单壁纳米碳管对大鼠主动脉内皮细胞损伤作用的研究

为了探索单壁纳米碳管(SWCNT)能否引起血管内皮细胞损伤及其可能的损伤机制,将大鼠主动脉血管内皮细胞暴露于不同浓度的SWCNT水溶液中(0.8、1.6、3.12、6.25、12.5、25、50、100、200μg·mL-1)中染毒,染毒不同时间后测定细胞存活率、细胞内LDH和GSH含量并进行综合分析.结果表明,随着SWCNT染毒浓度和染毒时间的上升,大鼠主动脉血管内皮细胞存活率逐渐下降,死亡率逐渐上升;细胞内LDH在SWCNT染毒浓度为0￣100μg·mL-1范围内其释放随染毒剂量的增加而逐渐上升,在200μg·mL-1剂量组,其释放有所减弱;而细胞内GSH在SWCNT染毒浓度为0￣200μg·mL-1范围内其含量随染毒剂量的增加而逐渐下降.以上结果说明,SWCNT可致血管内皮细胞损伤,其机制可能为氧化损伤途径.     

活性氧参与多壁碳纳米管诱导的RAW264.7细胞毒性

碳纳米管以其独特的结构和性能,在生物医药和电子等领域广泛应用,而其生态安全性也成为科学界关注的焦点。为探究多壁碳纳米管(MWCNTs)诱导的细胞毒性机制,将小鼠肺泡巨噬细胞(RAW264.7)暴露于6个浓度梯度(0、25、50、100、150和200μg.mL-1)的MWCNTs中,应用噻唑蓝(MTT)法测定细胞存活率,用2’,7’-二氯荧光素二乙酸(DCFH-DA)荧光染色法测定细胞内活性氧的生产量,用流式细胞方法测定MWCNTs对细胞周期的影响。同时使用抗氧化剂氮乙酰半胱氨酸(NAC)验证MWCNTs诱导的细胞氧化损伤的作用机理。结果显示,MWCNTs对RAW264.7的细胞毒性呈剂量依赖性。暴露于不同浓度的MWCNTs(25、50、100、150和200μg.mL-1)下24h后,细胞活力分别为对照的74%、62%、59%、51%和45%。MWCNTs对RAW264.7的周期阻滞作用主要发生在G0/G1期。200μg.mL-1的MWCNTs处理3h后活性氧较对照组上升6.6倍。NAC对MWCNTs细胞毒作用有明显的抑制作用,且NAC能减弱MWCNTs对RAW264.7的细胞周期阻滞作用。研究表明,活性氧能够介导MWCNTs对小鼠巨噬细胞RAW264.7的损伤,并且MWCNTS通过细胞周期G0/G1期的阻滞,诱导细胞凋亡。     

Raw single-walled carbon nanotube-induced cytotoxic effects in human bronchial epithelial cells: comparison to asbestos

Single-walled carbon nanotubes (SWCNT) are being developed to be used in many industrial and biomedical applications. However, SWCNT's durability and likely fibrous morphology have raised health concerns. The present investigations were focused on understanding the cellular and molecular mechanisms induced by raw SWCNT (SWCNT) in human bronchial-epithelial cells (BEAS-2B). Asbestos (crocidolite) was used as a positive control. Exposure of BEAS-2B cells to SWCNT induced apoptosis, DNA damage, and oxidative stress. The generation of hydroxyl radical (^?OH) and increase of superoxide dismutase (SOD) activity were concentration-dependent. The increase in apoptosis was associated with activation of caspase-3, caspase-7, and poly (ADP-ribose) polymerase-1 (PARP-1). A short recovery period of 6?h of cells from SWCNT exposure resulted in reversal of caspase-3 and caspase-7, and a partial reversal of PARP-1 activation. The activation of PARP-1, caspase-3, and caspase-7 was only partially diminished after a recovery of 6?h from the exposure to crocidolite. Exposure of BEAS-2B cells to SWCNT resulted in the phosphorylation of protein p42/44 (p42/44) and protein p38 (p38). SWCNT did not induce protein serine-threonine kinase (AKT) phosphorylation. For all the above end points, crocidolite induced a greater response compared to SWCNT. SWCNT induced a significant activation of activator protein-1 (AP-1) and nuclear factor kappa B (NF-κB), and the effect was inhibited by mitogen-activated protein kinase (MAPK) inhibitors. SWCNT also induced significant increase in the expression levels of c-Jun, βIGH3, and CD44 genes. The results of this study show that the molecular mechanism for raw SWCNT-mediated toxicity in BEAS-2B cells is through the activation of caspase-3, caspase-7, and PARP-1. Furthermore, the mechanism of AP-1 and NF-κB activation is through MAPK. This bioactivity of raw SWCNT is associated with the generation of oxidative stress and DNA damage. Considering the role of airway epithelium as a critical barrier for normal pulmonary function and focal point for tumor development, this study demonstrates that raw SWCNT activate molecular events which may be linked to adverse biological responses implicated in pulmonary diseases.     

Effect of Zinc Oxide nanoparticles on cellular oxidative stress and antioxidant defense mechanisms in mouse liver

Zinc oxide nanoparticles (ZnO₂), a common ingredient of cosmetics has a huge variety of applications. Previous studies reported oxidative stress mediated toxicity of ZnO₂ nanoparticles on various mammalian cell lines. Although zinc (Zn) is an essential mineral at higher concentrations this metal is toxic. The present study focused on size determination by monitoring changes in activities of antioxidant defense mechanism in response to oxidative stress induced by ZnO₂ nanoparticles using mouse liver tissue homogenates. The study also investigated effects of oxidative stress induced DNA damage by determining formation of 8-OHdG in mouse liver homogenate. A cytotoxicity assay was also carried out in L929 cells to determine cell viability. The results of the study indicated that 50μg/ml of ZnO₂ nanoparticles induced 50% cell death. Alterations in antioxidant parameters and 8-OHdG were also noted. Data showed that there was a concentration-dependent fall in cell viability, decrease antioxidant enzyme levels and increase formation of DNA adduct (8-OHdG) when mouse liver tissue homogenate were exposed to ZnO₂ nanoparticles.     

三邻甲苯磷酸酯对大鼠C6星形胶质细胞的氧化损伤和细胞周期阻滞作用

三邻甲苯磷酸酯(tri-o-cresyl phosphate,TOCP)是一种有机磷酸酯类化合物,具神经毒性作用。研究表明星形胶质细胞是有机磷化合物(organophosphorus compounds,OPs)神经毒性作用的靶点之一。为了探讨TOCP对星形胶质细胞的毒性作用,采用大鼠C6星形胶质细胞分别经0.1、0.3、1.0和3.0 mmol·L-1TOCP染毒处理24 h,应用MTT比色法和乳酸脱氢酶(LDH)活力分析法检测细胞活力,在电子相差显微镜下观察细胞形态,二硫代二硝基苯甲酸(DNTB)比色法测定谷胱甘肽(GSH)含量和谷胱甘肽过氧化物酶(GSH-Px)活性,流式细胞仪检测分析细胞周期。结果显示,经TOCP处理24 h后,大鼠C6星形胶质细胞存活率降低,LDH释放增加,细胞形态也发生了明显的变化。GSH含量和GSH-Px活性降低,G1期细胞数量也逐渐增加。上述结果表明,TOCP对星形胶质细胞具有毒性作用,引起氧化损伤和细胞周期阻滞。     

过敏症状儿童室内PM_(2.5)对小鼠巨噬细胞的氧化损伤及VE的抗氧化保护作用研究

越来越多的研究提示,主要空气污染物PM_(2.5)暴露浓度的升高与儿童过敏性疾病的发病率有着密切的关系,然而PM_(2.5)暴露与过敏性疾病之间的关联尚未完全阐明。为探究患有过敏症状儿童的室内PM_(2.5)对小鼠巨噬细胞的氧化损伤作用以及维生素E(vitamin E,VE)的抗氧化保护作用,从5户患有1种或1种以上的过敏性症状(如过敏性鼻炎、哮喘)儿童的室内采集PM_(2.5),分别考察了不同剂量PM_(2.5)暴露24 h后如何影响小鼠巨噬细胞的氧化应激水平,指标包括活性氧(ROS),还原型谷胱甘肽(GSH),丙二醛(MDA),8-羟基脱氧鸟苷(8-OH-dG),以及炎症因子水平,指标包括肿瘤坏死因子ɑ(TNF-ɑ),白介素8β(IL-8β)的影响。结果表明,200μg·mL~(-1)PM_(2.5)暴露组与对照组比较,细胞内ROS积累,出现脂质过氧化以及DNA损伤,并伴有炎症反应的发生,差异均有统计学意义(P0.05或P0.01);VE(50 mg·mL~(-1))+200μg·mL~(-1)PM_(2.5)组的ROS、MDA、8-OHdG、TNF-ɑ、IL-8β含量低于200μg·mL~(-1)PM_(2.5)组,GSH含量高于200μg·mL~(-1)PM_(2.5)组。较高剂量(200μg·mL~(-1))PM_(2.5)可诱导小鼠腹腔巨噬细胞出现氧化损伤,VE在该应激过程中起着一定的保护作用。     

甲醛及苯系物混合暴露对小鼠肺脏的氧化损伤作用

为探讨甲醛、苯、甲苯及二甲苯混合气体急性暴露对小鼠肺脏的氧化损伤作用,选用雄性健康昆明种小鼠50只,随机分为对照组和4个染毒组。染毒组1到4中甲醛、苯、甲苯和二甲苯浓度依次为:1.0+1.1+2.0+2.0μg·L-1、3.0+3.3+6.0+6.0μg·L-1、5.0+5.5+10.0+10.0μg·L-1、10.0+11.0+20.0+20.0μg·L-1,各染毒组混合气体的浓度分别是我国室内空气质量标准(GB/T18883-2002)的10、30、50和100倍。用静式吸入染毒方式,每天染毒2h,共染毒10d,实验结束后,测定小鼠肺脏中的氧化损伤指标。结果表明:染毒组小鼠的体重增加幅度均低于对照组,肝脏和脾脏系数显著低于对照组,肺脏ROS、MDA含量随染毒剂量的增加而增加,T-AOC、GSH、CAT、GSH-Px及SOD活力随染毒剂量的增加而降低,并且ROS、MDA含量与混合气体的浓度呈显著的正相关关系,GSH含量与混合气体的浓度呈显著的负相关关系。研究结果显示,甲醛、苯、甲苯及二甲苯混合气体急性暴露对小鼠肺脏具有氧化损伤作用,混合气体的联合毒性效应强于单一组分,ROS、MDA和GSH可以作为评价VOCs急性暴露对机体氧化损伤作用的敏感生物学标志。     

硫化镉量子点对人胚肝细胞L-02的毒性研究(Cadmium Sulfide Quantum Dots Induce Cytotoxicity in Human Embryo Liver Cells)

采用乳化液膜法自组合成硫化镉量子点(CdS quantum dots,CdS QDs),探讨CdS QDs的体外毒性作用及可能的作用机制.选用人胚肝细胞(L-02)作为细胞模型,采用不同浓度的CdS QDs(0.00、1.25、2.50、5.00、10.00、20.00、40.00μg·mL-1)对L-02细胞进行染毒.24h后,检测细胞内乳酸脱氢酶(LDH)释放量、谷胱甘肽(GSH)含量和超氧化物歧化酶(SOD)活力,并比较加入抗氧化剂N-乙酞半胱氨酸(NAC)后细胞存活率的变化,同时测定了细胞内外的镉离子浓度.结果表明,与空白对照组相比,CdS QDs单独染毒组细胞存活率显著降低(p<0.05或p<0.01);加入抗氧化剂NAC后,10.00、20.00、40.00μg·mL-1染毒组细胞存活率与单独染毒组相比显著上升(p<0.01).CdS QDs浓度为5.00μg·mL-1时,细胞内Cd2+的浓度略高于细胞外Cd2+的浓度,在其他浓度下,细胞外Cd2+的浓度均显著高于细胞内Cd2+的浓度.当作用浓度上升至10.00μg·mL-1时,人胚肝细胞内LDH含量显著增加,且随着作用剂量的升高,LDH含量逐渐增加.与空白对照组相比,40.00μg·mL-1CdS QDs染毒组SOD活力和20.00μg·mL-1CdS QDs染毒组GSH含量均显著降低(p<0.05).Cd2+易透过L-02细胞的细胞膜而进入细胞内,从而造成细胞损伤.氧化损伤可能是CdSQDs对L-02细胞毒性作用的机制之一.     

纳米四氧化三铁吸附水中六价铬后的复合物对HEK293细胞的毒性研究

磁性纳米粒子是一种环境友好型吸附剂,广泛应用于废水中重金属的处理。目前,有不少关于纳米粒子毒性的研究,但对处理后的纳米粒子和金属的复合物的毒性却鲜有研究。本文利用纳米四氧化三铁(MNPs)吸附水中的铬离子,以人胚胎肾细胞HEK293为生物模型,通过测定细胞活力、活性氧含量以及细胞摄取量等试验,评估磁性纳米四氧化三铁吸附六价铬后的复合产物对HEK293细胞的毒性。实验结果显示:在本实验浓度和作用时间下,Cr(Ⅵ)离子能够进入细胞,产生氧化应激,并引起细胞毒性;与Cr(Ⅵ)离子相比,磁性纳米四氧化三铁吸附Cr(Ⅵ)后的修复产物MNPs/Cr(Ⅵ)对HEK293细胞无明显毒性效应,MNPs/Cr(Ⅵ)复合物在细胞内的摄取极少,只有极少数颗粒通过内吞的方式进入细胞,且没有进入细胞核内。因此,在本实验的作用浓度和时间下,利用MNPs吸附水环境中Cr(Ⅵ)后的复合物对HEK293细胞没有明显毒性,本研究为深化了解MNPs及其重金属复合物对环境的影响提供了实验依据和参考价值。     

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。     

Nanosilica exerts cytotoxicity and apoptotic response via oxidative stress in mouse embryonic fibroblasts

Nanoscale silica is an important industrial material and extensively used in medicines. The objective of this study was to determine potential cytotoxicity and genotoxic effects attributed to nanosilica exposure in mouse embryonic fibroblasts (L929) cells. Nanosilica produced mild cytotoxicity in L929 cells. Results showed that nanosilica increased thiobarbituric acid reactive substance levels and enhanced superoxide dismutase activity but decreased levels of glutathione. This was accompanied by a concomitant generation of reactive oxygen species, loss of mitochondrial membrane potential, and activation of caspase-3 activity. In addition, in the single-cell gel test, nanosilica (50–300 μg/ml) at two treatment times 24 and 48 hr produced concentration- and time-dependent increase of DNA damage. Therefore, the obtained results indicate that nanosilica may induce genotoxic effects in cultured L929 cells associated with induction of oxidative stress.     

Indium tin oxide nanoparticles-mediated DNA fragmentation and cell death by apoptosis in human lung epithelial cells

Indium tin oxide (ITO) nanoparticles (NP) have extensive applications in industrial fields, and concerns regarding their potential toxicity in humans and environmental impact have increased. Since exposure to ITO NP is mainly via skin and inhalation, this study was conducted utilizing human lung epithelial (A549) cell line. Cells were exposed to different concentrations of the ITO NP for 24 and 48 hr. A severe cytotoxic response of ITO NP was observed as evident by the (3-4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide and neutral red uptake assays after 48 hr exposure. ITO NP significantly reduced glutathione levels with a concomitant increase in lipid hydroperoxide levels, superoxide activity, and reactive oxygen species (ROS) generation after exposure. A significant induction in caspase activity and formation of condensed chromosomal bodies was also observed after ITO NP (10 or 25 µg/ml) exposure. Furthermore, a significant induction in DNA damage was observed by the Comet assay in cells exposed to ITO NP. Our data demonstrate that ITO NP display cytotoxic and genotoxic potential. However, increase in ROS levels and oxidative stress leading to oxidative DNA damage and condensed chromosomal bodies formation, suggests involvement of apotosis. Thus, ITO NP-mediated effects on cell viability indicate cytotoxicity, and therefore, exposures need to be carefully monitored in the industrial sector.     

4种典型纳米材料对小鼠胚胎成纤维细胞毒性的初步研究

为探讨不同种类纳米材料对原代培养小鼠胚胎成纤维细胞(Mouse embryo fibroblasts,MEF)的毒性效应及作用机制,选择4种典型的纳米材料(纳米碳、单壁碳纳米管、纳米氧化锌、纳米二氧化硅)制备颗粒悬液,设立5个剂量组(5、10、20、50、100μg·mL-1)对BALB/c小鼠MEF细胞进行24、48、72h染毒培养,利用细胞形态学观察和噻唑蓝实验(MTT比色法)检测上述4种纳米材料对MEF细胞活性的影响,同时,测定染毒24h后细胞培养液上清中乳酸脱氢酶(LDH)活性以探讨纳米颗粒对细胞膜完整性的影响.结果显示:1)4种纳米材料均能明显影响MEF细胞的生长形态.染毒24h后,MEF细胞发生不同程度的回缩变形,细胞间隙增大,排列稀疏,胞内颗粒物增多,细胞透明度下降.2)纳米碳、纳米氧化锌、纳米二氧化硅对MEF细胞增殖的抑制作用和对细胞膜完整性的损伤作用均随染毒剂量的升高而增强,具有明显的剂量-效应关系,其半数致死浓度(24h-IC50)分别为21.85、21.94、461.10μg·mL-1;碳纳米管组的剂量-效应之间不呈对数线性关系,未能得出其24h-IC50.3)在不同染毒剂量水平上,4种纳米材料的毒性对比差异显著:低剂量水平上纳米碳与碳纳米管的毒性强于纳米氧化锌和纳米二氧化硅,随着剂量的升高纳米氧化锌的细胞毒性升高最为显著.结果提示,纳米材料能够对MEF细胞造成毒性损伤,破坏细胞膜的完整性可能只是作用途径之一;纳米材料的毒性可能受粒径、形状、化学组成等许多因素的影响.     

Protective role of epigallocatechin 3-gallate against lead-induced toxicity in human neuroblastoma cells

Lead (Pb) is a heavy metal, known to induce oxidative stress and produce damage to the antioxidant defence system ultimately leading to cell death. Antioxidants such as epigallocatechin 3-gallate (EGCG), a green tea polyphenol, was shown to play a protective role during Pb-exposure. In this study, human SH-SY5Y neuroblastoma cells were exposed to different concentrations (0.01–10?µM) of Pb for 48?h to determine effects on the viability of cells. It was observed that IC₅₀ was at 5?µM and at this concentration the cells exhibited a significant increase in caspase-3 activity, an indicator of apoptosis at least by 10-fold and the decrease of 59.4% in glutathione (GSH) content. The total cellular prostaglandin-E₂ (PGE₂) level was found to be elevated at least 10-fold upon Pb exposure. However, the effects of Pb on cells pre-incubated with 50?µM EGCG followed by 5?µM Pb showed 40% inhibition in cell viability, 17.3% decrease in caspase-3 activity, 23% increase in GSH content, and 11.4% fall in PGE₂ levels when compared with cells exposed to Pb only. Data suggest that EGCG exerted a significant protection to cell viability in preventing cell death and elevation in levels of GSH in cells exposed to Pb. However, EGCG did not elicit any significant effect on release of PGE₂ indicating the nature of EGCG as an effective anti-apoptotic, antioxidant, and anti-inflammatory agent.     

Cytotoxicity of single-walled carbon nanotubes,multi-walled carbon nanotubes,and chrysotile to human lung epithelial cells

Carbon nanotubes (CNTs) have found numerous applications in various industries. Recently, adverse effects of these materials on human and animal cells in vitro have been reported. In the present study, the cytotoxicity of single-walled carbon nanotubes (SWCNTs), multi-walled carbon nanotubes (MWCNTs), and chrysotile asbestos in human lung epithelial cells has been studied using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. The cells were exposed for 6 h and 24 h to between 0.97 and 1500 μg mL^?1 of CNTs and chrysotile fibers prepared in two culture media containing 5% serum and 0.5% dimethylsulfoxide. Dose–response curves were obtained to determine the nonobservable adverse effect concentration and the half-maximum inhibitory concentration (IC₅₀). The way of dispersion affects the cytotoxicity of CNTs. For MWCNT, the toxicological indexes were lower than for SWCNT. Chrysotile fibers were even less cytotoxic than CNTs. Therefore, workplace control measures are recommended as priority for occupational and environmental conditions.     

Involvement of mitochondrial dysfunction in nanosized lead oxide induced cellular damage in human lung alveolar epithelial cells

High levels of industrial lead (Pb) exposure have decreased in the last 10 years as an outcome of removal of the metal from gasoline and paints. However, environmental Pb exposures remain extensive and may be correlated with adverse human health outcomes. The present study was designed to examine molecular mechanisms underlying cytotoxicity of lead oxide nanoparticles (PbONPs) on human lung alveolar epithelial (A549) cells. When A549 cells were incubated with PbONPs, the production of reactive oxygen species was enhanced as observed by 2',7'-dichlorodihydrofluorescein diacetate. PbONPs significantly reduced proliferation of A549 cells and increased caspase3 activity. In addition, exposure of PbONPs decreased levels of glutathione, and increased lipid peroxide levels and activities of superoxide dismutase and catalase. Exposure of PbONPs enhanced DNA damage as evidenced by tail DNA (%) and olive tail moment. Taken together, these finding indicated that PbONPs diminished cell proliferation and increased apoptotic cell death of A549 cells.     

H_2O_2致大鼠RTE细胞系氧化应激作用及GSH保护作用的体外研究

许多具有氧化作用的空气污染物,均能使细胞产生氧化损伤,使胸腺基质淋巴生成素(thymic stromal lymphopoietin,TSLP)含量上升。而TSLP是一种启动过敏性炎症的重要因子,会导致哮喘等疾病发生率的上升。在本研究中用过氧化氢(H_2O_2)模拟具有氧化作用的空气污染物进行染毒,研究细胞氧化应激水平的变化,并讨论还原型谷胱甘肽(GSH)对细胞受氧化损伤的保护作用。将大鼠支气管上皮细胞(RTE)分组培养,每组设置6个平行实验,分别用低、中、高剂量H_2O_2染毒3 h;高剂量设置1个重复,作为保护组,在染毒前用GSH保护2 h。结果显示,高剂量组H_2O_2(3.2 mmol·L~(~(-1)))染毒的细胞,其细胞活力下降(P0.01),丙二醛(MDA)水平上升(P0.01),TSLP水平上升(P0.05),与之相比,用GSH保护后的同剂量染毒组,上述指标得到全面缓解(P0.01)。这表明高浓度的H_2O_2会损伤细胞活力,并使MDA及TSLP水平上升,而GSH对TSLP及MDA的升高有极显著的抑制作用,即对细胞有一定的保护作用。     

Induction of apoptosis and cytokine markers in colon cancer cells by magnesium oxide (MgO) nanoparticles

Magnesium oxide nanoparticles (MgONP) are predominantly utilized in industrial products. This study was undertaken to elucidate the mechanisms underlying toxic effect of MgONP in human colon cancer (HT 29) cells over 48 hr period. Cytotoxicity was evaluated by using MTT and neutral red uptake assays. Data demonstrated that MgONP reduced cell viability in concentration- and time-dependent manner. MgONP induced oxidative stress by decreasing glutathione (GSH) concentrations and elevation of reactive oxygen species (ROS) and lipid peroxidation levels. Increased caspase-3 enzyme activity and greater condensed, damaged chromosome was observed following MgONP exposure in HT 29 cells. The level of interleukin-4 (IL-4), tumor necrosis factor (TNF-α), and DNA fragmentation were significantly higher in MgONP incubated cells. The results showed that MgONP-induced toxicity in HT 29 cells may be mediated through oxidative stress.     

三氯乙烯和四氯乙烯的细胞毒性及氧化应激机制研究

采用离体细胞测试技术,研究三氯乙烯(TCE)、四氯乙烯(PCE)对中国仓鼠卵巢细胞(CHO)的细胞毒性作用。3-(4,5-二甲基噻唑-2)-2,5-二苯基四氮唑溴盐(MTT)试验结果显示三氯乙烯、四氯乙烯对CHO细胞的半数生长抑制浓度(IC_(50))分别为590 mg·L~(-1)、281 mg·L~(-1)。三氯乙烯、四氯乙烯暴露可导致CHO细胞膜损伤,并且诱导细胞活性氧的产生。经不同浓度的三氯乙烯、四氯乙烯作用24 h后,细胞内超氧化物歧化酶(SOD)活性受到抑制;染毒浓度较低时细胞过氧化氢酶(CAT)活性呈激活势,染毒浓度过高CAT酶活性受到抑制。研究表明在体外培养条件下,氯乙烯类污染物诱导氧化应激可能是其产生细胞毒性的作用机制之一。     

Neurotoxicity and oxidative stress induced by permethrin in gills of the freshwater mussel Unio ravoisieri

Pyrethroids are contaminants found in the aquatic environment, and their toxicological effects on aquatic organisms have received extensive attention. However, the impact on freshwater bivalve of exposure to these chemicals is still largely unknown. Freshwater mussels Unio ravoisieri were exposed to two nominal permethrin (PM) concentrations C1?=?50?µg/L and C2?=?100?µg/L during 7 days. The measured concentrations of PM using gas chromatography (GC/ECD) in the treated aquariums were, respectively, 28.7–62.3?µg/L. Catalase (CAT), Glutathione-S-transferase (GST), and Acetylcholinesterase (AChE) activities, Glutatione (GSH) and Malondialdehyde (MDA) levels were determined in gills of U. ravoisieri. Significant increase in CAT activity by the lowest concentration and decrease by highest concentration were observed. Additionally, GST activity was increased in a concentration-dependent manner. However, statistically significant decrease in GSH levels (about 39%) was observed only at high concentration of this compound (100?µg/L). PM generated an increase in MDA levels reaching the highest value at the high concentration. AChE activity of mussel ranging from 51% inhibition at lowest concentration 50?µg/L to 89% inhibition at highest concentration 100?µg/L. The results indicated that oxidative stress and cell damage might be one of the main mechanisms of PM toxicity to freshwater mussels.