ZnO nanoparticles induced cytotoxicity on human pulmonary adenocarcinoma cell line LTEP-a-2

Novel nanoparticles (NPs) such as zinc oxide (ZnO) NPs are widely produced and applied in our daily lives at a rapid pace. Thus, the toxicity of ZnO NPs should be monitored as an important standard for environmental risk assessment. Here we assessed the in vitro cytotoxicity of ZnO NPs on human pulmonary adenocarcinoma cells LTEP-a-2 by tetrazolium salt colorimetric assay of cell proliferation in the presence or absence of ZnO NPs. ZnO NPs-induced morphological changes in LTEP-a-2 cells were examined by light and scanning electron microscopy. The mechanism by which ZnO NPs impose the cytotoxic effect was investigated by a combination of active oxygen test, lactose dehydrogenase-release assay, and apoptosis detection. Results showed that ZnO NPs significantly inhibited the proliferation and induced evident morphological changes (cell shrinkage and chromosome condensation) in LTEP-a-2 cells. Additionally, ZnO NPs increased the level of intracellular reactive oxygen species and induced the formation of apoptotic vesicles as well as the lysis of cell nuclei. Zn²⁺ ions released from ZnO NPs into aqueous solution are important components that exert cytotoxic effects on LTEP-a-2 cells. This study provides new insights to the cytotoxicity of ZnO NPs against human health.     

Early genetic amniocentesis and its relationship to respiratory difficulties in paediatric patients: A report of findings in patients and matched controls 3–5 years post-procedure

This study evaluates the long-term pulmonary complications of 25 children from a prospective, matched-control, pilot study evaluating short-term complications of early (11–14 weeks' gestation) versus traditional (15 weeks' gestation and later) genetic amniocentesis. Five children in the early amniocentesis group were found to have various respiratory difficulties, a morbidity rate comparable to that of paediatric patients in the general population. These data identify the need for larger, multicentre trials.     

汽车尾气暴露对小鼠运动力竭时间的影响

汽车尾气是城市中大气污染物的主要来源,为探究汽车尾气对机体的损伤作用及其机制,通过建立汽车尾气暴露动物模型,利用轮式疲劳仪评估汽车尾气对小鼠运动力竭时间的影响。结果表明,汽车尾气连续暴露30 d后,暴露组小鼠的运动力竭时间较正常对照组明显缩短,支气管-肺泡灌洗液(BALF)中细胞因子白介素-1β(IL-1β),白介素-6(IL-6)和肿瘤坏死因子-α(TNF-α)水平较正常对照组明显升高,血清中谷胱甘肽(GSH)和超氧化物歧化酶(SOD)活性明显降低,丙二醛(MDA)含量显著升高。汽车尾气长时间暴露组(8 h·d-1)BALF中白细胞计数和中性粒细胞百分比较正常对照组明显升高。肺组织切片染色后可见汽车尾气长时间暴露组小鼠肺泡间质中有较多中性粒细胞及淋巴细胞浸润。上述研究结果表明,汽车尾气可能通过引起呼吸系统损伤和降低机体抗氧化应激能力减少小鼠的运动力竭时间。     

纳米二氧化钛暴露人胚肺细胞差异表达基因分析

为探讨纳米二氧化钛(Nano-TiO2)颗粒对人胚肺(HPF)细胞基因表达和基因功能的影响,使用粒径10nmTiO2暴露体外培养的人胚肺细胞24h,提取RNA,应用基因芯片方法,寻找差异表达基因,并对差异基因进行基因本体(GeneOntology,GO)分类.结果表明,纳米TiO2暴露人胚肺细胞,导致514条肺中表达的基因发生差异表达,基因分类显示400条基因涉及生物学过程;415条基因涉及分子学功能;391条基因涉及细胞构成.纳米TiO2作为外界刺激物质,与细胞膜上的受体结合,影响钙、钾离子通道,上调细胞免疫和炎症反应相关的细胞因子TNF、IL1B、IL1A等基因表达.     

苯并[a]蒽与肺表面活性剂混合磷脂的相互作用

为探究多环芳烃对肺表面活性物质（PS）膜的影响,选取1,2-二棕榈酰-sn-甘油-3-磷酸胆碱（DPPC）和1-棕榈酰-2-油酰-sn-甘油-3-磷酸胆碱（POPC）混合磷脂为PS模型,研究了苯并[a]蒽与DPPC/POPC混合磷脂的界面化学相互作用.结果表明,苯并[a]蒽对DPPC/POPC混合膜的相变影响显著,会削弱膜的抗形变能力、干扰膜分子的致密有序排列,这一不利影响随POPC占比增多更加明显.DPPC/POPC混合磷脂胶束会包裹苯并[a]蒽对其产生增溶作用,当DPPC浓度为200mg/L时,苯并[a]蒽的表观溶解度接近水溶液的3倍且POPC含量增加会促进胶束的分散使增溶更显著.苯并[a]蒽与DPPC/POPC混合磷脂的相互作用既抑制PS的生理功能,又会影响苯并[a]蒽的溶解迁移,进一步增加苯并[a]蒽的暴露风险.同时生理条件变化引起PS组分的改变可能导致苯并[a]蒽潜在毒性的差异,对患有相关肺部疾病的人群造成的肺损伤可能更严重.     

工业矿物粉尘对肺泡巨噬细胞影响的体外研究

为了评价来自全国6个矿床的6种工业矿物粉尘的细胞毒性,采用细胞培养技术,观察6种纤维状粉尘对兔肺泡巨噬细胞膜受损的程度及方式、氧化与抗氧化系统、膜流动性的影响．结果表明,纤维状硅灰石、斜发沸石无细胞毒性;纤状海泡石、纤维状坡缕石、纤维状水镁石、纤维状蛇效石石棉则表现出不同程度的细胞毒性．矿物纤维粉尘的细胞毒性与其表面它能团OH^－及其数量有关．