低剂量镉诱导细胞氧化损伤的机理研究

镉是一种有毒重金属,能诱导酿酒酵母的氧化损伤.为了研究低剂量镉诱导细胞氧化损伤的作用,通过有葡萄糖和无葡萄糖的酵母培养基,用浓度2 μmol/L和10 μmol/L的CdCl2染毒酿酒酵母10 h后,统计酿酒酵母细胞的存活率,并用HPLC-EC法测定酿酒酵母线粒体DNA中8-OH-dG/105dG比值.结果表明:无葡萄糖条件下,10μmol/L的CdCl2染毒时酿酒酵母对Cd2 的耐受性比有葡萄糖时明显高(P＜0.01),而且线粒体DNA氧化损伤程度也明显低(P＜0 01);但2 μmol/L的CdCl2染毒时,酿酒酵母对Cd2 的耐受性和线粒体DNA氧化损伤程度与有葡萄糖条件下相比差异不显著(P＞0.05).因此,本文认为低浓度Cr主要对酿酒酵母细胞质中蛋白造成氧化损伤,浓度升高时则对线粒体DNA也产生氧化损伤.     

松花江佳木斯江段水环境质量变化状况及趋势(水生生物指标)分析

根据近十年来的松花江佳木斯江段水环境质量监测数据,从水生生物指标对松花江佳木斯江段水环境质量变化趋势进行了评价分析,水生生物指标分析结果表明:近十年来佳木斯江段水环境质量得到显著持续改善,规律性的由轻-中污染变化为轻污染状况。标志着近十年水污染治理取得了一定成效。     

2000年1月15日姚安6.5级地震余震序列震源机制解与震源区应力场分析

本文利用垂直向的Pg和Sg波的最大振幅比方法,计算2000年1月15日云南姚安6.5级地震后余震序列震源机制解,通过统计和系统聚类分析,再结合震中分布图,综合分析了云南姚安6.5级地震的震源机制解和震源区应力场破裂特征,研究结果表明震源断层的走向为SEE-NWW占主导,其平均解为120°,震区主压应力轴平均解为145°,即SSE向,与震源区现今构造应力场主压应力方向一致,表明余震的应力场主要受区域应力场的控制.     

松花江佳木斯江段水环境质量变化状况及趋势分析研究

根据近十年来的松花江佳木斯江段水环境质量监测数据,介绍了松花江佳木斯江段水质现状,探讨了松花江佳木斯江段水质的主要污染物,从理化指标对松花江佳木斯江段水环境质量变化趋势进行了评价分析,分析结果表明：主要污染指标高锰酸盐指数、化学需氧量、氨氮、生化需氧量浓度值均有不同幅度的下降,2005年水质状况为轻度污染,2013年已达到良好水平.水环境质量呈规律性的逐年提高和改善,确保了松花江更好地休养生息.     

Primary neuronal-astrocytic co-culture platform for neurotoxicity assessment of di-(2-ethylhexyl) phthalate

Plastics such as polyvinyl chlorides （PVC） are widely used in many indoor constructed environments; however, their unbound chemicals, such as di-（2-ethylhexyl） phthalates （DEHP）, can leach into the surrounding environment. This study focused on DEHP＇s effect on the central nervous system by determining the precise DEHP content in mice brain tissue after exposure to the chemical, to evaluate the specific exposure range. Primary neuronal-astrocyte co-culture systems were used as in vitro models for chemical hazard identification of DEHP. Oxidative stress was hypothesized as a probable mechanism involved, and therefore the total reactive oxygen species （ROS） concentration was determined as a biomarker of oxidative stress. In addition, NeuriteTracer, a neurite tracing plugin with ImageJ, was used to develop an assay for neurotoxicity to provide quantitative measurements of neurological parameters, such as neuronal number, neuron count and neurite length, all of which could indicate neurotoxic effects. The results showed that with 1 nmol/L DEHP exposure, there was a significant increase in ROS concentrations, indicating that the neuronal-astrocyte cultures were injured due to exposure to DEHP. In response, astrocyte proliferation （gliosis） was initiated, serving as a mechanism to maintain a homeostatic environment for neurons and protect neurons from toxic chemicals. There is a need to assess the cumulative effects of DEHP in animals to evaluate the possible uotake and effects on the human neuronal system from exoosure to DEHP in the indoor environment.     

Fuelwood assessment at the micro-watershed level:a case study in Garhwal Himalaya,India

Biomass,as fuelwood,is one of the major sources of energy in rural areas,especially in the mountainous regions of the world.As the increasing human population exerts more pressure on the forest thereby inducing an adverse effect on the sustainability of the ecosystem,which consequently causes fuelwood crisis at a local level,this crisis is spatio-temporal in nature.Thus,the major objective of this study is to assess the sustainability of fuelwood at different probable scenarios at a micro watershed level.The present study was conducted in the Phakot watershed,the Tehri Garhwal district of central Himalaya in India,during 2006-2008.Based on the vegetation composition in the study area,the net primary productivity(NPP)value of the Oak forest,and mixed oak and sal forests,was used for the quantification of fuelwood availability in evergreen and deciduous forests,respectively.The fuelwood demand was calculated on the basis of seasonal fuelwood consumption values.Nine probable permutations for availability-demand scenarios assuming the existence of high(H),low(L)and average(A)conditions were analyzed for evaluating the stress.The available annual harvestable fuelwood in the watershed is in the minimum and maximum ranges of 2283.28 to 4066.00 tons,respectively,per year whereas it has a demand of 110.76 tons as the minimum to 3659 tons as the maximum annually.This shows that in the current availabilitydemand scenario,the watershed does not have fuelwood crisis in the present situation but needs to maintain the sustainability of the system.Based on our study,it is concluded that,globally,more spatio-temporal study is required to understand the issues at the local level.     

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.     

乌鲁木齐大气PM2.5对质粒DNA的损伤研究

2012年1月~2012年12月采集乌鲁木齐大气PM2.5样品,使用质粒DNA评价法研究了不同季节PM2.5的氧化能力,并进行氧化性毒性与相应气象因素和质量浓度之间的相关性研究.结果表明,乌鲁木齐大气PM2.5的质量浓度具有冬季最高,春季和秋季次之,夏季最低的季节性变化特征;PM2.5全样和水溶部分氧化能力的季节差异较大,对质粒DNA的氧化性损伤具有冬季最大,春季和夏季之次,秋季最低.冬、春、夏、秋季大气PM2.5全样的TD30(PM2.5对质粒DNA造成破坏达到30%所需要的颗粒物的剂量)平均值分别为440,491,503,515μg/mL,水溶部分分别为474,721,666,600μg/mL.绝大部分PM2.5样品全样的TD30值均小于水溶部分样,表明全样的毒性大于相应的水溶部分样.全样TD30值与平均温度显著(P<0.05)正相关,表明寒冷的天气/季节可能造成PM2.5的高毒性.水溶样TD30值与风速显著(P<0.01)正相关,与相对湿度显著负相关.这表明,高的风速和低的相对湿度可能跟较低和较高的PM2.5的毒性有关.PM2.5氧化性损伤能力的大小与其质量浓度之间的相关性不明显,表明仅以颗粒物的质量浓度来评价大气颗粒物氧化性损伤能力大小的方法并不能真实地反映其对人体健康的危害程度,起决定作用的还是颗粒物的化学组成及其表面吸附的有害成分.     

挥发性有机污染物排放控制标准制订中的关键技术问题研究

研究分析了挥发性有机污染物排放标准制订中4个关键技术问题:污染因子选择、控制指标确定、限值的确定以及技术管理措施.结果表明,应根据毒性和光化学反应性选择污染因子;确定控制指标应既考虑有组织控制指标,又考虑无组织的控制指标;确定排放限值应明确是基于控制技术还是基于健康风险;同时制定技术管理措施以通过源头和过程控制挥发性有机污染物排放.     

Involvement of mitochondrial-mediated caspase-3 activation and lysosomal labilization in acrylamide-induced liver toxicity

Acrylamide (ACR) is a chemical frequently used in both industrial and synthetic processes and may be produced during food processing. ACR at very high concentrations is postulated to exert its toxicity through the stimulation of an oxidative stress. ACR in excessive doses induces the central nervous system, reproduction, and genetic toxicity. However, ACR effects on the liver, a major organ of drug metabolism, have not been adequately explored. In addition, the role of mitochondria in an ACR-mediated hepatotoxicity is still unclear. The aim of this study was to investigate the cytotoxic mechanisms attributed to ACR using isolated rat hepatocytes. Hepatocytes were isolated by the collagenase perfusion method and incubated with an EC50_2hr concentration of ACR for 3 hr. The EC50_{2 hr} of ACR on isolated rat hepatocytes was determined to be 1 mM. Based on our results, hepatocytes cytotoxicity of ACR (1 mM) was mediated by a reactive oxygen species formation and lipid peroxidation. Incubation of hepatocytes with ACR produced rapid hepatocyte glutathione depletion which is another marker of the cellular oxidative stress. ACR cytotoxicity was also associated with mitochondrial injury as evidenced by the decline of mitochondrial membrane potential and lysosomal membrane leakiness. Our results also showed that ACR induced caspase-3 activation, the final mediator of apoptosis signaling. These findings contribute to a better understanding underlying mechanisms involved in ACR hepatotoxicity originating from the oxidative stress and ending in mitochondrial/lysosomal damage and cell death signaling.