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.     

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。     

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.     

三种典型纳米颗粒物造成的人体肺细胞氧化应激和炎症效应(Oxidative Stress and Inflammatory Effect on A549 Cell Line Induced by Three Typical Nano-Particles )

采用体外细胞暴露实验研究了人肺腺癌细胞系(A549)单层细胞暴露于50和500μg·mL-1两种浓度纳米氧化钛、纳米氧化硅、碳纳米管和晶体石英砂等四种颗粒物后产生的氧化应激和炎症反应.用细胞活度、细胞内活性氧总量和细胞上清液中白细胞介素8(IL-8)表达量表征暴露效应.研究结果表明,纳米氧化钛、纳米氧化硅和碳纳米管在体外暴露实验过程中均发生不同程度的聚集;细胞暴露48h后,三种纳米颗粒物均使A549细胞活度下降,诱导细胞产生过量活性氧,同时刺激细胞IL-8表达量增高;三种纳米颗粒物中,纳米氧化钛和纳米氧化硅对细胞活度影响较大,碳纳米管诱发的炎症效应较另两种纳米材料强.     

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.     

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.     

Combined toxic effect of airborne heavy metals on human lung cell line A549

Many studies have demonstrated that heavy metals existing as a mixture in the atmospheric environment cause adverse effects on human health and are important key factors of cytotoxicity; however, little investigation has been conducted on a toxicological study of a metal mixture from atmospheric fine particulate matter. The objective of this study was to predict the combined effects of heavy metals in aerosol by using in vitro human cells and obtain a suitable mixture toxicity model. Arsenic, nickel, and lead were selected for mixtures exposed to A549 human lung cancer cells. Cell proliferation (WST-1), glutathione (GSH), and interleukin (IL)-8 inhibition were observed and applied to the prediction models of mixture toxicity, concentration addition (CA) and independent action (IA). The total mixture concentrations were set by an IC₁₀-fixed ratio of individual toxicity to be more realistic for mortality and enzyme inhibition tests. The results showed that the IA model was statistically closer to the observed results than the CA model in mortality, indicating dissimilar modes of action. For the GSH inhibition, the results predicted by the IA and CA models were highly overestimated relative to mortality. Meanwhile, the IL-8 results were stable with no significant change in immune reaction related to inflammation. In conclusion, the IA model is a rapid prediction model in heavy metals mixtures; mortality, as a total outcome of cell response, is a good tool for demonstrating the combined toxicity rather than other biochemical responses.     

Single walled carbon nanotubes induce cytotoxicity and oxidative stress in HEK293 cells

The aim of the present study was to evaluate the potential toxicity and general mechanisms involved in single walled carbon nanotubes (SWCNTs)-induced cytotoxicity using human embryonic kidney cell line (HEK293) cells. Carbon nanotubes (coded as CNT) used in this study were synthesized by the chemical vapor deposition method. To elucidate the possible mechanisms underlying SWCNT-induced cytotoxicity, cell viability, cell membrane damage (lactate dehydrogenase activity (LDH) assay), reduced glutathione (GSH), interleukin-8 (IL-8) and lipid peroxidation products levels were quantitatively assessed following SWCNT exposure for 48 hr using HEK293 cells. Exposure of cells to SWCNT at 3–300 μg/ml produced significant reduction in cell viability in a concentration-dependent manner. The IC₅₀ value of SWCNT was found to be 87.58 μg/ml. Exposure of HEK cells to SWCNT at 10–100 μg/ml resulted in concentration-dependent cell membrane damage, increased production of IL-8, elevated levels of thiobarbituric acid reactive substances like malondialdehyde and decreased intracellular GSH levels. In summary, exposure to SWCNT resulted in a concentration-dependent cytotoxicity in cultured HEK293 cells that was associated with increased oxidative stress.     

ZnO纳米粒子抑制体外小鼠光感受器细胞MnSOD的表达及活性

随着纳米技术的发展,纳米材料在生物医药以及化工中已得到广泛应用。作为一类新型材料,其安全性也日益受到人们的高度关注。为探索氧化锌(ZnO)纳米粒子对小鼠视网膜光感受器细胞的毒性作用,本文通过MTT、荧光染色、流式细胞术、实时荧光定量PCR和酶联免疫吸附试验(ELISA)等技术,分别对经不同浓度ZnO纳米粒子处理的小鼠光感受器细胞活性、活性氧水平、锰超氧化物歧化酶(Mn SOD)的基因和蛋白表达及活性进行了检测。结果表明,ZnO纳米粒子可通过诱导细胞线粒体产生过多的活性氧,降低线粒体膜电位,导致小鼠视网膜光感受器细胞损伤;ZnO纳米粒子能显著减少Mn SOD在mRNA和蛋白质水平的表达,降低Mn SOD活性,加剧氧化应激介导的细胞损伤。因此,氧化应激水平的提高导致了过量的活性氧产生及Mn SOD表达和活性的下降,与ZnO纳米粒子引起的细胞毒性作用有关。     

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.     

In vitro cytotoxicity of multi-wall carbon nanotubes on human cell lines

The aim of this study was to evaluate the in vitro toxicity of two multi-wall carbon nanotubes on four different cell lines: human alveolar epithelial (A549) cells, hepatocytes (Hep 3B cells), human embryonic kidney cells, and intestinal (P407 cells) cells. The adverse effects of carbon nanoparticles were analyzed after 24 h incubation with different cell lines using the trypan blue dye exclusion method. Incubation of carbon nanotubes with different cells produced a concentration-dependent inhibition of growth of the cells. The TC₅₀ or IC₅₀ values (toxic concentration 50, i.e., concentration of particles inducing 50% cell mortality) of two nanoparticles were (1) found to be in the range 23.5–30.5 µg mL^?1, and (2) less than that of quartz (known toxic agent, 28.8–66.9 µg mL^?1), indicating the greater cytotoxic effect of carbon nanoparticles than quartz particles.     

Response in germination and seedling growth in Phaseolus mungo under salt and drought stress

The effect of salt and drought stress at the water potentials of-2, -4,-6and -8 bars induced by NaCl and PEG 6000 (Polyethylene glycol 6000) each, on germination and early seedling growth, were investigated for two varieties (PU-19 and Type-9). Electrical conductivity (EC) value of the NaCl solutions were 4.5, 8.8, 12.7 and 16.3 dS m(-1). Germination percentage, root and shoot length, and seedling fresh and dry weight were measured in the study. The objective was to determine genotypic differences among P. mungo varieties in terms of salt and drought stress and to determine factors (salt toxicity or osmotic stress due to PEG) inhibiting seed germination. The germination results revealed that the genotypes significantly differed for salt and drought stress. PU-19 appeared to be more tolerant to salt and drought stress comparable to var Type-9. Both NaCl and PEG inhibited germination and seedling growth in both the varieties, but the effects of NaCI compared to PEG was less on germination and seedling growth. All varieties were able to germinate at all NaCl levels without significant decrease in germination, while a drastic decrease in germination was recorded at -6 and -8 bars of PEG. It was concluded that inhibition in germination at equivalent water potential of NaCl and PEG was mainly due to an osmotic effect rather than salt toxicity.     

大气中细颗粒物对肺癌细胞A549迁移和侵袭作用的影响

采集大连城区大气中可吸入性细颗粒物(PM_(2.5)),研究其对肺癌A549细胞迁移、黏附和侵袭力的影响,利用明胶酶谱法检测细胞分泌的基质金属蛋白酶活性,利用Western blot法测定A549细胞中转移相关蛋白的表达。结果表明,在无明显细胞毒性浓度下,PM_(2.5)可增加A549细胞的迁移速率;细胞与细胞外基质的黏附率增加;细胞侵袭实验结果表明PM_(2.5)可增加A549细胞穿透基底膜的能力;用明胶酶谱法检测发现PM_(2.5)可使A549细胞分泌的基质金属蛋白酶-2(MMP-2)和基质金属蛋白酶-9(MMP-9)活性增强。转移相关蛋白——细胞钙粘蛋白-N(N-cadherin)的表达量升高,而钙粘蛋白-E(E-cadherin)的表达量下降,实验结果表明,PM_(2.5)可增强A549细胞的侵袭性,大气中的可吸入性颗粒可能导致肺癌转移发生率增加。     

汽油尾气对人肺腺癌A549细胞的氧化损伤效应研究

为研究汽油燃烧汽车尾气(简称汽油尾气)的氧化损伤效应及其可能的毒作用机制,以人肺腺癌A549细胞为研究对象,采用MTT试验测试汽油尾气对细胞的毒性作用;通过测定细胞内超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性了解细胞在汽油尾气作用下抗氧化水平的改变;并用彗星试验检测汽油尾气对细胞DNA氧化损伤及修复的影响．结果显示汽油尾气在浓度≥0．0625L·mL-1时即显示出明显的细胞毒性;汽油尾气作用下A549 细胞SOD及GSH-Px活性均下降,在一定的浓度范围内与对照组比较有统计学差异(p<0．05)．汽油尾气可诱导 A549细胞不同程度的DNA氧化损伤,且细胞拖尾率和DNA迁移长度均随着汽油尾气浓度的增加而增加;损伤后 A549细胞修复发生较快,3小时内基本修复完全．提示汽油尾气具有明显的细胞毒性作用,可影响A549细胞抗氧化酶活性,并可导致DNA的氧化损伤．     

Determination of nephrotoxicity and genotoxic potential of silver nanoparticles in Swiss albino mice

Silver nanoparticles (AgNPs) possess properties that are important for industrial and medical applications. This study is aimed to investigate intra-peritoneal toxicity of AgNPs at 26, 52 or 78 mg/kg/day for 5 days in mice Swiss albino mice. The effects on oxidative stress markers activities of serum superoxide dismutase (SOD) and catalase (CAT), levels of serum glutathione (GSH), apoptosis (TUNEL assay), DNA strand breaks (comet assay) in lymphocytes, as well as histopathological of kidney tissue were determined. AgNPs significantly increased SOD and CAT activities reduced GSH levels. In kidney apoptosis (TUNEL assay) while DNA strand breaks (comet assay) in lymphocytes revealed that AgNPs at concentration 78 mg/kg produced significant apoptosis and DNA damage. AgNPs also produced associated histological renal tissue damage. Evidence suggests that AgNPs-mediated alterations may be attributed to oxidative stress.     

Determination of F2-isoprostanes in cultured human lung epithelial cells after exposure to metal oxide and silica nanoparticles by high-performance liquid chromatography/tandem mass spectrometry

The environmental impact of nanotechnology has caused a great concern. Many in vitro studies showed that many types of nanoparticles were cytotoxic. However, whether these nanoparticles caused cell membrane damage was not well studied. F₂-isoprostanes are specific products of arachidonic acid peroxidation by nonenzymatic reactive oxygen species and are considered as reliable biomarkers of oxidative stress and lipid peroxidation. In this article, we investigated the cytotoxicity of different nanoparticles and the degree of cellular membrane damage by using F₂-isoprostanes as biomarkers after exposure to nanoparticles. The human lung epithelial cell line A549 was exposed to four silica and metal oxide nanoparticles: SiO₂ (15 nm), CeO₂ (20 nm), Fe₂O₃ (30 nm), and ZnO (70 nm). The levels of F₂-isoprostanes were determined by using high-performance liquid chromatography/mass spectrometry. The F₂-isoprostanes’ peak was identified by retention time and molecular ion m/z at 353. Oasis HLB cartridge was used to extract F₂-isoprostanes from cell medium. The results showed that SiO₂, CeO₂, and ZnO nanoparticles increased F₂-isoprostanes levels significantly in A549 cells. Fe₂O₃ nanoparticle also increased F₂-isoprostanes level, but was not significant. This implied that SiO₂, CeO₂, ZnO, and Fe₂O₃ nanoparticles can cause cell membrane damage due to the lipid peroxidation. To the best of our knowledge, this is the first report on the investigation of effects of cellular exposure to metal oxide and silica nanoparticles on the cellular F₂-isoprostanes levels.     

铅与纳米SiO2联合染毒对A549细胞氧化损伤的影响

为了研究铅与纳米SiO2联合染毒所致的细胞损伤特征,并从氧化应激方面探讨其可能的作用机制。用铅和SiO2处理A549细胞,采用四唑盐(MTT)比色法检测细胞存活率,评价铅和SiO2联合染毒所致的细胞损伤特征;采用硫代巴比妥酸(TBA)比色法检测细胞内丙二醛(MDA)含量,评价铅与SiO2联合染毒所致细胞的氧化应激状态;检测了细胞内抗氧化物还原型谷胱甘肽(GSH)含量以及细胞内抗氧化酶的活性,以评价铅与SiO2联合染毒对细胞抗氧化系统的影响。将实验数据进行ANOVA分析。结果表明,铅、SiO2单独染毒组各指标没有明显改变;而联合染毒能造成细胞氧化损伤,表现为细胞存活率、GSH水平、超氧化物歧化酶(SOD)及谷胱甘肽过氧化物酶(GSH-Px)活性显著低于对照组及2个单独染毒组(P<0.05),细胞内MDA含量显著高于对照组及各单独染毒组(P<0.05)。可见,联合染毒可引起明显的细胞毒性,氧化损伤可能是铅与SiO联合染毒致肺细胞毒性损伤的作用机制之一。     

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。     

活性氧和钙信号参与铅对酵母细胞的毒性作用

以模式生物酵母菌为材料,研究铅对细胞的毒性效应,探讨胞内活性氧(ROS)和Ca~(2+)在铅诱导细胞死亡中的作用。结果显示,浓度为5~100 mg·L~(-1)的硝酸铅可降低酵母细胞活性,诱导酵母细胞死亡,随着铅浓度的提高和作用时间的延长,细胞死亡率增高。在铅处理组酵母细胞中,ROS和Ca~(2+)水平显著升高,线粒体膜电位明显下降;用1 mmol·L~(-1)的外源抗坏血酸(AsA)能降低铅引发的酵母细胞死亡,0.5 mmol·L~(-1)的钙离子螯合剂乙二醇双四乙酸(EGTA)或0.1 mmol·L~(-1)的质膜Ca~(2+)通道特异性抑制剂氯化镧(LaCl_3)亦可明显抑制铅引起的酵母细胞死亡。研究结果表明,铅诱发的酵母细胞死亡与处理组胞内ROS和Ca~(2+)升高有关,高浓度的Ca~(2+)可能通过诱导线粒体膜通透性转变孔道开放,或者高水平ROS可能损伤线粒体膜,致线粒体膜电位下降,继而激活相关下游信号导致细胞死亡。     

纳米硫化镉对A549细胞的损伤研究

研究纳米硫化镉(Nano-Cd S)材料对肺癌细胞系A549的毒性及氧化损伤作用。培养A549细胞,经传代后接种于6孔板中,每孔2 m L完全培养基,接种次日进行染毒。用直径20~30 nm、长度80~100 nm的Nano-Cd S进行染毒,染毒浓度分别为0、5、10、20、40和80 mg·L~(-1)。染毒24 h后用MTT检测细胞存活率,以存活率在80%左右的浓度为后续实验染毒浓度。应用流式细胞技术,用荧光探针法检测A549细胞的活性氧(reactive oxygen species,ROS)含量,PI-Annexin-V法检测细胞凋亡情况;用试剂盒检测细胞中超氧化物岐化酶(superoxide dismutase,SOD)和过氧化氢酶(catalase,CAT)活性以及丙二醛(malondialdehyde,MDA)含量,判断细胞氧化损伤情况。不同浓度Nano-Cd S处理细胞24 h之后,细胞存活率随剂量的增加而下降,浓度为10、20、40和80μg·L~(-1)时,存活率分别为(88.71%±0.80%)、(81.93%±3.06%)、(75.23%±1.13%)和(70.66%±5.63%),且各组间差异均具有统计学意义(P0.05)。以浓度为10和20 mg·L~(-1)的Nano-Cd S染毒24 h后,胞内ROS含量和细胞凋亡率随染毒剂量的增加而增加(P0.05);浓度为10 mg·L~(-1)时,细胞凋亡率为(6.26%±0.44%)。与对照相比,各染毒组SOD和CAT活性和MDA含量升高,20 mg·L~(-1)染毒组SOD和CAT活性和MDA含量高于10 mg·L~(-1)染毒组(P0.05)。研究表明,纳米硫化镉能引起A549细胞的氧化损伤和细胞凋亡,具有明显的细胞毒性。