Cytotoxicity and DNA damage of five organophosphorus pesticides mediated by oxidative stress in PC12 cells and protection by vitamin E

Previous studies have demonstrated that pesticides could induce cytotoxicity and genotoxicity in vivo and in vitro, and that oxidative stress may be an important factor involved. However, investigations comparing the capability of different organophosphorous (OP) compounds to induce cytotoxicity, genotoxicity and oxidative stress are limited. Hence, the aim of this paper was to access the cytotoxic and genotoxic effects of five OPs or metabolites, Acephate (ACE), Methamidophos (MET), Chloramidophos (CHL), Malathion (MAT) and Malaoxon (MAO), and to clarify the role of oxidative stress, using PC12 cells. The results demonstrated that MET, MAT and MAO caused significant inhibition of cell viability and increased DNA damage in PC12 cells at 40 mg L^?1. MAO was more toxic than the other OPs. ACE, MET, MAT and MAO increased the levels of intracellular reactive oxygen species (ROS) and malondialdehyde (MDA), and decreased the activity of superoxide dismutase (SOD), catalase (CAT) and glutathione (GSH) at 20 mg L^?1 and 40 mg L^?1 to different degrees. Pre-treatment with vitamin E(600 μM)caused a significant attenuation in the cytotoxic and genotoxic effect; pre-treatment reversed subsequent OP-induced elevation of peroxidation products and the decline of anti-oxidant enzyme activities. These results indicate that oxidative damage is likely to be an initiating event that contributes to the OP-induced cytotoxicity.     

工程塑料环境因素与载荷应力耦合作用试验装置研究

目的 设计一种能够模拟工程塑料实际服役工作环境的试验装置,在多型自然环境中,构建兼具环境因素侵蚀与载荷应力耦合作用的试验条件。方法 研制工程塑料环境因素与载荷应力协同作用试验装置,采用包括拉伸加载、弯曲加载、控制系统等组件的模块化设计,实现0.01~16 Hz加载频率的拉伸及弯曲载荷,最大1 550 kg的拉伸载荷,最大375 kg的弯曲载荷。结果 将研制完成的试验装置置于多型自然环境下对试验施加恒定和交变载荷,以真实模拟工程塑料实际服役中的环境因素与载荷应力协同作用。结论 试验装置制造加工难度小,结构稳定可靠,可用于评价和研究工程塑料等系列类型材料的环境损伤性能演变。     

哈尔滨市城乡居民生活消费的环境压力分析

论文用生态足迹理论和方法,定量研究哈尔滨市城乡居民食物、生活用品、生活用能、水资源、住区和生活污染等6类消费项的环境压力,为引导城市化发展和城乡居民建立可持续消费模式提供科学依据。结果显示,1985～2003年哈尔滨市人均生活消费的环境压力不断增大,并在此期间超过生态承载力,产生生态赤字。城镇居民生活消费及各分项足迹均大于农村居民,差距呈加大趋势。在消费构成上,城镇和农村居民的食物消费足迹最大,2003年两者分别为1.054hm²/人和0.711hm²/人,城镇人均动物性食物消费数量显著大于农村,是其食物足迹较大的主要原因;在生态空间占用上,耕地占用面积最大,城乡居民分别为0.947hm²/人和0.700hm²/人,分别占其总足迹的58.7%和73.4%。研究表明,城镇化发展和消费升级将进一步加大区域环境压力。     

基于PM2.5的中国雾霾灾害风险评价

基于雾霾胁迫、人口暴露和适应能力,结合遥感数据与统计数据,对2014年中国286个地级及以上城市的雾霾灾害风险进行评价,在此基础上,识别雾霾灾害风险热点区的风险主导因子.结果表明:中国城市雾霾灾害风险整体水平不高且内部差异显著,雾霾灾害风险大体呈"东高西低、北高南低"的空间布局特征.雾霾灾害风险热点区范围涵盖96个城市,占据国土面积92.4万km~2,波及人群数量5.9亿.风险主导因子分区方面,适应能力主导区分布在汕头、揭阳、邵阳、娄底、玉林、汕尾、达州、巴中、天水、昭通、潮州和贵港等12个城市;雾霾胁迫主导区分布在郑州、上海、成都、泰州、济南、西安、武汉、鄂州、南京、扬州、天津、无锡、嘉兴、南昌、常州、芜湖、淄博、合肥、镇江、黄石、马鞍山、南通和日照等23个城市,其余61个城市则属于雾霾胁迫-适应能力综合主导区.     

纳米氧化锌颗粒物通过氧化应激和离子通道失调诱导大鼠气管上皮细胞凋亡的机理

纳米氧化锌具有广泛的工业用途,其生态安全性受到广泛关注,针对纳米氧化锌诱导的呼吸道细胞毒性及其作用机理研究尚不广泛.本研究分别采用不同浓度和粒径(30 nm和90 nm)的氧化锌颗粒物处理大鼠气管上皮细胞(rat tracheal epithelial cells,RTE cells),暴露时间为12 h,通过检测细胞内锌元素含量,细胞增殖抑制率,细胞凋亡率,凋亡相关caspsae 3基因与蛋白相对表达量,细胞内金属硫蛋白活性,ROS和MDA含量、细胞内Ca~(2+)-ATP酶和Na~+/K~+-ATP酶活性来分析纳米氧化锌诱导细胞毒效应机理.在90 nm纳米氧化锌高浓度暴露时,其细胞内锌元素浓度为0.845μg·L~(-1),约为低浓度暴露组的4.7倍,是30 nm低浓度暴露组的9倍;纳米颗粒物诱导的细胞增殖和凋亡毒效应具有剂量和尺寸依赖效应;30 nm处理组的pro-caspase 3和cleaved-caspase 3蛋白表达量均高于90 nm暴露组;暴露浓度为10 mg·L~(-1)的90 nm处理组的金属硫蛋白增加量为0.533μg·L~(-1),增幅达到46%;不同粒径氧化锌颗粒物处理后,细胞内ROS和MDA含量显著上升,且30 nm处理组结果均高于90 nm处理组;纳米氧化锌颗粒物暴露诱导细胞Ca~(2+)-ATP酶和Na~+/K~+-ATP酶活性显著下降,30 nm氧化锌颗粒物暴露组,其Na~+/K~+-ATP酶活性分别是对照组的1.8倍和3.5倍.纳米氧化锌颗粒物进入RTE细胞,通过干扰锌在细胞内代谢,诱导细胞内ROS和MDA水平升高,产生氧化应激,进而诱导细胞凋亡是导致纳米氧化锌产生细胞毒性的主要原因之一.纳米氧化锌会导致细胞内Ca~(2+)-ATPase和Na~+/K~+-ATPase活性下降,离子通道失调,破坏细胞内离子平衡,进一步造成细胞凋亡.     

CdSe/ZnS量子点对稀有鮈鲫胚胎发育的影响及其氧化应激作用

本研究以稀有鮈鲫(Gobiocypris rarus)为对象,研究了不同浓度CdSe/ZnS量子点(QDs)暴露下,稀有鮈鲫胚胎发育过程中自主运动频率、内心率和体长的变化,以及利用体内超氧化物歧化酶(SOD)和丙二醛(MDA)作为毒性指标,反映CdSe/ZnS QDs暴露对稀有鮈鲫胚胎发育的氧化应激作用.结果显示:CdSe/ZnS QDs对稀有鮈鲫胚胎72 hpf(hours post fertilization)的半致死浓度(LC50)为319.629 nmol·L-1,96 hpf的半致畸浓度(EC50)为203.312 nmol·L-1.CdSe/ZnS QDs暴露不仅影响稀有鮈鲫胚胎死亡率、畸形率、自主运动频率、孵化时间和孵化率,而且使其内心率减缓、体长缩短,导致胚胎卵凝结,心包囊肿,出现脊椎弯曲等多种毒性现象.同时发现,CdSe/ZnS QDs暴露导致稀有鮈鲫体内MDA含量增加以及SOD活力的降低.这表明CdSe/ZnS QDs对稀有鮈鲫胚胎发育具有致畸、致死作用,而氧化应激可能是引起其胚胎致畸、致死的重要机制之一.     

The Water Poverty Index: An application in the Indian context

For developing countries, the proportion of households covered by improved water resources is conventionally used to assess the water stress situation. However, in a developing country like India with a high population growth rate, water demand and supply are considerably mismatched. An agro-based economy with large variations in socio-economic conditions and changing rainfall patterns across the states imposes greater challenge on water resources. Therefore, there is a need to assess the water situation across the country in a holistic manner. This paper proposes application of the Water Poverty Index as a comprehensive policy tool to assess actual water-stress situation across 20 major states in India. This index covers important socio-economic parameters such as access, capacity, use and environment in addition to water resources of each state. The results and findings are expected to be of use to policymakers and implementing agencies. In view of policy formulation, a state performing well on a Water Poverty Index component can act as a benchmark for another state.     

Mitochondrial toxicity and in vitro biological effects of ambient PM2.5 from an urban site in China

Abstract

The roles of PM_2.5-induced mitochondrial damage and oxidative stress on mast cell degranulation were examined in vitro. Mast cells were treated with suspensions of PM_2.5 in Dulbecco’s modified Eagle’s medium at concentrations from 25 to 200?mg/L in the absence or presence of 10?mmol/L N-acetyl-L-cysteine. Biological effects and mitochondrial function were assessed by determining cell viability, β-hexosaminidase release, interleukin-4 secretion, reactive oxygen species generation, adenosine triphosphate production, potential alteration of mitochondrial membrane, and activities of mitochondrial electron transport chain complexes I and III. Exposure of mast cells to PM_2.5 induced reduction of adenosine triphosphate production, collapse of mitochondrial membrane potential, and inhibition of the activity of complex III. Co-treatment of mast cells exposed to PM_2.5 with N-acetyl-L-cysteine attenuated cytotoxicity and the production of reactive oxygen species, and decreased the release of β-hexosaminidase and interleukin-4. Evidently, PM_2.5-induced oxidative stress plays an essential role in mitochondrial toxicity and mast cell activation.     

交通荷载作用下饱和软粘土孔压-应变分析模型

针对交通荷载的作用特点设计了循环三轴试验,进而对交通荷载作用下饱和软粘土的动力特件进行厂研究.结果表明:循环荷载作用下,饱和软粘土存在临界循环应力比,采用孔压曲线所得到的临界循环应力比要小于采用应变曲线所得到的临界循环应力比.当土样不存在初始剪应力时,随着循环次数的增加,土样的应力-应变关系曲线近似原点对称,但随着初始剪应力的增大,应力-应变关系曲线逐渐表现为一系列平行曲线,峰值孔压与循环孔压幅值均逐渐减少;同时,轴应变的发展加快,但循环应变幅值逐渐减小.当循环应力比小于临界循环应力比时,对于同一初始剪应力,不同循环应力比下的孔压比-动应变曲线近似集中在同一条曲线上.通过对试验数据进行回归分析,得到了交通荷载作用下饱和软粘土残余孔压-累积塑性应变关系模型.     

焊点热疲劳失效原因分析

某PCBA样品在使用约半年后出现功能失效,该PCBA在封装后进行整体灌胶,将失效样品剥离,发现部分器件直接脱落,通过表面观察、切片分析、EBSD分析、应力分析、热膨胀系数测试等手段对样品进行分析,结果表明:各封装材料存在热失配,且焊点缺陷较多且存在应力集中区,加速焊点的疲劳失效进程,导致PCBA功能失效。