草甘膦对GC-1小鼠精原细胞的毒性作用及N-乙酰半胱氨酸的干预效应

为探讨41%草甘膦水溶液(农达)对雄性生殖细胞的毒性及其作用机制以及N-乙酰半胱氨酸(N-acetylcysteine,NAC)的干预效应。以GC-1小鼠精原细胞为受试细胞,设正常对照组、草甘膦染毒组(60、90、120、150、180 mg·L-1)、NAC干预组(10 mmol·L-1NAC+90 mg·L-1农达)。MTT法检测细胞存活率,Giemsa染色法观察细胞的形态学改变,彗星试验检测细胞DNA损伤,比色法检测细胞培养液乳酸脱氢酶(LDH)以及细胞内超氧化物歧化酶(SOD)、谷胱甘肽(GSH)及丙二醛(MDA)水平的变化。结果显示,随着草甘膦染毒浓度增加,细胞存活率逐渐下降(P0.01),彗星阳性率逐渐升高(P0.01);与对照组相比,草甘膦染毒组LDH活性增加(P0.05,60 mg·L-1组除外),MDA生成量增多(P0.05),GSH含量降低(P0.05)和SOD活性降低(P0.05)。抗氧化剂NAC预处理具有相应的拮抗作用。研究表明,60~180 mg·L-1浓度草甘膦对GC-1细胞有明显的损伤作用,其机制可能是草甘膦诱导氧化应激,导致细胞通透性增加和DNA损伤。抗氧化剂NAC对草甘膦的细胞毒性具有一定保护作用。     

ROS介导的氧化应激在INH诱导的细胞毒性中的作用及槲皮素的干预

为探讨ROS介导的氧化应激在异烟肼(INH)诱导L-02细胞毒性中的作用及槲皮素的干预作用,建立体外培养INH诱导L-02细胞氧化损伤模型,实验分为对照组(A)、INH组(B)、槲皮素低剂量组(C)及槲皮素高剂量组(D)。采用生化分析法检测L-02细胞培养液中天冬氨酸氨基转移酶(AST)和丙氨酸氨基转移酶(ALT)的活性;利用荧光探针检测L-02细胞线粒体内活性氧(ROS)水平;应用比色法检测L-02细胞内丙二醛(MDA)、谷胱甘肽(GSH)的含量以及主要抗氧化物酶的活性。结果表明,与对照组相比,INH能显著增加L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并显著减少L-02细胞内GSH的含量及超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)的活性(P0.01)。与INH组比较,槲皮素低剂量组L-02细胞培养液中AST的活性、线粒体内ROS水平及细胞内MDA的含量明显降低(P0.05),而细胞内SOD的活性明显增加(P0.05);高剂量槲皮素能显著降低L-02细胞培养液中AST和ALT的活性、细胞线粒体内ROS水平及细胞内MDA的含量(P0.01),并能显著增高L-02细胞内GSH的含量和主要抗氧化物酶的活性(P0.01)。与槲皮素低剂量组相比,槲皮素高剂量组的保护效应更明显(P0.05)。可见,ROS介导的氧化应激在INH诱导的L-02细胞毒性中发挥了重要作用,且槲皮素对INH诱导的L-02细胞氧化损伤具有保护作用。     

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.     

草甘膦对GC-1小鼠精原细胞的毒性作用及NAC的干预效应

为探讨41%草甘膦水溶液(农达)对雄性生殖细胞的毒性及其作用机制以及N-乙酰半胱氨酸(N-acetylcysteine, NAC)的干预效应。以GC-1小鼠精原细胞为受试细胞,设正常对照组、草甘膦染毒组(60、90、120、150、180 mg·L^-1)、NAC干预组(10 mmol·L^-1 NAC＋90 mg·L^-1农达)。MTT法检测细胞存活率,Giemsa染色法观察细胞的形态学改变,彗星试验检测细胞DNA损伤,比色法检测细胞培养液乳酸脱氢酶(LDH)以及细胞内超氧化物歧化酶(SOD)、谷胱甘肽(GSH)及丙二醛(MDA)水平的变化。结果显示,随着草甘膦染毒浓度增加,细胞存活率逐渐下降(p<0.01),彗星阳性率逐渐升高(p<0.01);与对照组相比,草甘膦染毒组LDH活性增加(p<0.05,60 mg·L^-1组除外),MDA生成量增多(p<0.05),GSH含量降低(p<0.05)和SOD活性降低(p<0.05)。抗氧化剂NAC预处理具有相应的拮抗作用。研究表明,60～180 mg·L^-1浓度草甘膦对GC-1细胞有明显的损伤作用,其机制可能是草甘膦诱导氧化应激,导致细胞通透性增加和DNA损伤。抗氧化剂NAC对草甘膦的细胞毒性具有一定保护作用。     

邻苯二甲酸二丁酯(DBP)与卵清白蛋白(OVA)联合染毒对小鼠肺脏和脾脏组织氧化应激的作用

为研究邻苯二甲酸二丁酯(dibutylphthalate,DBP)单独染毒及与卵清白蛋白(ovalbumin,OVA)联合染毒对小鼠肺脏和脾脏组织氧化应激的作用,将BALB/c小鼠随机分为8组:(1)未处理对照组(生理盐水组);(2)0.5mg·kg-1DBP染毒组;(3)5.0mg·kg-1DBP染毒组;(4)50mg·kg-1DBP染毒组;(5)1.67mg·kg-1OVA单独染毒组;(6)0.5mg·kg-1DBP与1.67mg·kg-1OVA联合染毒组;(7)5.0mg·kg-1DBP与1.67mg·kg-1OVA联合染毒组;(8)50mg·kg-1DBP与1.67mg·kg-1OVA联合染毒组。未处理对照组和DBP染毒组每天按体质量给予生理盐水和DBP灌胃。2周后,测定肺脏组织活性氧物种(ROS)、谷胱甘肽(GSH)和丙二醛(MDA)含量以及脾脏组织ROS、GSH含量。结果显示,联合染毒组相较于其他组的肺脏组织各指标均有不同的显著性差异(P<0.05),联合染毒组的脾脏组织中ROS含量较其他组有显著差异(P<0.05),而GSH含量无统计学意义(P>0.05)。结果说明,DBP与OVA联合染毒能够增强肺脏组织的氧化应激作用,对于脾脏组织的氧化应激作用不明显;DBP在联合染毒中显示一定免疫佐剂效应。     

邻苯二甲酸二丁酯(DBP)与卵清白蛋白(OVA)联合染毒对小鼠肺脏和脾脏组织的氧化应激

为研究邻苯二甲酸二丁酯(dibutyl phthalate,DBP)单独染毒及与卵清白蛋白(ovalbumin,OVA)联合染毒对小鼠肺脏和脾脏组织氧化应激的作用,将BALB/c小鼠随机分为8组:(1)未处理对照组(生理盐水组);(2)0.5 mg·kg-1DBP染毒组;(3)50 mg·kg-1DBP染毒组;(4) 50 mg·kg-1DBP染毒组;(5) 1.67 mg·kg-1OVA单独染毒组;(6) 0.5 mg·kg-1DBP与1.67 mg· kg-1OVA联合染毒组;(7) 5.0 mg·kg-1 DBP与1.67 mg·kg-1 OVA联合染毒组;(8) 50 mg· kg-1 DBP与1.67 mg·kg-1 OVA联合染毒组.未处理对照组和DBP染毒组每天按体质量给予生理盐水和DBP灌胃.2周后,测定肺脏组织活性氧物种(ROS)、谷胱甘肽(GSH)和丙二醛(MDA)含量以及脾脏组织ROS、GSH含量.结果显示,联合染毒组相较于其他组的肺脏组织各指标均有不同的显著性差异(P＜0.05),联合染毒组的脾脏组织中ROS含量较其他组有显著差异(P＜0.05),而GSH含量无统计学意义(P＞0.05).结果说明,DBP与OVA联合染毒能够增强肺脏组织的氧化应激作用,对于脾脏组织的氧化应激作用不明显;DBP在联合染毒中显示一定免疫佐剂效应.     

Promotive Effect of Glutathione on the Formation of DNA-Protein Crosslinks Induced by Formaldehyde in vitro and in vivo

研究发现,在环境水平的甲醛染毒之后,动物体内的谷胱甘肽(GSH)含量会发生显著减少,并呈现剂量-效应关系.值得思索的是,GSH的减少对甲醛所致的遗传毒性指标DNA-蛋白质交联(DPC)没有明显的保护作用.为了深入探讨GSH与甲醛的联合作用,进行了体外和体内两项实验.体外实验以Hela细胞为实验材料,实验组分为4组:对照组、250μMGSH组、250μM甲醛组、250μM甲醛和250μMGSH联合作用组;体内实验以昆明小鼠为实验材料,采用腹腔注射方法连续染毒两周.实验组分为4组:对照组、1mMGSH组、1mM甲醛组、1mM甲醛和1mM GSH联合作用组.体外实验与体内实验结果表明,单独GSH染毒组所致DPC与试剂对照组之间没有统计学差异(p>0.05;p>0.05),甲醛染毒组所致DPC显著高于对照组(p<0.01;p<0.05),联合作用组所致DPC不但显著高于试剂对照组(p<0.01;p<0.01)而且还显著高于甲醛染毒组(p<0.05;p<0.01).结果提示,GSH单独作用不能诱导DPC形成,但是GSH对甲醛所致的DPC具有促进作用.同时论文对这种协同作用的发生机制进行了讨论,作者认为GSH与甲醛的协同作用,和GSH与一氧化氮的协同作用的分子机制类似。     

纳米碳黑与重金属对BEAS-2B细胞的联合毒性作用模式评价

通过研究空气颗粒物的代表性组分纳米碳黑(nano particle carbon black,NPCB)与重金属(Pb/Cr/Cd)联合染毒对BEAS-2B细胞存活率和LDH漏出率的影响,旨在阐明NPCB与重金属对细胞毒性的联合作用模式。检测NPCB与重金属(Pb/Cr/Cd)联合染毒24 h后BEAS-2B细胞存活率(CCK-8法)和LDH漏出率(LDH活性比色法)的变化,采用析因方差分析判断其是否存在联合毒性作用及联合作用模式。NPCB与重金属(Pb/Cr/Cd)联合染毒在细胞存活率和LDH漏出方面存在联合作用;与对照组和单独染毒组相比,低剂量Pb(125μmol·L-1)与NPCB联合染毒对细胞存活率无交互作用,对LDH漏出表现为拮抗作用;高剂量Pb(1 000μmol·L-1)与NPCB联合染毒对细胞存活率表现为协同作用,对LDH漏出无交互作用;Cr和Cd与NPCB联合染毒在细胞存活率方面均表现为协同作用;低剂量Cr和Cd与NPCB联合染毒在LDH漏出方面无交互作用,高剂量时表现为协同作用。NPCB与重金属存在联合作用,金属不同、剂量不同以及评价指标不同,其联合作用模式不尽相同。     

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。     

谷胱甘肽对甲醛所致Hela细胞毒性的影响

为研究还原型谷胱甘肽(GSH)对甲醛所致Hela细胞毒性的影响,采用体外染毒方式,应用KC1-SDS法和MTT法分别检测GSH对甲醛引起Hela细胞DNA-蛋白质交联(DPC)和细胞活性的影响.结果表明,250μmol·L-1浓度下,DNA-蛋白质交联实验中甲醛染毒组所致的DPC显著高于对照组(p＜0.01),GSH+...     

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.     

Toxicity of nano-anatase TiO2 to mice: Liver injury,oxidative stress

There are concerns regarding the toxicity of nano-TiO₂, but data are limited on the mechanism underlying oxidative damage to liver of mice. In order to further study these mechanisms of nano-TiO₂ particles, nano-anatase TiO₂ (5 nm) were injected into the abdominal cavity of ICR mice daily for 14 days and biochemical parameters in liver were investigated. The increase of hepatic lipids peroxide produced by nano-anatase TiO₂ suggested an oxidative attack that was activated by a reduction of antioxidative defense mechanisms as measured by analyzing the activities of superoxide dismutase, catalase, ascorbate peroxidase, and glutathione peroxidase, as well as antioxidant levels such as glutathione and ascorbic acid. The antioxidative responses of liver were reduced in mice by nano-anatase TiO₂. The oxidative stress of nano-anatase TiO₂ on liver was greater than that seen with bulk-TiO₂.     

立方体和八面体微/纳米氧化亚铜对大型水蚤(Daphnia magna)的氧化胁迫和生理损伤

为了实现特定的功能和应用,越来越多不同结构特性的纳米材料逐渐被人们精确合成。一些研究指出纳米材料的物理化学特性能够显著影响纳米材料对水生生物的毒性作用,但是对于不同特性的纳米氧化亚铜的毒性研究依然比较缺乏。本研究制备了2种不同形貌和结构的微/纳米氧化亚铜(micro/nano-Cu_2O)晶体,通过对大型水蚤(Daphnia magna)进行72 h的急性暴露实验,测定了大型水蚤体内还原型谷胱甘肽(GSH)的含量以及超氧化物歧化酶(SOD)、过氧化氢酶(CAT)和钠/钾腺苷三磷酸酶(Na+/K+-ATPase)的活性变化。结果表明在2种不同特性的微/纳米氧化亚铜暴露体系中,大型水蚤体内Cu的积累量差别不大,但是不同结构的micro/nano-Cu_2O对大型水蚤抗氧化酶活性和钠/钾腺苷三磷酸酶活性影响存在差别。与立方体相比,八面体micro/nano-Cu_2O能够暴露更多的{111}面,并且其原子排列使其具有较高的表面能量,因此更容易在大型水蚤肠道内诱导产生活性氧(ROS)及溶出更多Cu2+,对大型水蚤产生更强的氧化胁迫和膜损伤。     

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。     

Salinity stress and hydrogen peroxide regulation of antioxidant defense system in Ulva fasciata

The regulation of antioxidant defense system in macroalgae exposed to salinity stress was examined in Ulva fasciata Delile. As compared to the 30‰ control, a long-term (4 days) exposure to hyposaline (5, 15‰) and hypersaline (60, 90, 120, 150‰) conditions inhibited growth rate and TTC reduction ability. A decrease in maximum quantum efficiency (F _v/F _m ratio) and the maintenance of superoxide dismutase activity under salinity stress indicate the potential generation of reactive oxygen species in chloroplasts. An exposure to 15, 60, and 90‰ decreased seawater H₂O₂ contents but increased thallus H₂O₂ contents that are positively correlated with TBARS and peroxide contents. Alleviation of oxidative damage and H₂O₂ accumulation at 15 and 90‰ by a H₂O₂ scavenger, dimethylthiourea, suggests that oxidative damage occurring under moderate hyposaline and hypersaline conditions is ascribed to accumulated H₂O₂. Increased glutathione reductase activity and glutathione content and decreased ascorbate content are responsible for accumulated H₂O₂ at 15, 60, and 90‰, while ascorbate peroxidase activity increased only at salinity ≥ 90‰. Catalase and peroxidase activities also increased at 60 and 90‰ for H₂O₂ removal, but only catalase showed activity increase at 15‰. For the regeneration of ascorbate, the activities of both dehydroascorbate reductase and monodehydroascorbate reductase were increased at 5 and 15‰ while only monodehydroascorbate reductase activity increased at 60 and 90‰. It is hypothesized that the availability of antioxidants and the activities of antioxidant enzymes are increased in U. fasciata to cope with the oxidative stress occurring in hyposaline and hypersaline conditions.     

Tualang honey supplementation improves oxidative stress status among chronic smokers

Free radicals induced by cigarette smoking have been linked to an increase in oxidative stress resulting in smoking-related cardiovascular diseases. However, the possible effect of honey that has antioxidant property in improving oxidative stress status among smokers has not yet been reported. Hence, this study was to determine the effects of 12-week Tualang honey supplementation on F₂-isoprostanes, superoxide dismutase, glutathione peroxidase, catalase, and total antioxidant status among chronic smokers. A total of 32 non-smokers and 64 chronic smokers were recruited from Quit Smoking Clinic and Health Campus, Universiti Sains, Malaysia. Smokers were randomized into two groups (n = 32/group) namely smokers without supplementation and smokers with honey supplementation (20 g/day) for 12 weeks. Blood was obtained from non-smokers and smokers at pre-intervention and from smokers at post-intervention. During pre-intervention, the levels/activity of F₂-isoprostanes, total antioxidant status, and catalase were significantly higher while superoxide dismutase and glutathione peroxidase were lower in smokers than non-smokers. During post-intervention, in supplemented smokers, there were significant decrease in F₂-isoprostanes and increase in total antioxidant status, glutathione peroxidase and catalase levels/activities compared with pre-intervention. This study indicates that honey supplementation improves oxidative stress status suggesting a beneficial role of honey in reducing the risk of cardiovascular diseases.     

Effects of Matricaria chamomilla L. on lipid peroxidation,antioxidant enzyme systems,and key liver enzymes in CCl4-treated rats

In this study, we investigated the effects of Matricaria chamomilla L. extract (MCE) on lipid peroxidation, antioxidant enzyme systems, and several liver enzymes in carbon tetrachloride (CCl₄)-treated rats. Rats were divided into five groups. The first group (control group) was fed on standard feed. The rats in the other groups (CCl₄, MCE50, MCE100, and MCE200) were injected intraperitoneally with 0.8?mL?kg^?1 CCl₄. Moreover, rats in the MCE50, MCE100, and MCE200 groups were gavaged with 50?mg?kg^?1, 100?mg?kg^?1, and 200?mg?kg^?1 MCE, respectively. Serum aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, whole blood malondialdehyde (MDA) and glutathione (GSH) levels, and erythrocyte superoxide dismutase (SOD), glutathione peroxidase (GPx), and catalase (CAT) activity levels were measured after 14 days of exposure. ALT and AST in the CCl₄ group increased significantly in comparison to the control group (p?4, MCE50, MCE100, and MCE200 groups at different significance levels. In conclusion, the findings suggest that, depending on the dose administered, MCE decreases CCl₄-induced damage and consequent oxidative stress in rats; it affects the antioxidant system positively.     

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.     

Impaired behavior and changes in some biochemical markers of bivalve (Ruditapes decussatus) due to zinc toxicity

Susceptibility and response of bivalves, the clam Ruditapes decussatus, to zinc (Zn) were studied by monitoring behavior using valve movement and some biochemical parameters. The LC₅₀ was 4.1 mg L^?1 at 7 days. Depuration of Zn from their tissues was also followed. Accumulation of Zn increased with concentration and duration of exposure. After 20 days, Zn caused impairment of valve movement as well as the antioxidant system, decreasing glutathione and protein levels and increasing the lipid peroxidation which is indicative of oxidative damage. Results suggested that behavior and biochemical parameters of clam R. decussatus were sensitive and suitable responses for assessing the effects of Zn on the aquatic ecosystems. It could be concluded that there is a time–dose–response relationship of Zn with behavior and oxidative stress of R. decussatus.     

Antioxidant responses in the polychaete Perinereis gualpensis (Nereididae) exposed to the carbon nanomaterial fullerene (C60)

The objective of this study was to analyse biochemical responses induced by the carbon nanomaterial fullerene (C₆₀) in the polychaete Perinereis gualpensis (Nereididae). The activity of glutathione-S-transferase (GST), glutathione reductase (GR) and glutamate cysteine ligase (GCL), as well as total antioxidant capacity, concentration of glutathione (GSH) and malondialdehyde (TBARS), were analysed. Estuarine worms were maintained in sediments collected at an unpolluted site and spiked with fullerene (3 mg C₆₀·g^?1 sediment). A control group was run in parallel. Scanning electron microscope (SEM) images of sediment and fullerene indicated that the size of the carbon nanomaterial should enable it to be ingested by the polychaete. No evidence of oxidative damage (TBARS) was observed in any of the treatments, and the same was true for GSH and GCL measurements (p>0.05). Total antioxidant capacity was higher in the C₆₀ group after 2 and 7 d when compared with the control group (p<0.05), suggesting that fullerene is acting as an antioxidant. The fact that P. gualpensis is an infaunal organism diminishes the chance of fullerene photoexcitation with consequent reactive oxygen species production. Thus, the data indicated an absence of toxic responses mediated by oxidative stress in estuarine worms exposed to C₆₀ mixed in sediments.