微波辐照对免疫功能的量效反应探讨

本文以2450MHz连续波为辐照源,在质量控制条件下,进行微波急性辐照实验。微波剂量分假辐照组、0.2mw·cm~(-2)、1.0mw·cm~(-2)和5.0mw·cm~(-2)4组,每组8只小鼠,每天辐照1h,连续辐照7天。结果表明:5.0mw·cmq在本实验条件下届热效应。控制微波剂量≤1.0mw·am~(-2)的急性辐照,对机体免疫功能有一定的促进作用。微波5.0mw·cm~(-2)辐照从免疫量效反应看不够安全。     

急性微波辐照对巯基、前白蛋白和循环免疫复合物的影响

急性大强度微波辐照大白兔头部(每天2.5小时,连续10天),10mw·cm~(-2)无明显改变,一定功率密度(50、100、200mw·cm~(-2))才可能影响巯基含量致明显降低,巯基与辐照强度呈明显负相关(r=一0.95,p<0.05)。前白蛋白(PA)和循环免疫复合物(CIC)未见明显改变。     

微波辐照剂量对精子畸变与微核的影响

以≤10mW·cm~(-2)的2450MHz微波照射健康成年雄性小鼠,观察骨髓PCE微核检出率及附睾精子畸变率。急性试验5—10mW·cm~(-2)剂量组精子畸变率显著增高,相关回归分析有随剂量增大而增高的趋势。畸变各型精子中以尾折叠型为主,约占1/2。表明5—10mW·cm~(-2)微波急性辐照对精子形态学转变过程有一定影响。亚急性试验停止辐照4天后,发现精子畸形减少,与阴性组无差异。提示该剂量下微波辐照引起生殖细胞损伤属可逆性,机体的代偿修复能力对较轻的畸变在短期内可使之修复。急性、亚急性辐照后小鼠PCE微核检出率均在正常范围。表明在有效控制辐照剂量条件下,10mW·cm~(-2)微波SB不足以引起微核率的增高。从监测微波剂量对机体损伤角度探讨,微核试验不宜作为卫生标准衡量的敏感指标。     

微波引起(大鼠)体温、血清皮质酮和促甲状腺素的相关

作者用142只雄性Long-Evans大鼠分A、B两组进行微波(2.45 GHz)照射实验。A组每天照射1小时,微波功率密度(PD)为1～70mw/cm~2;B组每天照射4小时,PD为0.1～40mw/cm~2。动物间所受辐射的功率密度变动小于10%。微波平均吸收比率(SAR)是0.21±0.01(SE)w·kg~(-1)·mw~(-1)·cm~2。用放射免疫法测定促甲状腺激素(TSH),用竞争蛋白粘合物测定皮质酮(CS),体温(Tcol)则为直接测定结肠温度。实验结果表明,大鼠结肠温度随微波照射功率的增大而增加,照射时间如超过1小时,大鼠结肠温度的增加与照射微波的时间无关,A、B两组之间无区别;大鼠皮质酮亦随着照射微     

微波辐照对体液免疫功能的实验研究

本文以2450MHz连续微波为辐照源,在控制环境条件的情况下,对小鼠体液免疫功能进行了急性、亚慢性和慢性三阶段的实验研究,以揭示微波辐照对体液免疫功能作用的某些规律和特点.1 材料和方法微波辐照源为WB-74型微波电疗仪发射的2450MHz连续微波,实验在恒温、恒湿、反射系数近于零的微波暗室内进行.微波剂量分假辐照、0.2mw·cm~(-2)、1mw·cm~(-2)和5mw·cm~(-2)四个组.每组8～12只、体重18～20g的Balb/c小白鼠.每天辐照1h,连续7天(急性)、45天(亚慢性)和90天(慢性),分别于停止辐     

大强度微波对兔全血维生素C含量的影响

采用频率为2450MHz,强度为10、50、100、200mw·cm~(-2)微波辐照大白兔,每天2.5小时,前三组连续照10天,后一组照5天.10和50mw·cm~(-2)未见明显改变,100和200mw·cm~(-2)致全血维生素 C 明显升高,可作为大强度微波辐照影响评价指标之一。     

CO_2-激光辐照眼角膜的形态功能分析

实验选用42只新西兰雄性家兔,用ЛГН-703型CO_2-激光器(输出功率30W)作照射源,黄铜屏、石英板或锗反射镜和网状减弱器减弱或分散激光辐照。角膜受照斑直径为0.8 cm,辐照能量为4×10~(-2)W/cm~2。每天照射102 s共120 d,分别于辐照前、辐照第5,10,30,60,90,120 d及恢复期第30 d,用活体组织显微镜观察角膜变化,并做眼血流图检查。家免     

低功率微波致雄性小鼠生殖细胞DNA损伤作用

目的 探讨低功率微波对小鼠雄性生殖细胞DNA的损伤作用.方法 选择清洁级昆明种雄性小鼠40只,随机分为1个对照组和3个辐照组,每组10只.微波辐射源平均功密度为250μW/cm²,频率为900 MHz的连续波,全身24 h暴露.分别于照射后5,10,15 d处死小鼠,观察小鼠睾丸细胞拖尾率、尾长、尾部DNA%和Olive尾矩(OTM)等.结果 微波辐射连续照射使小鼠睾丸细胞拖尾率、尾长、尾部DNA%和OTM明显升高,照射后15 d拖尾率达45.8%,尾长、尾部DNA%和Olive尾矩分别为(33.81±16.87)μm,(33.92±20.32)%和(11.08±8.54),与对照组比较差异均有统计学意义(P<0.01).结论 连续微波辐射对雄性小鼠生殖细胞DNA有损伤作用,具有时间效应关系.     

长期低剂量微波辐射对血液的影响

不少苏联及东欧学者报导了低剂量微波可引起外周血液及造血系统的变化,而英美科学工作者大多对此持相反意见。由于低剂量微波辐射与实际职业接触密切相关,尤其是关于10mw/cm~2以下的微波辐射的生物学作用问题,存在着大量混乱和错误的报导,因而有必要进行低剂量微波辐射对血液系统影响的研究。本实验采用Wistar种雄性大鼠,体重180g,实验组与对照组各30只,实验组每天微波辐射1小时,平均功率密度为5mw/cm~2,连     

安多霖胶囊对高功率雷达微波辐照雄性SD大鼠性激素损伤的防护作用

目的探讨安多霖胶囊对高功率雷达微波辐照下雄性SD大鼠性激素的影响及防护。方法将成年雄性SD大鼠分为两组(分别进行单次微波辐照实验研究和连续微波辐照实验研究)。每组按大鼠体质量随机分为对照组、微波辐照组和药物防护组,每组10只。辐照后1 d,左心室穿刺取血,检测血液性激素水平的变化情况,对检测数据进行方差分析。结果单次微波辐照实验组:与对照组相比,辐照组促卵泡生成激素(FSH)、睾酮(T)浓度显著降低,雌二醇(E2)显著升高(P0.05),药物防护组无显著变化。连续微波辐照实验组:与对照组相比,辐照组FSH、T浓度显著降低(P0.05),E2显著升高(P0.01),药物防护组无显著变化。结论高功率雷达微波辐照能够对雄性机体的生殖系统造成一定程度的损伤,表现为使机体雄性激素浓度下降,雌性激素浓度上升。安多霖胶囊表现出对雄性机体生殖系统较好的防护效果。     

微波辐照致大鼠小胶质细胞活化与JAKs磷酸化

目的 探讨微波辐照后Janus激酶/信号转导与转录激活子途径(JAK/STAT)信号通路中JAK家族(JAKs)蛋白磷酸化水平的变化与小胶质细胞活化之间的关系。方法 以90 mW/cm²的微波一次辐照大鼠20 min,在辐照后不同时相点采用免疫组化方法检测海马脑区小胶质细胞同工凝聚素(GSA-IB4)的表达情况,采用蛋白印迹Westernr blot方法检测JAK/STAT信号通路上游分子JAKs在海马脑区蛋白磷酸化水平的变化。结果 微波辐照后3 h和24 h大鼠海马脑区小胶质细胞GSA-IB4表达明显增高:Jak1、Jak2、Jak3蛋白磷酸化水平在微波辐照后都有所升高,Jak1于辐照后即刻开始升高,12 h达到峰值,而Jak2磷酸化水平在辐照后即刻就达到峰值,并且24 h内都维持在较高水平,Jak3仅在辐照后3 h以内明显升高,72 h后所有Jak家族成员蛋白磷酸化水平恢复至正常。结论 微波辐照可明显诱导海马脑区小胶质细胞活化,JAK/STAT信号转导系统的Jak1,Jak2,Jak3磷酸化水平出现不同形式的升高,表现为差别激活,3条SAK/STAT信号通路在微波辐照致小胶质细胞活化过程可能具有不同作用。     

微波辐射对小鼠免疫功能影响

目的 研究微波辐射对小鼠免疫功能的影响。方法微波辐射后测定血清IgG浓度，T淋巴细胞，酸性α-醋酸萘酯酶（ANAE）阳性率，腹腔巨噬细胞吞噬功能，小鼠胸腺、脾脏指数。结果与对照相比。1，5mW／cm^2组IgG含量明显升高（P〈0．01），15mW／cm^2组则显著降低（P〈0．01）；各辐射组ANAE阳性率均显著降低（P〈0．01）；1mW／cm^2组吞噬率有显著提高（P〈0．05）；与对照组相比。脾脏指数在15mW／cm^2组明显下降。在辐射21d后。暴露组小鼠血清IgG浓度明显增高（P〈0．05）；微波辐射15，21d后，暴露组吞噬率、吞噬指数与对照组相比显著降低（P〈0．01）；辐射9，21d后脾脏指数较对照组显著增高（P〈0．01）。结论微波辐射对小鼠机体免疫功能具有明显的影响，表现为体液免疫、细胞免疫和非特异免疫功能的改变。微波对免疫功能的影响因微波辐射的强度和辐射时间的不同而有不同的表现。     

低频超声抗兔妊娠对胎盘组织细胞Bax mRNA、Bcl-2 mRNA的影响

目的:探讨低频超声终止妊娠的可能性并观察低频超声对兔胎盘组织细胞Bax mRNA、Bc l-2 mRNA表达的影响。方法:利用低频聚焦声束超声(353 kHz“超声终止早孕治疗机”样机)6种声强各90 s体内直接照射妊娠第10天兔胚胎,妊娠20天时观察各组胚胎死亡率;选用完全抗孕剂量(40 W/cm2×90 s)照射胚胎,照后24、48、72、96、120、168、192 h留取胎盘,原位杂交技术检测各组BaxmRNA、Bc l-2 mRNA表达情况。结果:对照组胚胎总死亡率为11.36%(30/264);照射组中声强25 W/cm2、30 W/cm2及≥35 W/cm2组的胚胎死亡率分别为24.49%(12/49)、71.15%(37/52)和100.00%(62/62、45/45、40/40、35/35)。超声辐照胚胎后24 h胎盘组织细胞表达Bax mRNA增加,96 h增加最明显,120 h表达下降,192 h恢复至对照组水平;Bc l-2 mRNA表达趋势与Bax mRNA表达相反:照射后24 h开始下降,96 h下降至最低点,120 h开始恢复,照后192 h接近对照组水平。结论:低频超声抗早孕具有潜在的可行性,低频超声辐照胚胎可诱导胎盘组织细胞Bax mRNA表达增加,Bc l-2 mRNA表达下降,从而诱导胎盘组织细胞凋亡增加,但具有一定的可复性。     

不溶性镍化合物对人肺癌A549细胞镍含量影响

目的 探讨不溶性镍化合物对细胞中镍含量的影响.方法 用不同浓度的水不溶性氧化镍(NiO)和二硫化三镍(Ni3S2)分别处理人肺癌A549细胞,用原子吸收分光光度计(AAS)检测染毒48 h后细胞内镍含量并估算其摄取率.结果 经过终浓度为0,0.5,1.0,1.5,2.0,2.5,3μg/cm²的Ni3S2处理后,平均每105个细胞中含镍量为0.002 4,0.077 1,0.015 7,0.226 8,0.475 4,0.7,0.988 2μg;终浓度为0,0.5,1.0,2.0,4.0,8.0,16μg/cm²的NiO处理后,平均每105个细胞中含镍量为0.003,0.07,0.108,0.255,0.628,1.543,6.571μg;相同浓度(0.5,1.0,2.0μg/cm²)镍颗粒物处理下,Ni3S2处理组细胞镍含量分别为(0.077 1±0.006 6,0.157 4±0.019 0,0.475 4±0.112 1)μg/105个细胞,均高于NiO处理组(0.070 1±0.003 2),(0.108 1±0.015 9),(0.255 2±0.041 5)μg/105个细胞,各剂量组间比较差异均有统计学意义(P<0.05).结论 人肺癌A549细胞对不溶性镍化合物的摄取与其染毒剂量成正比,且相同浓度下对NiS的摄取率高于NiO.     

低频超声终止妊娠的实验研究

目的探讨低频超声止孕可能性。方法低频聚焦超声(353 kHZ)6种声强直接照射妊娠第10 d兔胚胎,10 d后观察胚胎死亡率,并用免疫组化法检测胎盘组织细胞p53的变化。结果声强30 W/cm2、35 W/cm2及≥40 W/cm2组的胚胎死亡率分别为25.00%、72.88%和100%;照射后胎盘组织细胞p53表达增加,96 h升至最高点,192 h接近对照组水平。结论低频超声抗孕具有可行性,可诱导胎盘组织细胞p53表达增加,但具有可恢复性。     

Characterisation of a human sperm cell subpopulation marked by the presence of the TSH2B histone

During the process of mammalian spermiogenesis, a significant reorganisation of the chromatin structure occurs involving the sequential substitution of somatic histones with protamines. In the human sperm nucleus, approximately 15% of the basic nuclear protein complement is maintained as histones. Human testis/sperm-specific histone H2B (hTSH2B) is a variant of the histone H2B expressed exclusively in spermatogenic germline cells and present in some mature sperm cells. Thus, this protein marks a subpopulation of sperm cells in the ejaculate. Using indirect immunofluorescence, we examined the influence of hTSH2B on zona pellucida binding and sperm head decondensation in amphibian egg cell-free extract. As suggested by previous studies, we found that hTSH2B can be localised in only approximately 30% of sperm cells within a given ejaculate. We established that the presence of hTSH2B does not influence sperm zona pellucida binding capacity. Finally, we found that decondensation occurred more rapidly and to a greater extent in those cells containing hTSH2B. We propose that the presence or absence of hTSH2B within spermatozoa influences pronuclei formation and the activation of paternal genes following fertilisation and during early embryonic development.     

Effect of lonophores and Inhibitors and Uncouplers of Oxidative Phosphorylation on Sperm Respiration

The respiration rates of human, bovine and monkey spermatozoa were measured by means of O₂ electrode technique and the effect of perturbants of energy metabolism on these rates was determined. For sperm cells respiring with added substrate, addition of oligomycin, a specific inhibitor of mitochondrial ATP synthesis, followed by an uncoupler of oxidative phosphorylation gave the unperturbed rate, the slow resting rate with oligomycin, and the fastest uncoupled rate. Two indices can be calculated from these rates. One is the energy index E, the ratio of the unperturbed and oligomycin rates. The other is the respiratory control index C., the ratio of the uncoupled and oligomycin rates. A value of 4 or greater for C indicates that cell metabolism is tightly coupled to energy production. A value of E about 30% that of C indicates a high intracellular level of ATP. These indices and the uncoupled respiration rate characterize the metabolic capacity of a sperm sample and are easily obtained in a single experiment with a small volume of suspended cells. The respiration rate, induced by addition of Ca⁺² to sperm cells respiring with substrate and oligomycin, compared to the rate induced by subsequent addition of the ionophore A23187, provides a way to determine the fraction of intact cells with bovine sperm. The ease of obtaining quantitative parameters directly related to the metabolic capacity and degree of intactness of sperm cells in a semen sample by means of O₂ electrode techniques recommends its use in evaluating such samples for fertilizing capacity.     

高功率微波对大鼠血睾屏障通透性的影响及防护研究

目的探讨高功率雷达微波辐照对大鼠血睾屏障通透性的影响及防护研究。方法将成年雄性SD大鼠随机分为两大组（分别进行单次和连续微波辐照实验研究）。每大组又随机分为对照组、微波辐照组、药物防护组和物理防护组4个小组,每组10只。药物防护组大鼠在辐照前用安多霖药物灌胃。对微波辐照组、药物防护组和物理防护组大鼠进行辐照,其中物理防护组辐照盒外面套有防电磁波辐射面料。对照组大鼠行假辐照。辐照后取大鼠睾丸组织用含有硝酸镧颗粒的戊二醛固定液固定,用透射电镜观察血睾屏障通透性的变化。结果与对照组相比,辐照组的睾丸组织生精细胞间隙明显增大,发生不同程度的变性、线粒体空泡化,血睾屏障紧密连接处可见镧颗粒沉积,而在药物防护组和物理防服组,硝酸镧颗粒未穿过血睾屏障紧密连接。结论高功率雷达微波辐照能够使大鼠血睾屏障通透性显著增加,对机体产生一定程度的生殖毒性,安多霖胶囊和防电磁波辐射面料表现出了较好的防护效果。     

Chenopodium album seed extract-induced sperm cell death: exploration of a plausible pathway

BACKGROUND: This study was conducted for to explore the plausible pathway of Chenopodium album seed extract (CAE)-mediated sperm cell death. STUDY DESIGN: The role of CAE for its spermicidal action was assessed by (a) measuring lipid peroxidation, protein carbonyl content and intracellular glutathione content in CAE exposed sperm cells; (b) assaying antioxidant enzymes like catalase and superoxide dismutase (SOD); (c) analyzing protein expressions by using sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Western blot analysis; (d) fluorimetric measurement of intracellular H(2)O(2) level and generation of reactive oxygen species (ROS) in CAE-treated sperm cells; and (e) DNA ladder formation study. RESULTS: CAE-induced sperm death is due to (a) lipid peroxidation of the sperm cell membrane, oxidation of some critical cellular proteins and depletion of intracellular reduced gluthathione, indicating production of ROS; (b) activation of Mn-SOD and inactivation of catalase favoring endogenous accumulation of H(2)O(2); (c) generation of O(2)(*-) at an enhanced rate during oxidative stress as evidenced by increased Mn-SOD activity and protein expression; (d) accumulation of ROS in spermatozoa reflected in the fluorimetric experiments; and (e) increased production of O(2)(*-) and H(2)O(2) induced apoptosis-like death in sperm cells as observed by DNA ladder formation. CONCLUSION: The sperm death mediated by CAE is due to oxidative damage of cellular macromolecules by in situ generation of ROS.