicits an HSP-related stress response in rat hippocampus.

The issue of possible neurobiological effects of the electromagnetic field (EMF) exposure is highly controversial. To determine whether electromagnetic field exposure could act as an environmental stimulus capable of producing stress responses, we employed the hippocampus, a sensitive target of electromagnetic radiation, to assess the changes in its stress-related gene and protein expression after EMF exposure. Adult male Sprague-Dawley rats with body restrained were exposed to a 2.45 GHz EMF at a specific absorption rate (SAR) of 6 W/kg or sham conditions. cDNA microarray was performed to examine the changes of gene expression involved in the biological effects of electromagnetic radiation. Of 2048 candidate genes, 23 upregulated and 18 downregulated genes were identified. Of these differential expression genes, two heat shock proteins (HSP), HSP27 and HSP70, are notable because expression levels of both proteins are increased in the rat hippocampus. Result from immunocytochemistry revealed that EMF caused intensive staining for HSP27 and HSP70 in the hippocampus, especially in the pyramidal neurons of cornu ammonis 3 (CA3) and granular cells of dentate gyrus (DG). The gene and protein expression profiles of HSP27 and HSP70 were further confirmed by reverse transcription polymerase chain reaction (RT-PCR) and Western blot. Our data provide direct evidence that exposure to electromagnetic fields elicits a stress response in the rat hippocampus.

[The morphology and thickness of cornea in patients with Marfan syndrome].

OBJECTIVE: To search for the characteristics of MFS in corneal morphology and thickness. METHODS: Twenty-four patients (48 eyes) with MFS and 24 healthy age- and gender-matched volunteers (48 eyes) were recruited in this clinical prospective, and comparative series study. Firstly, biomicroscopic examination and Type-A ultrasonometry was conducted to search for ectopia lentis and axis length. Secondly, the corneal morphologic parameter [including the height of anterior and posterior surface, the centre corneal curvature, the mean astigmatism in the 3.0-mm central zone (Mean A), the mean simulated astigmatism (Sim A), the mean keratometry in the 3.0-mm central zone (Mean K), the mean simulated keratometry (Sim K), the 3.0-mm zone irregularity (3.0ZI), the 5.0-mm zone irregularity (5.0ZI), corneal thickness index (CTI)] and thickness (at the central location and at eight midperipheral locations) were obtained by the the autorefractometer and the Orbscan II Z corneal topography. Last, the statistics method including Crosstabs, One-way ANOVA, student-t test and discriminant analysis were applied and the correlations were established. RESULTS: There is no statistically significance between MFS group and control group in ages (38 ± 7) and (37 ± 8) years, gender (8/16) and (9/15), and axis length (23.12 ± 1.06) mm and (24.26 ± 2.96) mm (age χ(2) = 0.091, P = 0.763;gender t = 0.324, axis length t = 1.976, P > 0.05). Flat cornea ratio (66.7% and 12.5%) and topography of the oval (25.0% and 16.7%), irregular bow-shaped (41.7% and 37.5%) and irregular-shaped (12.5% and 8.3%) were increased significantly in patients with MFS. The corneal topography (MFS/control) showed that there are statistically significance in the thinnest thickness of cornea (489.8 ± 42.9)µm and (544.8 ± 25.7)µm, Mean K (40.60 ± 1.30) D and (42.80 ± 1.40) D, Sim K (40.50 ± 1.30) D and (42.80 ± 1.20) D, Sim A (1.08 ± 0.86)D and (0.91 ± 0.46) D, CTI 1.57 ± 0.24 and 1.21 ± 0.14, 3.0ZI (1.76 ± 0.96) D and (1.54 ± 0.82) D, and 5.0ZI (1.91 ± 1.26) D and (0.92 ± 0.68) D (thinnest thickness t = 6.996, Mean K t = 2.554, Sim K t = 3.326, Sim A t = 2.324, CTI t = 3.116, 3.0ZI t = 2.686, 5.0ZI t = 3.768, P < 0.05), while no statistically significance in the Mean A between the MFS (1.11 ± 0.89) D and control group (0.99 ± 0.49) D (Mean A t = 1.898, P = 0.08); except for temple inferior, the significant decrease of pachymetry (including the center and the seven midperipheral locations) appeared in the MFS group compared with the control group. CONCLUSION: The characteristic of MFS in corneal topography is that corneal axial refractive power descends and corneal thickness decreases.

L-carnitine protects against nickel-induced neurotoxicity by maintaining mitochondrial function in Neuro-2a cells.

Mitochondrial dysfunction is thought to be a part of the mechanism underlying nickel-induced neurotoxicity. L-carnitine (LC), a quaternary ammonium compound biosynthesized from the amino acids lysine and methionine in all mammalian species, manifests its neuroprotective effects by improving mitochondrial energetics and function. The purpose of this study was to investigate whether LC could efficiently protect against nickel-induced neurotoxicity. Here, we exposed a mouse neuroblastoma cell line (Neuro-2a) to different concentrations of nickel chloride (NiCl2) (0.25, 0.5, 1, and 2 mM) for 24 h, or to 0.5 mM and 1 mM NiCl2 for various periods (0, 3, 6, 12, or 24 h). We found that nickel significantly increased the cell viability loss and lactate dehydrogenase (LDH) release in Neuro-2a cells. In addition, nickel exposure significantly elevated reactive oxygen species (ROS) and malondialdehyde (MDA) levels, disrupted the mitochondrial membrane potential (ΔΨ(m)), reduced adenosine-5'-triphosphate (ATP) concentrations and decreased mitochondrial DNA (mtDNA) copy numbers and mtRNA transcript levels. However, all of the cytotoxicities and mitochondrial dysfunctions that were triggered by nickel were efficiently attenuated by pretreatment with LC. These protective effects of LC may be attributable to its role in maintaining mitochondrial function in nickel-treated cells. Our results suggest that LC may have great pharmacological potential in protecting against the adverse effects of nickel in the nervous system.

[Relationship between activation of microglia and Jaks phosphorylation induced by microwave irradiation].

OBJECTIVE: To explore the relationship between microglial proinflammatory and electromagnetic radiation and unveil the role of microglia in microwave radiation induced central nervous system injury. METHODS: N9 microglia cells cultured in vitro were exposed to microwave at 90 mW/cm2. Cell flow cytometry was used to observe the expression of CD11b at different time points after exposure; ELISA was used to detect the concentration of TNF-alpha in N9 cell culture supernatant; RT-PCR analysis confirmed iNOS mRNA expression in N9 microglia cells; and Nitrate Reductase Method was used to test NO amount in culture supernatant. RESULTS: The CD11b positive microglial cells increased significantly at 3 h after microwave exposure (P < 0.05), continued to increase until 24 h and peaked at 6 h after exposure. The amount of TNF-alpha rose dramatically from 1 h to 24 h after exposure (P < 0.01) and peaked at 3 h [(762.1 +/- 61.5) pg/ml] after exposure (P < 0.01). The level of NO started to increase at 1 h [(4.48-0.59) micromol/L] and lasted for 24 h after exposure. The expression of iNOS mRNA increased significantly at 1 h (P < 0.05), and tripled the original expression at 6 h after exposure, hereafter, it decreased slightly, but all were higher than the control group within 24 h after exposure. CONCLUSION: Microwave radiation could induce the activation of microglia cells. The activated microglia cells could induce microglial proinflammatory by producing large amounts of TNF-alpha, NO, etc.

[Effects of occupational microwave irradiation on heat shock protein 70 expressions in rat hippocampus].

OBJECTIVE: To study the change of heat shock protein (HSP)70 expression after exposure to occupational microwave in rats hippocampus, and explore the role of HSP70 in the mechanism of bio-effect of microwave irradiation. METHODS: The animal model was established by whole body exposures in 90, 5 W/cm(2) microwave irradiation field for 20 min in rats. Changes of the mRNA of hsp70 expressions in rat hippocampus at different time were studied by RT-PCR, and the protein change by Western blot. RESULTS: The mRNA and protein expression of hsp70 in rat hippocampus increased after 90 W/cm(2) and 5 W/cm(2) microwave irradiation for 20 min. The anal temperature and the value of SAR increased significantly. These changes were positively correlated with power and irradiation time of microwave. The results indicated that microwave irradiation led to HSP70 syntheses effectively. CONCLUSION: Microwave irradiation can obviously induce the thermal effect and activate HSP70, and initiate the endogenous protective mechanism of central nervous system.

[Effects of high power microwave exposure on cholinergic neurotrophic factors protein in rabbit retina].

OBJECTIVE: To investigate the changes of cholinergic neurotrophic factors (CNTF) protein at different time points and the distribution of CNTF in rabbit retina after exposure to high power microwave (HPM), in order to determine the changes rule of CNTF protein. METHODS: The rabbits were irradiated by HPM (peak power 90 W/cm(2)) for 15 min respectively, and then killed at 0, 3, 6, 12, 24 and 72 h after irradiation. The changes of CNTF protein were investigated by immunohistochemistry and semi-quantity analysis. RESULTS: CNTF protein was distributed in full retinal layers, special in the cell membrane and cytoplasm. HPM irradiation could immediately down-regulated CNTF protein expression at 0 h, up-regulated and arrived at peak level at 6 h (P<0.05 vs 0 h group), and then kept control level. CONCLUSION: HPM may cause acute retinal injure and change the expression of CNTF protein in rabbit retina. These effects show the time-dependent feature. These results suggest that CNTF activation plays a central role in the retinal injures induced by HPM, and supplies a therapy method by using foreign-aid CNTF to remedy the retinal injure induced by HPM.

[Effects of electromagnetic irradiation on glucocorticoid in serum and its receptor expression in rat hippocampus].

OBJECTIVE: To explore the role and mechanism of glucocorticoid (GC) in the harmful bio-effects of electromagnetic irradiation. METHODS: Rats were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. At 10 min, 30 min, 3 h, 12 h after irradiation, their learning and memory abilities were tested by Morris water maze. The levels of corticosterone (CORT) in serum were measured by radioimmunoprecipitation assay and the changes of total glucocorticoid receptor (GR) expression and GR nuclear translocation in rat hippocampus were measured by reverse transcription-polymerase chain reaction and Western blot. RESULTS: The rats had learning and memory deficits at 10 min, 30 min and 3 h after irradiation, but at 12 h had no difference from the normal control. The levels of corticosterone in serum increased significantly at 10 min, 30 min, decreased at 3 h and increased significantly compared with 12 h after irradiation. GR mRNA and total GR protein expression in rat hippocampus had no significant changes at 10 min, 30 min after irradiation. At 3 h, 12 h GR mRNA expression significantly decreased by 69%, 76% respectively and GR total protein decreased by 58%, 67% respectively. There were significant differences between the two groups and the corresponding controls (P<0.05). And compared with the control, the GR nuclear translocation increased significantly at 3 h and 12 h (P<0.05). CONCLUSION: GC may take part in the injury to learning and memory abilities after electromagnetic irradiation, and the non-genomic and genomic effects of GC may play a major role in the early and late stage, respectively.

[Differential activation of mitogen-activated protein kinase in PC 12 cells apoptosis induced by electromagnetic irradiation].

OBJECTIVE: To explore the relationship between differential activation of mitogen-activated protein kinase (MAPK) signal transduction system and apoptosis in PC12 cells induced by electromagnetic irradiation. METHODS: Cultured PC12 cells were exposed to 65 mW/cm(2) electromagnetic wave for 20 min. The PC12 cells apoptosis was detected by flow cytometry 0, 3, 12, 24 h after electromagnetic irradiation. The phosphorylations of ERK1/2, JNK and P38 MAPK were tested by Western-blot. RESULTS: Electromagnetic irradiation induced apoptosis in PC12 cells soon after irradiation. The apoptotic rate of PC12 cells increased to about 23.5% at 3 h. But compared with that at 3 h, there was no significant difference in the apoptotic rate at 12 h (P > 0.05). The apoptotic rate of PC12 cells increased sharply again at 24 h. After exposure to electromagnetic irradiation, the phosphorylations of ERK1/2 and JNK increased significantly. The increased phosphorylation of ERK1/2 lasted for 3 hours, but of JNK lasted for 12 hours, and 24 hours after irradiation. The phosphorylation of both ERK1/2 and JNK were significantly lower than that of control. The phosphorylation of P38 MAPK was always higher after electromagnetic irradiation, and there were two phosphorylation peaks at 3 h and 24 h. CONCLUSION: The electromagnetic irradiation can induce the activation of MAPK signal transduction system, and ERK1/2, JNK, P38 MAPK showed differential activation. The differential activation of MAPKs may play an important role in the apoptosis of PC12 cells induced by electromagnetic irradiation.

[Influence of electromagnetic irradiation on P450scc mRNA expression in rat testis tissues and protective effect of the shield].

OBJECTIVE: To study the influence of electromagnetic irradiation on cytochrome P450 cholesterol side chain lyase (P450scc) in adult rat testis tissues and to assess the protective effect of the copper shield. METHODS: Healthy male Wistar rats were randomized into a control group, an electromagnetic irradiation group and a wholly shielded group (with the copper shielding net). The electromagnetic irradiation group and the shielded group were set for 4 phases of 3, 6, 24 and 72 hours after irradiation, 15 rats for each phrase. The testosterone contents in the serum of the irradiated rats at 3, 6, 24 and 72 hours and in that of the controls were measured by radioimmunoassay(RIA), and so was the level of the P450scc mRNA in the testis tissues by semi-quantitative RT-PCR. And the effect of the copper shielding net on testosterone and P450scc mRNA was observed. RESULTS: The contents of testosterone and the P450scc mRNA level in the irradiated group were significantly lower than in the control rats, decreased by 83.9% and 56.9% at 3 hours (P < 0.01), 54.8% and 27.3% at 6 hours (P < 0.01), restored to normal at 24 hours, but again reduced by 60.1% and 56.1% respectively (P < 0.01). While in the shielded group, no significant change was observed either in the testosterone of the serum or in the P450scc mRNA expression in the testis tissues. CONCLUSION: Electromagnetic irradiation may affect the transcription of P450scc in adult rat Leydig cells and thereby decrease the testosterone synthesis. Whole-body shielding with the copper net may achieve satisfactory effect.

[Effects of electromagnetic radiation in metropolis environment on teenagers' electrocardiogram and blood cells].

OBJECTIVE: Our previous investigation indicated that electromagnetic radiation level of city environment in some frequency range has gotten close to national standard limits. This study is to investigate the effects of these frequency electromagnetic waves coexisted in same environment on teenagers' electrocardiogram and blood cells. METHODS: Electrocardiogram and blood cells were examined in 106 cases of teenagers by using electrocardiograph and blood counting instruments respectively. RESULTS: There were not significantly different in heart rate, P-R interphase, QRS-wave time, Q-T interphase, blood hemoglobin content and blood platelet number in teenagers between high and low electromagnetic radiation environment (P > 0.05). The total blood leucocyte number in teenagers was statistically lower in high electromagnetic radiation environment than that in low electromagnetic radiation environment (P < 0.05). With regard to classification of blood leucocyte, the blood monocyte number in 14 - 18 years old of teenagers and the blood eosinophil number in boy were significantly higher in high electromagnetic radiation environment than those in low electromagnetic radiationenvironment (P < 0.05). CONCLUSION: The electromagnetic radiation nowadays in metropolis environment may have no harmful effects on teenagers' electrocardiogram and have harmful effects on teenagers' blood leucocyte-mainly showing decreased total blood leucocyte number, increased percentages of monocyte and eosinophil number.

[Effect of microwave irradiation on neurocyte mitochondrial ultrastructure and mtTFA mRNA expression in rats cerebral cortex and hippocampus].

OBJECTIVE: To explore molecular controlling mechanism of mitochondrial injury induced by different density of microwave irradiation. METHODS: Rats were exposed to microwave irradiation for 1 hour at average power density of 3 mW/cm(2) or 30 mW/cm(2). After microwave irradiation, the changes of pathological ultrastructure of rat cerebral cortex and hippocampus were observed by electron microscope, and mitochondrial transcription factor A (mtTFA) mRNA expression level were determined by RT-PCR. RESULTS: After 3 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure and mtTFA mRNA expression level didn't significantly change in rat cerebral cortex and hippocampus. After 30 mW/cm(2) microwave irradiation for 0, 3, 24 h, mitochondrial ultrastructure obviously changed, mtTFA mRNA expression in rat hippocampus significantly increased by 67.00%, 80.00%, 30.00% respectively, and in rat cerebral cortex by 133.00%, 86.00%, 233.00% respectively. There were significant differences between the corresponding groups of hippocampus and cerebral cortex (P < 0.01). CONCLUSION: No obvious change in mitochondria was found after 3 mW/cm(2) microwave irradiation, but it was found after 30 mW/cm(2) microwave irradiation. Mitochondria injury in cerebral cortex was more severe than that in hippocampus. mtTFA mRNA may have certain regulation in mitochondrial energy metabolism.