Microwave Exposure Impairs Synaptic Plasticity in the Rat Hippocampus and PC12 Cells through Over-activation of the NMDA Receptor Signaling Pathway

Objective The aim of this study is to investigate whether microwave exposure would affect the N-methyl-D-aspartate receptor (NMDAR) signaling pathway to establish whether this plays a role in synaptic plasticity impairment.
Methods 48 male Wistar rats were exposed to 30 mW/cm2 microwave for 10 min every other day for three times. Hippocampal structure was observed through H&E staining and transmission electron microscope. PC12 cells were exposed to 30 mW/cm2 microwave for 5 min and the synapse morphology was visualized with scanning electron microscope and atomic force microscope. The release of amino acid neurotransmitters and calcium influx were detected. The expressions of several key NMDAR signaling molecules were evaluated.
Results Microwave exposure caused injury in rat hippocampal structure and PC12 cells, especially the structure and quantity of synapses. The ratio of glutamic acid and gamma-aminobutyric acid neurotransmitters was increased and the intracellular calcium level was elevated in PC12 cells. A significant change in NMDAR subunits (NR1, NR2A, and NR2B) and related signaling molecules (Ca2+/calmodulin-dependent kinase II gamma and phosphorylated cAMP-response element binding protein) were examined.
Conclusion 30 mW/cm2 microwave exposure resulted in alterations of synaptic structure, amino acid neurotransmitter release and calcium influx. NMDAR signaling molecules were closely associated with impaired synaptic plasticity.     

葡萄糖干预对电磁辐射所致大鼠学习记忆功能障碍的影响

目的观察平均功率密度为30 mW/cm2的连续微波辐射对大鼠学习记忆功能和海马葡萄糖摄取(glucose uptake)的影响及葡萄糖干预作用。方法成年雄性SD大鼠48只,其中18只用于Morris水迷宫实验,分为对照组、暴露组、葡萄糖干预暴露组,每组6只;暴露组、葡萄糖干预暴露组接受平均功率密度30 mW/cm2的微波连续暴露28 d,每天20 m in,暴露结束后Morris水迷宫检测大鼠学习记忆功能变化,Morris水迷宫训练前30 m in,葡萄糖干预暴露组大鼠按500 mg/kg腹腔注射葡萄糖,对照组和暴露组腹腔注射生理盐水。另30只用于海马葡萄糖摄取实验,分为对照组,暴露7、14、21、28 d组,每组6只,分别接受0、7、14、21、28 d平均功率密度为30 mW/cm2的微波暴露,各组暴露期满后,液体闪烁计数法检测大鼠海马组织对3H-2脱氧葡萄糖(3H-2DG)的摄取量变化。结果平均功率密度为30 mW/cm2的微波连续暴露28 d后,暴露组大鼠第4、5、6、7天逃避潜伏期较对照组延长(P<0.05),葡萄糖干预暴露组大鼠逃避潜伏期较对照组差异无显著性(P>0.05);暴露组大鼠在目标象限停留时间[(18.66±2.77)s]和跨越虚拟平台次数(1.60±0.54)均较对照组[(30.75±8.02)s,(2.80±0.83)]下降(P<0.05),葡萄糖干预暴露组大鼠目标象限停留时间[(26.84±4.75)s]和跨越虚拟平台次数(3.20±1.03)较对照组无显著性差异(P>0.05)。微波暴露21 d组和28 d组大鼠海马对3H-2-D-G lu-cose摄取量[(3 959±390),(3 764±192)]较对照组(5 284±711)显著减少(P<0.05)。结论腹腔注射葡萄糖可以改善微波暴露引起的学习记忆功能障碍,海马葡萄糖摄取减少可能是电磁辐射致学习记忆功能障碍的重要因素。     

1800MHz电磁波出生前暴露对大鼠海马NCAM表达的影响

目的了解1 800 MHz电磁波出生前暴露对大鼠海马NCAM表达的影响.方法 7周龄SD雌性大鼠32只,雄性16只,适应环境1周后以雌：雄=2：1交配,受孕后雌鼠随机分为四组（两个实验组和两个对照组）;实验组采用1 800 MHz射频电磁波对大鼠于孕0～20 d进行21 d连续全身暴露,每天12 h,功率密度为0.5 mW/cm2和1.0 mW/cm2,各实验组分别设置虚拟暴露作为对照组.暴露期间的温度、湿度、背景噪声等环境条件稳定.暴露完成后在F1代子鼠长至3周龄和7周龄,每组随机抽取8只子鼠采用免疫组织化学方法分别对海马NCAM进行染色,然后采用图像分析系统分析海马CA1、CA3和DG区（齿状回）NCAM的表达.结果 1.0 mW/cm2暴露组未发现对3周龄、7周龄F1代大鼠海马各区NCAM表达有影响,其表达与对照组无统计学意义;0.5 mW/cm2暴露组3周龄F1代大鼠海马各区NCAM表达和对照组差异无统计学意义（P〉0.05）,0.5mW/cm2暴露组7周龄F1代大鼠海马各区NCAM表达出现了下调,其表达与对照组相比有统计学意义（P〈0.05）.结论 1 800 MHz功率密度0.5 mW/cm2电磁波出生前暴露使7周龄大鼠NCAM在海马各区表达下调.     

脉冲微波对大鼠胚胎发育及其后天学习记忆功能的影响

目的观察Ｘ波段脉冲波的胚胎发育生物学效应。方法以功率密度５～４０ｍＷ／ｃｍ２的脉冲微波对孕鼠进行孕期慢性辐照（孕６～１６日隔日一次,每次２０分钟）,研究足月胎鼠一般生长发育指标、畸形学指标及后天记忆行为学指标变化。结果４０ｍＷ／ｃｍ２对孕鼠有明显的升温效应,并对胚胎和胎鼠生长发育及其后天的学习记忆功能有明显影响和表现出一定的致畸性;２０ｍＷ／ｃｍ２只有轻微的升温效应,１０ｍＷ／ｃｍ２以下无升温作用,两者均不致畸但亦影响胎鼠后天的学习记忆功能;５ｍＷ／ｃｍ２剂量无上述作用。结论热效应是主要的致畸因素,非热或微热功率的脉冲微波孕期辐照主要影响胎鼠脑功能发育。     

Changes in gap junctional intercellular communication in rabbits lens epithelial cells induced by low power density microwave radiation

Objective To demonstrate the changes in gap junctional intercellular communication (GJIC) mediated by low power density microwave radiation in rabbits lens epithelial cells (LECs) and its mechanisms.Methods Rabbits’ eyes were exposed to 5 mW/cm(2) and 10 mW/cm(2) power densities of microwave radiation for 3 hours. The fluorescence-recovery-after-photobleaching (FRAP) method was used to determine the GJIC. The localization and function of connexin 43 in LECs was detected by laser scanning confocal microscopy.Results The GJIC of rabbits LECs was inhibited by microwave radiation especially in the 10 mW/cm(2) irradiated samples. A decrease in connexin 43-positive staining was seen in 5 mW/cm(2)×3 h treated LECs. Intracellular space accumulation and cytoplasmic internalization were clearly demonstrated in 10 mW/cm(2) group.Conclusions Low power densities microwave radiation (5 mW/cm(2) and 10 mW/cm(2)) induces damage to connexin 43 and inhibits the GJIC of rabbits LECs. These changes result in an osmotic imbalance within the lens and induce early cataract. 5 mW/cm(2) or 10 mW/cm(2) microwave radiation is cataractogenic.     

电磁辐射对大鼠海马NMDA受体NR1亚单位蛋白及其mRNA表达的影响

目的 探讨2000 μW/cm2电磁辐射对大鼠海马N-甲基-D-门冬氨酸(NMDA)受体NR1亚单位蛋白及其mRNA水平表达的影响,揭示电磁辐射对大鼠学习记忆功能的损伤机制.方法 实验分为空白对照组,假辐射组,1 h/d、2h/d、3 h/d辐射组.将辐射组大鼠固定体位,头部接受功率密度为2000μW/cm2的近场辐射,连续辐射30d.通过Morris水迷宫检测大鼠的空间学习记忆能力,采用免疫组化法和Western-Blot法检测大鼠海马组织NR1蛋白表达的变化,RT-PCR法检测大鼠海马组织NR1 mRNA表达的变化.结果 各辐射组大鼠在水迷宫检测第4天寻找安全平台的逃避潜伏期分别为1 h/d[(12.29±1.36)s]、2 h/d[(17.99±2.25)s]、3 h/d[(24.66±5.56)s],均明显长于空白对照组[(8.8±1.66)s](P＜0.05);1 h/d、2 h/d和3 h/d辐射组大鼠海马神经元均排列紊乱,NR1阳性细胞比率明显低于空白对照组,海马组织NR1蛋白[分别为(0.122±0.026)、(0.102±0.023)、(0.060±0.009)]及其mRNA[分别为(0.46±0.07)、(0.35±0.05)、(0.12±0.02)]表达水平较空白对照组[(10.70±0.11)、(0.68±0.11)]均明显降低(P＜0.05).而假辐射组大鼠各项指标与空白对照组相比均无显著差异(P＞0.05).结论 2000μW/cm2电磁辐射可导致大鼠学习记忆功能下降,其机制可能与大鼠海马组织NR1蛋白及其mRNA的表达降低有关.

Abstract：

Objective To evaluate the effects of electromagnetic irradiation of 2000 μW/cm2 exposure on mRNA and protein expression levels of immunoreactive protein and mRNA of NMDAR1 in rats hippocampal,and to explore the impaired mechanism of electromagnetic irradiation on learning and memory.Methods Rats were randomly divided into normal control group, sham-radiated group, and 1 h/d, 2 h/d, and 3 h/d radiation groups.The rats in the radiation groups were fixed and recieved microwave exposure of 2000 μW/cm2, then their learning and memory abilities were tested by Morris water maze experiment, the change of NR1 protein in hippocampal neurons of each group of rats was measured with immunohistochmistry and western blot techniques, and the expression of NR1 mRNA in hippocampus was determined by RT-PCR.Results In the water maze test,compared with the normal control group (8.8 ± 1.66 ), the escape latency of three radiated groups rats ( 1 h/d ( 12.29 ±1.36) s,2 h/d ( 17.99 ±2.25) s,and 3 h/d (24.66 ±5.56) s) were significantly longer (P＜0.05).In the radiation group,the hippocampal neurons of rats showed evident reduction in the ratio of NR1 positive cells,irregular,and arrayed in disorder.Moreover,compared with the normal control group ( (0.70 ±0.11 ), (0.68 ±0.11 ) ) ,the expession of NR1 protein ( 1 h/d (0.122 ±0.026) ,2 h/d (0.102 ±0.023) ,and 3 h/d (0.060 ± 0.009) ) and its mRNA ( 1 h/d (0.46 ±0.07) ,2 h/d (0.35 ±0.05) ,and 3 h/d (0.12 ±0.02) ) in hippocampal neurons was significantly decreased (P＜0.05).Among the indicators, there was no significant difference between sham-radiated group and normal control group.Conclusions Electromagnetic irradiation of 2000 μW/cm2 exposure can impair the learning and memory abilities of rats possibly through a mechanism correlated with the lower expression of NR1 protein and its mRNA in hippocampus.     

电磁辐射对大鼠海马神经元钙调蛋白激酶Ⅱ和环磷腺苷反应元件结合蛋白表达的影响

目的探讨2000μW／cm2电磁辐射后钙调蛋白激酶Ⅱ（CaMKⅡ）和环磷腺苷反应元件结合蛋白（CREB）在元代培养海马神经元中表达的变化和意义。方法体外培养新生大鼠大脑海马神经元,实验分为空白对照组,假辐射组和1h／d、2h／d、3h／d辐射组。辐射组接受功率密度为2000μW／cm。的近场辐射,连续辐射5d。采用Western—Blot法检测海马神经元CaMKII和CREB蛋白的表达,RT—PCR法检测CaMKII和CREBmRNA表达的变化。结果电磁辐射后,1h／d、2h／d、3h／d辐射组大鼠海马神经元CaMKⅡ蛋白[分别为（0．59±0．05）、（0．44±0．08）、（0．18±0．04）]及其mRNA[分别为（0．41±0．08）、（0．34±0．04）、（0．24±0．02）]表达水平较空白对照组[（0．78±0．07）、（0．62±0．12）]明显降低（P〈0．05）;CREB蛋白[分别为（0．49±0．05）、（0．40±0．04）、（0．17±0．03）]及其mRNA[分别为（0．68±0．11）、（0．53±0．08）、（0．30±0．03）]表达水平较空白对照组[（0．69±0．10）、（0．80±0．12）]明显降低（P〈0．05）。结论海马神经元CaMKⅡ和CREB的表达变化可能参与了电磁辐射致大鼠学习记忆功能改变的病理生理过程。     

微波对大鼠脾脏超微结构的影响

用功率密度10mW/cm~2、20mW/cm~2和40mW/cm~2的微波,全身1次照射大鼠,见到各实验组淋巴细胞显示不同程度的变性和坏死。其中40mW/cin~2组尤甚。淋巴细胞多趋退变坏死,核质外溢,胞质溶解等。浆细胞各实验组也有不同程度的变化,尤以40mW/cm~2组更明显,核变形,异染色质普遍浓缩,分布异常,核膜局部缺失,粗面内质网扩大。网状细胞10mW/cm~2组变化不明显,20mW/Cm~2和40mW/cm~2组可见核变形,线粒体肿胀,嵴溶解或局部空化等。实验表明一定功率密度的微波对大鼠脾脏超微结构有一定影响。     

低强度微波辐射对小鼠NK细胞活性的影响

目的观察低强度微波辐射对小鼠NK细胞活性的影响。方法小鼠脾细胞体外经不同强度微波直接辐射不同时间后,用LDH法测定小鼠NK细胞的活性,并用MTT法测定脾细胞的生长代谢。结果①4种不同强度的微波(0.05mW/cm     

微波辐照对鼠脑MDA、NOS含量和LDH活性的影响

为研究手机微波对小鼠脑是否有损害 ,选用 4种不同频率和不同发射功率的微波照射小鼠 ,用TBA比色法、二硝基苯肼显色法 (DNPH显色法 )和吩嗪二甲脂比色法 (PMS显色法 )检测小鼠脑组织中脂质过氧化产物丙二醛(MDA)、乳酸脱氢酶 (LDH)和一氧化氮合酶 (NOS)。统计学分析显示 :2 45 0MHz微波辐射后MDA含量升高 (P <0 .0 0 1 ) ,LDH活性降低 (P <0 .0 5 ) ,NOS不变 (P >0 .0 5 ) ;870、45 0和 45MHz微波分别辐照后 ,MDA含量和LDH活性均变化不大 (P >0 .0 5 )。提示 :在强辐照条件下 (2 45 0MHz) ,微波通过使脑中自由基产生过量参与脑损伤 ;而在手机弱辐照条件下 (870、45 0、45MHz) ,微波辐照对脑基本无损伤 ,手机使用是安全的     

1 800 MHz射频电磁场暴露对大鼠海马GFAP、NCAM和GABA受体表达的影响

  目的  探究1800 MHz射频电磁场对大鼠的体重和海马体胶原纤维酸性蛋白（GFAP）、神经细胞黏附分子（NCBA）和γ-氨基丁酸（GABA）受体表达的影响。  方法  购买SD大鼠14只,分为暴露组和对照组,暴露组雌雄比例3∶4,对照组雌雄比例4∶3。暴露频率1800 MHz,强度0.5 mW/cm2。全身暴露3周,每天12 h（20:00～08:00）。暴露结束后,对2组老鼠分别称重。应用免疫组织化学技术对大鼠海马组织切片GFAP、NCBA、GABA受体进行染色,并测定GFAP、NCBA和GABA受体在海马CA1、CA3和DG区的表达变化。  结果  暴露组与对照组体重指标无明显不同（P > 0.05）;暴露组海马CA1区、DG区GFAP的表达下降（P < 0.05）,其他各组比较无明显不同（P > 0.05）。  结论  在1800 MHz,0.5 mW/cm2射频电磁场使SD大鼠暴露3周,大鼠海马CA1和DG区GFAP表达下降,可能对某些脑部疾病有所影响。     

电磁辐射对小鼠免疫功能的抑制作用

目的：研究电磁辐射对小鼠免疫功能的影响。方法：288只BALB／c小鼠随机分为4组,分别接受频率为2856MHz、辐射剂量依次为0mW／cm^2、5mW／cm^2、10mW／cm^2、20mW／cm^2的辐射,辐射时间均为10min×6／d,连续照射5d。于照射后1h、1d、3d、7d、15d、30d检测外周血细胞计数、外周血T细胞亚群（CIM、CD8）、胸腺指数。结果：照射组在所有检测时间点与对照组（0mW／cm^2）相比白细胞计数及淋巴细胞计数均下降、CD4^＋／CD8^＋比值升高、胸腺指数下降（P〈0．05）,至检测后期差异尤为显著,且免疫抑制作用随照射剂量增大而增强。结论：电磁辐射能抑制小鼠的免疫功能,且随着功率密度增大而抑制作用增强。     

Microwave-induced Apoptosis and Cytotoxicity of NK Cells through ERK1/2 Signaling

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

慢性持续高剂量电磁辐射对小鼠外周血象的长期影响

目的通过研究慢性持续高剂量电磁辐射对小鼠外周血细胞变化的影响,探讨慢性持续高剂量电磁辐射对小鼠外周血象的长期影响。方法采用随机、平行对照分组法,将30只雄性Babl／c小鼠分为正常对照组（0mW／cm。）、辐射组（10mW／cm2）、环磷酰胺给药（CTX组）,每组10只。辐射组动物予以30min／d,持续20个工作日,功率密度为10mW／cm2电磁辐射;CTX组在小鼠开始辐照的时间点给药,每3d给药一次,每次每只30mg／kg,共7次;各组于辐照结束后30,45,60,75,90,105d和120d分别采集尾静脉血,应用全自动细胞分析仪检测外周血中红细胞、白细胞、血小板、血红蛋白、中性粒细胞等数量的变化。结果经持续高剂量电磁辐射后,与正常对照组相比,辐射组白细胞数量显著减少（P〈0．05）;辐射组红细胞数量于照射后60—90d开始显著上升（P〈0．05）;外周血血小板数量于照射后30—45d明显上升,结果有统计学意义。辐射组小鼠外周血免疫细胞及中性粒细胞的数量均低于正常对照组。辐照组血象各指标的变化情况与环磷酰胺给药组（CTX组）变化趋势一致。结论慢性持续大剂量电磁辐射可导致小鼠免疫系统的损伤,造成小鼠机体的炎症反应,通过检测外周血象各项指标峦化可了解辐射后生物机体的龟疫状杰。     

Low power density microwave radiation induced early changes in rabbit lens epithelial cells

Objective To determine whether low power density microwave radiation can induce irreversib le changes in rabbit lens epithelial cells (LECs) and the mechanisms of the chan ges.Methods One eye of each rabbit was exposed to 5 mW/cm(2) or 10 mW/cm(2) power density microwaves for 3 hours, while the contralateral eye served as a control. Annex in Ⅴ-propidium iodide (PI) two-color flow cytometry (FCM) was used to detect the early changes in rabbit lens epithelial cells after radiation.Results Lots of rabbit LECs were in the initial phase of apoptosis in the 5 mW/cm(2) mi crowave radiation group. A large number of cells became secondary necrotic cell s, and severe damage could be found in the group exposed to 10 mW/cm(2) microwa ve radiation. Conclusion Low power densities of microwave radiation (5 mW/cm(2) and 10 mW/cm(2)) ca n induce irreversible damage to rabbit LECs. This may be the non-thermal effec t of microwave radiation.     

孕哺期铅暴露对仔鼠学习记忆能力及海马组织中P-JNK表达的影响

目的:研究孕哺期铅暴露对仔鼠学习记忆能力及海马组织中磷酸化JNK蛋白(P-JNK)表达的影响。方法:0.3(低剂量铅暴露)、1.0(中剂量铅暴露)和3.0(高剂量铅暴露)g/L醋酸铅溶液以自由饮水方式对母鼠孕哺期染毒,每组10只,并设未染毒对照组。每组取10只仔鼠用于实验,仔鼠出生第21天用水迷宫实验检测其学习记忆能力,并检测其血液和海马组织中铅的含量,采用Western Blot法测定其海马组织中P-JNK蛋白的表达水平。结果:迷宫实验中,各组仔鼠错误次数和平均逃避潜伏期时间比较,差异有统计学意义(F=302.475和26.902,P<0.001);组间两两比较,差异均有统计学意义(P<0.05)。各组仔鼠血及海马组织铅水平比较,差异有统计学意义(F=53.139和9.392,P=0.003和0.001),组间两两比较,差异均有统计学意义(P<0.05)。各组仔鼠海马组织中P-JNK蛋白表达比较,差异有统计学意义(F=67.103,P<0.001),各剂量铅暴露组P-JNK蛋白的表达明显高于对照组(P<0.05)。结论:铅经血脑屏障,可能通过上调海马中JNK磷酸化水平并激活其信号传导通路,造成子代神经系统的损伤,从而影响学习记忆功能。     

Effect of Chronic Noise Exposure on Expression of N-Methyl-D-Aspartic Acid Receptor 2B and Tau Phosphorylation in Hippocampus of Rats

Objective To study the effect of chronic noise exposure on expression of N-methyl-D-aspartic acid receptor 2B (NR2B) and tau phosphorylation in hippocampus of rats. Methods Twenty-four male SD rats were divided in control group and chronic noise exposure group. NR2B expression and tau phosphorylation in hippocampus of rats were detected after chronic noise exposure (100 dB SPL white noise, 4 h/d×30d) and their mechanisms underlying neuronal apoptosis in hippocampus of rats with TUNEL staining. Results The NR2B expression decreased significantly after chronic noise exposure which resulted in tau hyperphosphorylation and neural apoptosis in hippocampus of rats. Immunohistochemistry showed that the tau hyperphosphorylation was most prominent in dentate gyrus (DG) and CA1 region of rat hippocampus. Conclusion The abnormality of neurotransmitter system, especially Glu and NR2B containing NMDA receptor, and tau hyperphosphorylation in hippocampus of rats, may play a role in chronic noise-induced neural apoptosis and cognition impairment.     

微波对内耳及眼,脑影响的实验研究

采用频率９３７０ＭＨｚ微波脉冲式输出，在不同的平均功率密度辐射下对豚鼠进行耳部照射，观察内耳功能与形态学改变及邻近眼球和脑组织的形态学变化。辐射强度为８９２ｍＷ／ｃｍ＾２和１９１７ｍＷ／ｃｍ＾２时未造成内耳、眼球及脑的损害。     

孕期及哺乳期铅暴露对仔代大鼠学习记忆能力的影响及其机制

目的：探讨孕期及哺乳期铅暴露对仔代大鼠学习记忆能力和海马组织c-fos蛋白及小清蛋白（PV）表达的影响,阐明铅对仔代大鼠神经系统发育期记忆功能损害的可能机制。方法：8只孕期Wistar雌性大鼠随机分为对照组和低、中及高剂量铅暴露组。低、中和高剂量铅暴露组大鼠分别给予含0.05%、0.10%和0.20%醋酸铅的去离子水,对照组大鼠饮用去离子水。仔代大鼠出生10d后,采用Morris水迷宫法检测各仔代大鼠的学习记忆能力,原子吸收光谱法检测各组仔代大鼠血液和海马组织中铅质量浓度,生化方法测定各组仔代大鼠海马组织中一氧化氮（NO）水平和一氧化氮合酶（NOS）活性,蛋白免疫印迹法检测各组仔代大鼠海马组织中c-fos和PV蛋白表达水平,Pearson相关分析法分析仔代大鼠海马组织中c-fos和PV蛋白表达水平与学习能力指标、海马组织中NO水平及NOS活性的相关性。结果：定位航行实验,与对照组比较,中和高剂量铅暴露组仔代大鼠平均逃避潜伏期和游泳距离明显增加（P<0.05）。空间探索实验,与对照组比较,中和高剂量铅暴露组仔代大鼠目标象限停留时间和穿越次数明显减少（P<0.05）。各组仔代大鼠血液和海马组织中铅质量浓度比较差异有统计学意义（F=176.44,P<0.01;F=37.37,P<0.01）;与对照组比较,不同剂量铅暴露组仔代大鼠血液和海马组织中铅质量浓度明显升高（P<0.05）。各组仔代大鼠海马组织中NO水平和NOS活力比较差异有统计学意义（F=4.105,P<0.05;F=3.443,P<0.05）;与对照组比较,高剂量铅暴露组NO水平和NOS活力明显下降（P<0.05）。与对照组比较,不同剂量铅暴露组仔代大鼠海马组织中c-fos蛋白表达水平明显降低（P<0.05）,中和高染铅暴露组仔代大鼠海马组织中PV蛋白表达水平明显升高（P<0.05）。Pearson相关分析法,仔代大鼠海马组织中c-fos蛋白表达水平与水迷宫实验中学习能力指标、海马组织中NO水平和NOS活性呈正相关关系（P<0.01）,PV蛋白表达水平与水迷宫实验中学习能力指标、海马组织中NO水平和NOS活性呈负相关关系（P<0.01）。结论：孕期及哺乳期铅暴露可损伤仔代大鼠的学习记忆能力,其毒性作用机制可能与海马组织中c-fos蛋白表达水平降低和PV蛋白表达水平升高有关。     

抗氧化营养素对电磁辐射致大鼠肝损伤的防护效果

目的研究抗氧化微量营养素硒、锌、维生素E、维生素C对电磁辐射致大鼠肝损伤的保护作用。方法幼年Wistar大鼠80只,按性别和体质量分别喂养普通饲料和添加抗氧化营养素的营养饲料,并分别分为对照组、慢性辐照组、急性辐照组3 h、急性辐照组24 h、急性辐照组72 h。检测肝组织细胞凋亡率、丙二醛(MDA)、超氧化物歧化酶(SOD)、羟自由基(ROS)、谷胱甘肽过氧化物酶(GSH-Px)。结果电磁辐射急慢性辐照均能引起各组大鼠肝脏细胞凋亡率增加(P<0.01),而营养干预可以显著减少细胞凋亡发生(P<0.05)。并且电磁辐射急慢性辐照后各组大鼠肝脏SOD活性、GSH-Px活性、抑制ROS能力明显下降(P<0.05,P<0.01),MDA含量明显增加(P<0.05,P<0.01);而营养干预在电磁辐射急性辐照后期(辐照后24、72 h)以及慢性辐照时能够显著增加SOD、GSH-Px活性(P<0.05),降低MDA含量,有效促进抑制ROS能力的恢复(P<0.05)。结论电磁辐射急慢性辐照均导致大鼠肝组织过氧化损伤;抗氧化营养素干预能促进电磁辐射急性辐照后期及慢性辐照后大鼠肝组织损伤的恢复。