工伤保险与安全管理

从我国安全管理实际出发,分析了借助于工伤保险的经济杠杆作用实现国家对企业安全管理制约机制的必要性,并对建立制约机制有关的指标体系及综合评估模型,以及该机制实现等问题进行了深入探讨.     

Ecologically neglected tannins and their biologically relevant activity: chemical structures of plant ellagitannins reveal their in vitro oxidative activity at high pH

Summary.  Chemical structures of 27 ellagitannins were systemically compared in respect of their in vitro oxidative activity at high pH found e.g. in lepidopteran insects. The analysis revealed over six-fold differences in the oxidative activities of individual ellagitannins which could be explained by the chemical divergences of the ellagitannins. These findings allowed the formulation of a simple equation that can be used to estimate the oxidative activities of other ellagitannins with known structures. The results suggest that, in future studies of plant-herbivore interactions, ellagitannins should be (1) taken into account as possible oxidative stress -based defences of plants against herbivores, (2) chemically characterized from the study plants, and (3) quantified individually, not as chemically ill-defined group. These actions together with the utilization of the created equation would allow the clarification of the role of ellagitannins in plant-herbivore interactions as natural pro-oxidants.     

Modification of the biochemical pathways of plants induced by ozone: what are the varied routes to change?

When plants are observed under a low dose of ozone, some physiological and metabolic shifts occur. Barring extreme injury such as tissue damage or stomata closure, most of these disruptive changes are likely to have been initiated at the level of gene expression. The belief is oxidative products formed in ozone exposed leaves, e.g. hydrogen peroxide, are responsible for much of the biochemical adjustments. The first line of defense is a range of antioxidants, such as ascorbate and glutathione, but if this defense is overwhelmed, subsequent actions occur, similar to systemic acquired resistance or general wounding. Yet there are seemingly unrelated metabolic responses which are also triggered, such as early senescence. We discuss here the current understanding of gene control and signal transduction/control in order to increase our comprehension of how ozone alters the basic metabolism of plants and how plants counteract or cope with ozone.     

丙烯酰胺对斑马鱼各器官的毒性作用及生殖细胞的DNA损伤

在我国,聚丙烯酰胺(PAM)主要应用于石油开采,其长期暴露于环境中可以降解成有毒的丙烯酰胺(AM)。为探究在降解过程中AM的毒性作用,选择斑马鱼作为受试动物,进行AM长期毒性暴露40 d,考察了对斑马鱼的肝脏、脑组织、心脏、腮等器官的影响情况。结果表明:在2.04 mg·L~(-1)、6.12 mg·L~(-1)和18.36 mg·L~(-1)暴露浓度下,形态学观察斑马鱼的鳃丝,鳃小片和鳃细胞有严重的受损现象;随着浓度的升高斑马鱼肝脏、脑组织和心脏中MDA含量、LDH活力的升高,SDH和Na+-K+-ATPase活力的降低,均对其肝脏、脑组织和心脏造成氧化损伤作用,从而影响了斑马鱼体内细胞能量代谢过程。采用彗星试验检测斑马鱼的生殖腺细胞DNA损伤,结果显示暴露于浓度为2.04 mg·L~(-1)~18.36 mg·L~(-1)的AM后,斑马鱼的DNA损伤均表现为显著差异(P0.01)。上述研究结果均确定了AM对斑马鱼的毒性效应并可造成其生殖腺细胞的DNA损伤。     

酰胺类除草剂对铜绿微囊藻的生长影响及氧化损伤效应

酰胺类除草剂的广泛使用对水生生态环境构成了潜在风险。为探究其对藻类的毒性作用,以铜绿微囊藻为对象,分别从藻类生长和氧化损伤效应角度探讨了甲草胺、乙草胺和丁草胺对铜绿微囊藻的毒性影响。实验结果显示,酰胺类除草剂对藻类的影响存在明显的滞后效应和剂量–效应关系,低浓度暴露组刺激藻类增长,高浓度表现为抑制作用;3种酰胺类除草剂增加了铜绿微囊藻的氧化压力,并随着暴露时间的延长和浓度的增加而增强。其中,藻体内过氧化脂质降解产物丙二醛(MDA)含量明显增加,同时超氧化物歧化酶(SOD)和过氧化物酶(POD)活性也显著增强。经96 h暴露后,甲草胺(32.0 mg·L~(-1))、乙草胺(32.0 mg·L~(-1))和丁草胺(15.0 mg·L~(-1))暴露溶液中相对MDA含量分别为138%、204%和154%,相对SOD活性分别为116%、87%和115%,相对POD活性分别475%、278%和627%。结合生物量及氧化损伤效应实验结果可知,3种除草剂对铜绿微囊藻的毒性大小顺序为丁草胺乙草胺甲草胺。     

植物重金属伤害及其抗性机理

讨论了二个问题：（1）重金属对植物伤害效应及伤害机理。其中包括重金属对植物细胞质膜透性,水分代谢、光合作用、呼吸作用、碳水化合物代谢、氮素代谢、核酸代谢、植物激素等生理生化过程,生境以及矿质营养的伤害效应,在伤害机理中讨论了植物体内原有的离子平衡系统,大分子物质活性和自由基与伤害的关系。（2）植物对重金属抗性及抗性机理。其中包括植物对重金属的抗性概念,例证,分类,抗性机理包括植物限制重金属离子吸收,重金属与体外分泌物结合,重金属的排除,根系富集,与细胞壁结合,在液泡中积累,形成类－金属硫蛋白或植物络合素,加强抗氧化系统等与植物抗性的关系,参85     

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.     

零价铁类Fenton试剂氧化降解废水中有机污染物的研究进展

综述了近年来国内外Fe0类Fenton试剂氧化反应降解废水中有机污染物的研究现状,介绍了Fe0-H2O2体系、紫外光-Fe0-H2O2体系和可见光-Fe0-H2O2体系处理有机污染物的机理、特点和效果,并对未来Fe0类Fenton试剂氧化反应体系处理有机污染物的发展前景进行了展望。     

酸雨与镧对大豆幼苗生长的复合伤害效应研究

为探索酸雨与稀土镧对大豆幼苗生长的复合影响及其内在机制,以重要油粮作物大豆(Glycine max)为材料,研究在模拟酸雨pH分别为3.0、3.5、4.5与稀土镧La(Ⅲ)浓度分别为60、100和300mg·L-1处理下大豆幼苗生长及光合作用的变化.结果表明,相对单一酸雨与镧处理,酸雨与La(Ⅲ)复合处理组中大豆幼苗的生长受抑制程度增大,两者呈协同效应,且pH越低,La(Ⅲ)浓度越高,抑制效应越明显.光合参数的变化规律与生长指标近同,相同处理组各光合参数的降幅不一致,其中最大荧光(Fv/Fm)和叶绿素含量(Chl)的降幅范围分别为9.53%～22.75%和9.14%～24.53%,较净光合速率Pn(22.78%～84.7%)、希尔(Hill)反应速率(15.52%～73.38%)和Mg2+-ATPase活性(14.51%～71.54%)小,表明各光合参数对2个胁迫因子的敏感程度存在差异.进一步相关性分析发现,Pn变化主要受Hill反应速率与Mg2+-ATPase活性的影响,而Chl、Fv/Fm次之.表明酸雨与La(Ⅲ)对植物光合过程各环节的作用机制不同,光合作用受阻是影响植物生长的重要因素之一.     

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.