稀土矿城市不同季节大气可吸入颗粒物中稀土含量特征及颗粒物细胞毒性

为探讨典型稀土矿城市不同季节大气可吸入颗粒物(inhalable particulate matter,PM10)中稀土元素污染特征及其细胞毒性响应,将前期采集于包头市的PM10颗粒物进行提取,检测PM10中的稀土元素(rare earth elements,REEs)含量,并将人肺上皮细胞(A549)暴露于不同浓度水平(25,50,100μg·m L-1)的PM10样品和标准颗粒物1649b(standard reference material,SRM1649b)暴露液,用WST-1法测定暴露24 h后的细胞活性,用2’7’二氯荧光素二醋酸盐(2’7’-dichlorofluorescein diacetate,DCFH-DA)荧光探针法和彗星实验分别测定暴露3 h后的细胞内活性氧(reactive oxygen species,ROS)产生水平和DNA双链损伤程度。结果表明,包头春、夏季大气PM10和SRM1649b均引起A549细胞活性下降,并诱导细胞内ROS生成量增加,造成显著的细胞内DNA损伤,含REEs的大气颗粒物毒性显著高于标准颗粒物。与春季相比,包头夏季PM10对细胞活性的抑制程度更高,造成更多的DNA双链损伤,从而表现出更强的细胞毒性和遗传毒性。包头PM10呈现明显的轻稀土元素(light rare earth elements,LREEs)富集,铈(Ce)、钷(Pm)、镧(La)和钕(Nd)含量占稀土总量的50%以上。LREEs均与细胞活性和细胞内ROS产生水平呈负相关性,包头春季和夏季PM10中稀土元素含量的差异是导致包头PM10细胞毒性效应不同于标准颗粒物且具有季节性差异的原因之一。     

载带苯并[a]芘的纳米碳／二氧化硅颗粒引起大鼠氧化应激作用的研究

通过人工制备载带B[a]P的纳米碳(C)和纳米二氧化硅(SiO2)颗粒,采用气管滴注染毒方式,以7.5mg·kg-1(以体重计)的染毒剂量急性染毒大鼠,观察染毒24小时后载带B[a]P的纳米C/SiO2颗粒对机体产生氧化应激损伤的联合毒性效应.结果表明,在急性染毒后大鼠外周血中反映机体脂质过氧化损伤程度指标的丙二醛(MDA)含量表现为染毒组较对照组显著增加(p<0.05),表明纳米颗粒诱发机体发生了氧化应激反应.在急性染毒后各组大鼠肺泡灌洗液中谷胱苷肽过氧化物酶(GSH-PX)和超氧化物岐化酶(T-SOD)活力与对照组相比显著增加(p<0.05)(载带B[a]P的纳米SiO2组除外);载带B[a]P的纳米SiO2组肺泡灌洗液中GSH-PX活力与对照组相比无显著差异,而与单纯纳米SiO2组和B[a]P组比较显著降低,推测与抗氧化酶的一过性增高有关;载带B[a]P的纳米C组肺泡灌洗液T-SOD活力与其单纯纳米C组和单纯B[a]P组比较显著增加(p<0.05),由此表明载带B[a]P的复合纳米C/SiO2颗粒在致机体氧化损伤效应方面二者存在一定的协同作用.     

水体中铊对泥鳅外周血红细胞的遗传毒性的时效性

铊(T1)是剧毒的重金属元素,会对生态环境和人体健康造成威胁.目前各国铊的环境安全标准存在差异.本文利用泥鳅红细胞微核技术,研究泥鳅Misgurnus anguillicaudatus红细胞微核率和核异常率与铊污染时间的关系,为该技术在铊毒理研究中的可行性和铊环境安全标准提供依据.结果表明:水体铊质量浓度为0.5μg·L~(-1)下,随处理时间的延长,泥鳅红细胞微核率、核异常率显著增加,并与时间呈显著的正相关,其中微核率、核异常率分别在处理24 h和48 h时达到最大值;随后两指标逐步下降,与时间呈显著的负相关.在此铊质量浓度和处理时间内,核异常率与微核率均显著高于空白无铊对照处理,表明水体铊质量浓度0.5 μg·L~(-1)对泥鳅血红细胞具有遗传毒性.     

微囊藻毒素-LR致小鼠肝细胞DNA-蛋白质交联作用的研究

为探讨微囊藻毒素-LR致小鼠肝细胞的DNA-蛋白质交联作用,将20只昆明雄性小鼠随机分为4组:1个对照组和3个染毒组,采用腹腔注射进行染毒7d,染毒剂量分别为3.0、6.0和12.0μg·kg-1,检测小鼠肝细胞DNA-蛋白质交联程度.结果显示,3.0、6.0和12.0μg·kg-1微囊藻毒素-LR均可导致小鼠肝细胞显著的DNA-蛋白质交联作用(与对照组相比,p<0.01,p<0.01,p<0.05),当微囊藻毒素为6.0μg·kg-1时,这种作用最明显.     

Histopathology of cerebro neuronal cells in freshwater snail Bellamya bengalensis: impact on respiratory physiology,by acute poisoning of mercuric and zinc chloride

Mercuric (Hg) and zinc (Zn) chloride toxicity was investigated in cerebroneuronal cells and gills of Bellamya bengalensis using sublethal concentrations under lab conditions. Freshwater snail B. bengalensis was exposed to mean LC₅₀ concentration (1.56 ppm and 12.7 ppm) of Hg and Zn chloride, respectively. Bioaccumulation of Hg and Zn was observed in nervous and gill tissue in proportion to the time of exposure. Respiratory mechanisms and rate of oxygen consumption was depleted by both metals. Histopathological alterations in cerebro neuronal cells (giant, large, medium, and small) and gill filamental epithelia were apparent in Hg and Zn-exposed snails. Histopathology demonstrated increased cytoplasmic basophilia, extreme indentation of plasma membrane, karyolitic and eccentric nuclei, nuclear envelope with irregular size, and shrunken appearance of cerebroneuronal cells. Histologically, gill filamental epithelia showed hypertrophy, enlarged ciliated margins reduced length of cilia, nuclear dilations, thickening of basal lamina, and hemocytic accumulations in induced cells and severe loss of goblet mucus cells at the tip. Histopathology was accompanied by dysfunctioning cilia with decreased rate of respiration. Overall, neuronal impairment with damaged gill filament produced improper gaseous exchange leading to sluggish movement.     

Enzymatic and cellular level effects of chromium∗

Exposure of Cr to four hepatic enzymes activities of tilapia, viz. acid‐ and alkaline phosphatases, catalase and glucose‐6‐phosphatase, was contrary to the results obtained for Cd and Ni. This is the only heavy metal investigated thus far that dramatically augmented glucose‐6‐phosphatase by approximately 83% at a concentration of 12 mg L^‐1 in vivo in lieu of the fact of an initial inhibition of approximately 45 % at a lower concentration of Cr; 6 mg L^‐1. In the case of acid phosphatase and catalase activities progressive increment was observed up to 50 and 217% respectively at a concentration of 12 mg L^‐1 Cr. On the other hand, in contrast to all the investigated enzymes interestingly alkaline phosphatase was inhibited continuously at all concentrations up to 46% at 12 mgL^‐1 Cr. In vitro experiments were contrary to the above mentioned results, whereby all hepatic enzymes were inhibited with major inhibition observed for acid phosphatase of approximately 60% from 5 mgL^‐1 Cr onwards in the system.

At cellular level, Cr exposure at a lethal dose of 12 mgL^‐1 demonstrated similar effects to that of Cd. In general, the glycogen and fat reserves were depleted while lysosomal activity is increased. As compared to the effects of Cd, the mitochondria did not indicate any prominent reflection in the formation of intramitochondrial bodies. Further, similar to Cd, the cell membrane as well as nucleus were not affected.     

活性氧介导砷诱导的蚕豆保卫细胞死亡

采用蚕豆(Vicia fabaL.)表皮条生物法,研究砷的细胞毒性作用机制。结果发现,一定浓度的NaAsO2可使气孔保卫细胞活性降低,部分细胞死亡,细胞死亡率呈浓度依赖性增高;砷处理组保卫细胞内活性氧(reactive oxygen species,ROS)水平升高。抗氧化剂抗坏血酸和过氧化氢酶及Ca2+特异性螯合剂EGTA、Ca2+通道抑制剂LaC13与NaAsO2共同作用时,砷诱发的细胞死亡被显著抑制;MAPK激酶抑制剂PD98059亦能有效阻止NaAsO2诱发的细胞死亡。研究结果表明,砷胁迫引起的胞内ROS合成增加可能通过Ca2+信号途径介导了保卫细胞的死亡过程,MAPK途径参与了砷诱导的细胞死亡。     

量子点对Cu2+诱导L02细胞毒性的影响及机理研究

量子点(QDs)和Cu~(2+)可能共存于肝脏,对肝细胞产生联合毒性,威胁人体健康。本研究以人胚肝细胞(L02)为研究对象,考察了低/无毒的QDs(3.6%的细胞致死率)对Cu~(2+)诱导L02细胞毒性的影响及相关机理,为其可能的健康和环境风险提供参考。结果显示,QDs的加入使得Cu~(2+)的细胞毒性有了很大的提高,细胞存活率最高下降了26.0%,两者表现为协同作用;另外QDs存在使得Cu~(2+)细胞蓄积量增大,伴随着Cu~(2+)天然解毒蛋白CTR1和ATP7A等表达水平的升高,从侧面印证了Cu~(2+)的蓄积量增加对细胞的影响;同时,QDs的存在使得细胞乳酸脱氢酶(lactate dehyfrogenase,LDH)泄露相对于Cu~(2+)单独处理组提高,暗示QDs可能破坏了细胞膜,导致Cu~(2+)在细胞内蓄积量增加,从而使细胞毒性增加,两者的联合毒性表现为协同作用。     

高等植物细胞中的钙通道

钙通道在高等植物细胞中参与众多的信号转导过程,对钙通道的研究最近几年获得长足的进步：不仅在质膜中直接发现了电位依赖性的钙通道、牵张刺激激活的机械敏感性钙通道等,而且在液泡膜中发现了众多具有不同开放调控机制的钙通道：受化学信使控制的钙释放通道、电位依赖性钙通道、钙离子诱导的钙释放通道．本文对高等植物细胞中钙通道的研究进行了综述     

高含硅量高盐地下水处理工艺

本文通过对高含硅量，高盐地下水这一特殊水质进行纯化处理研究，经实际运行及分析，得出一套行之有效的工艺流程。