50Hz低频环境磁场对细胞增殖的影响及其机理探讨

本文以细胞株LO2(人肝细胞)和CHL(中国仓鼠肺成纤维细胞)为研究对象，用50Hz正弦磁场以不同强度、不同时间作用于细胞。长时间作用后，2种细胞的增殖均受到抑制，但抑制程度与磁场作用量并非呈简单的线性关系；磁场短时间作用对细胞增殖无明显影响，但细胞膜的流动性变差，在磁场撤去后膜的流动性又有所恢复。这一现象说明，低频弱磁场引起宏观生物效应需要时间的积累。同时观察到磁场短时间作用导致的CHL细胞上表皮生长因子受体(EGFR)的聚集，这可能是低频弱磁场引起宏观生物效应的一种机制。     

纳米乳化油修复地下水硝酸盐过程中产气及微生物增殖代谢对多孔介质堵塞的模拟评估

为有效评估纳米乳化油原位处理地下水硝酸盐过程中,产气及微生物增殖代谢对含水层多孔介质的堵塞作用,以纳米乳化油为碳源,采用市售反硝化菌剂接种微生物进行硝酸盐降解批实验研究,探讨产气及微生物增殖代谢的动态变化及特征,并基于Kozeny-Carman(K-C)方程、Clement、Pham及Kozeny Grain(KG)模型,对假定含水层一维流模拟柱,预估产气及微生物增殖代谢造成的渗透性损失,识别堵塞过程及主导因素.结果显示,反硝化菌降解效果良好,硝氮总去除率达90.23%.CO_2及N_2为主要产气成分,降解1 mg硝氮对应的平均CO_2产气量为0.71 mL,平均N_2产气量为0.14 mL;微生物代谢产物胞外聚合物以蛋白质及多糖为主,降解1 mg硝氮平均蛋白产量为0.64 mg,平均多糖产量为0.16 mg.在含水层不与外界交换气体的假设前提下,K-C方程预测显示产气可在2个周期内造成渗透性完全损失,Clement、Pham及KG模型评估的微生物增殖代谢造成中、细砂渗透性损失分别为10.87%～31.10%、12.77%～48.32%,分析认为初期细胞生物量是导致渗透性骤降的关键因素,后期为细胞生物量和胞外聚合物共同作用.此外,封闭体系中产气是堵塞的主导因素,随着含水层开启程度增加,产气的贡献占比会下降,微生物的贡献占比提高.因此,对于相对封闭的含水层系统,探索增强其开放状况是缓解堵塞的有效途径之一.     

大气颗粒物对小鼠淋巴细胞的免疫毒性研究

采用大气颗粒物提取液观察对小鼠淋巴细胞免疫功能的影响，结果表明，各浓度的颗粒物液均能抑制小鼠淋巴细胞增殖反应，其中５ｍｇ／ｍＬ浓度的抑制效果最显著，脾淋巴细胞ＩＬ－２的诱生也受各浓度颗粒物液的抑制，以１０ｍｇ／ｍＬ组抑制效果最明显。     

Prenatal testing for inherited immune deficiencies by fetal blood sampling

We attempted to develop a prenatal diagnosis in fetuses at risk for immunodeficiency by fetal blood sampling performed under fetoscopy at 18–22 weeks of gestation. In order to obtain normal values, we first investigated thirty-five control fetuses whose blood punctures were undertaken for the diagnosis of haemoglobinopathies. Surface markers and in vitro mitogen-induced proliferation of the fetal lymphocytes were studied using micromethods. We then examined two fetuses at risk for two different types of severe combined immunodeficiency and established their immunological integrity, hence avoiding an unjustified termination of pregnancy. This immunological integrity was confirmed after birth.     

毛兰素诱导结肠癌SW480细胞凋亡的分子机制

毛兰素是名贵中药材石斛的活性化合物之一,研究了其对人结肠癌SW480细胞的增殖抑制作用及其诱导的细胞凋亡分子机制.实验表明,毛兰素能显著抑制结肠癌SW480细胞的增殖,且随着药物浓度与时间增加,抑制率呈明显的剂量时间效应,48 h半数抑制浓度IC50为24.5 nmol/L;毛兰素能显著诱导结肠癌SW480细胞凋亡,并诱导细胞周期阻滞于G2-M期;分子机制研究显示,毛兰素通过下调XIAP、Bcl-xL蛋白表达以及激活Caspase-9、Caspase-7、Caspase-3和PARP活性从而诱导SW480细胞凋亡.结果表明毛兰素可能对结肠癌的防治具有潜在药用价值.图6参17     

Effects of lead on calmodulin content,proliferation and interleukin-2 in lymphocytes of mice

The mechanism inderlying lead (Pb)-induced toxicity was presumed to involve interaction between Pb²⁺ and calcium (Ca²⁺) associated with calmodulin-dependent systems. The aim of this study was to (1) examine the hypothesis that Pb alters calmodulin content and (2) assess the effects of Pb on proliferation and interleukin-2 (IL-2) levels in lymphocytes. The influence of Pb on calmodulin content in mouse lymphocytes was assessed by western blot, while the proliferation of lymphocytes was studied using MTT test, and IL-2 level by ELISA assay. The results showed that 100?µM PbCl₂ decreased calmodulin content, phytohemagglutinin (PHA)-induced proliferation, and IL-2 levels, but a lower concentration (1?µM PbCl₂) did not appear to be effective. Evidence indicates that IL-2 levels and lymphocyte proliferation might not be calmodulin content dependent. Our data suggested that Pb²⁺-induced toxicity was likely to be complex with multiple factors involved, including calmodulin, IL-2, and proliferation of lymphocytes.     

Effects of methyl-, phenyl-, ethylmercury and mercurychlorid on immune cells of harbor seals （Phoca vitulina）

Mercury (Hg) is present in the marine environment as a natural metal often enhanced through human activities. Depending on its chemical form, Hg can cause a wide range of immunotoxic e ects. In this study, the influence of methyl-, ethyl- and phenylmercury as well as mercurychloride on immune functions was evaluated. Two parameters of cellular immunity, proliferation and mRNA cytokine expression of interleukin-2, -4, and transforming growth factor , were investigated in harbor seal lymphocytes after in vitro exposure to Hg compounds. While all Hg compounds had a suppressive e ect on proliferation, di erences between juvenile and adult seals were found. Lymphocytes from juveniles showed a higher susceptibility to the toxic e ect compared to lymphocytes from adults. Furthermore, the degree of inhibition of proliferation varied among the four Hg compounds. The organic compounds seem to be more immunotoxic than the inorganic compound. Finally, for the cytokine expression of methylmercury-incubated lymphocytes, timedependent changes were observed, but no dose-dependency was found. Marine mammals of the North Sea are burdened with Hg, and lymphocytes of harbor seals may be functionally impaired by this metal. The present in vitro study provides baseline information for future studies on the immunotoxic e ects of Hg on cellular immunity of harbor seals.     

两种内分泌干扰物对鲫鱼淋巴细胞活性与功能的影响

从鲫鱼的血样中分离淋巴细胞,以内分泌干扰物甲草胺和莠去津染毒,体外培养48 h,采用四甲基偶氮唑盐(MTT)比色法测定两种除草剂对淋巴细胞生长活性的影响,并进行淋巴细胞的增殖实验,确定植物血凝素(PHA)刺激淋巴细胞增殖的适宜浓度,在此基础上开展两种除草剂对鲫鱼淋巴细胞增殖影响的研究.结果表明,甲草胺和莠去津对鲫鱼淋巴细胞生长活性的影响呈剂量-效应关系,其半数抑制浓度(IC50)分别为(27.7±7.6)、(97.6±26.4)μg/L;PHA的适宜刺激质量浓度是10.0/μg/mL;两种除草剂对鲫鱼淋巴细胞增殖存在影响,当甲草胺质量浓度大于7μg/L、莠去津质量浓度大于50μg/L时,淋巴细胞增殖受到明显抑制,表明其对鲫鱼存在潜在的免疫毒性.     

全氟辛烷磺酸（PFOS）对小鼠T、B淋巴细胞增殖功能和NK细胞活性的干扰效应研究（Disturbance of Mice Lymphocyte Proliferation Function and NK-cell Activity by Perfluorooctane Sulfonate（PFOS）Exposure）

为初步探讨全氟辛烷磺酸(Perfluorooctane sulfonate,PFOS)的细胞免疫毒性,采用每天1次经口灌胃染毒的方法,研究了PFOS经口重复剂量染毒对C57BL/6小鼠淋巴细胞增殖功能和NK细胞活性的影响.选择雄性C57BL/6小鼠40只,随机分为4组.实验组PFOS染毒剂量分别为5、10、20mg·kg-1(bw),对照组给予2%Tween-80.每天1次经口灌胃染毒7d后,制备脾脏T淋巴细胞悬液,以刀豆蛋白A(ConA)和大肠杆菌脂多糖(LPS)作为刺激源,采用MTT法检测T、B淋巴细胞增殖功能,乳酸脱氢酶释放法检测NK细胞活性.结果表明,10mg·kg-1和20mg·kg-1PFOS染毒组小鼠体重呈明显的下降趋势,且小鼠胸腺和脾脏指数显著低于对照组(p<0.05),而各PFOS染毒组小鼠肝脏指数均显著高于对照组(p<0.05).PFOS各染毒组T淋巴细胞的增殖功能均显著低于对照组(p<0.05);10mg·kg-1和20mg·kg-1PFOS染毒组小鼠NK细胞的活性显著降低(p<0.05).研究结果显示,PFOS暴露可降低小鼠淋巴细胞增殖功能和NK细胞活性,表明PFOS具有免疫抑制效应.     

磺胺与群体感应抑制剂对费氏弧菌发光和生长联合毒性效应对比研究

抗生素类药物在广泛应用的同时,也带来了细菌耐药性问题。因此,越来越多的抗生素替代品如群体感应抑制剂(QSIs)被研究和应用,在未来二者可能共存于环境之中。为了对它们混合物联合毒性评价进行系统的研究,本文选择费氏弧菌(Vibrio fischeri,V.fischeri)为受试生物,测定了5种磺胺类抗生素(SAs)与6种QSIs对V.fischeri的发光强度(HV)和生长量(OD600)的联合毒性作用,初步探讨了SAs与QSIs对V.fischeri发光联合毒性和生长联合毒性差异的原因。结果表明:SAs与QSIs联合作用于V.fischeri时,对发光的联合毒性表现为拮抗,对生长的联合毒性表现为拮抗或加和,且TUHVTUOD。这可能是由于QSIs对V.fischeri的发光的抑制作用可以削弱SAs对发光的促进作用,而SAs与QSIs对V.fischeri的生长都表现出抑制作用,两者没有互相削弱作用。同时,基于分子对接和回归分析法的研究表明了靶蛋白上结合的化合物有效浓度不同也可能是造成SAs与QSIs联合作用于V.fischeri时TUHVTUOD的主要原因。该研究可以为抗生素与QSIs联合暴露的生态风险评价提供借鉴。