单轴应力对煤自燃特性参数和导热系数的影响研究

为探究单轴应力作用下煤氧化和传热特性,利用自制荷载加压煤自燃特性参数测定装置对炉体内长焰煤煤样进行程序升温。结合程序升温过程中煤临界温度Tc和Tg,对其进行阶段划分:阶段1为30℃~Tc;阶段2为Tc~Tg。计算了不同单轴应力下2个阶段煤表观活化能和平均耗氧速率。根据能量守恒得出程序升温过程煤导热系数随温度的变化,进一步分析煤导热系数与单轴应力的关系。结果表明:阶段1单轴应力为4 MPa时为临界轴压,煤表观活化能最大,平均耗氧速率最小;阶段2煤表观活化能和平均耗氧速率随单轴应力增大均呈抛物线变化,单轴应力为2.7 MPa时为临界轴压,煤表观活化能最大,平均耗氧速率最小;阶段1和2煤导热系数随温度升高均先减小后增大,并且煤导热系数随单轴应力增大呈三次函数变化。     

化学环境下的应力-渗流耦合对尾 矿库稳定性影响试验

通过扫描电镜（FE-SEM）、能谱分析（EDX）、X射线衍射（XRD）、LMS-30激光粒度分析等室内试验探究了尾矿库内存在的酸、碱离子对尾矿颗粒的沉降、微观形貌、物质组成以及粒径级配的影响;建立酸、碱影响下的孔隙比与渗透系数的数学关系模型,并将建立的模型用来表征尾矿库内的应力渗-流场两场耦合机制,实现代入有限元计算软件的目的。结果表明:化学因素的存在影响着尾矿颗粒的多项性状,酸性环境下尾矿颗粒发生溶蚀,部分金属元素流失;碱性环境下尾矿颗粒间生成胶结物质,孔隙出现以含氢氧化铁为主的絮状、团簇状堵塞物,改变了渗流速度;尾矿库内浸润线高度在碱性、中性、酸性环境下依次降低,而渗流速度依次升高。     

非柔性连接石化储罐配管温差应力分析与对策

储罐配管在温差作用下产生热位移会导致管壁产生热应力,未采用柔性连接的配管由于热应力集中作用可能发生破漏。针对与石油化工储罐非柔性连接的配管的安全问题,应用ANSYS有限元分析软件模拟计算石化企业典型配管的热应力分布;根据不同类型配管的分析结果,提出了工程技术与管理方面的针对性安全措施。研究结果表明:温差效应对石化储罐配管热应力影响显著,随内外温差的增加,配管应力集中的区域增大,最大热应力值增大;补偿措施能够改善配管的柔性,降低配管应力;约束载荷限制配管热膨胀从而增大配管应力;三通管是多根配管接合的区域,这种复杂管道交汇处会形成明显应力集中。研究结果对于提高石油化工非柔性连接配管安全性有一定的指导意义。     

环境污染物导致氧化应激的关键信号通路及其检测方法

环境污染物能够以多种途径进入生物体内,在体内产生含氧自由基等活性氧物质,并通过多种信号通路及酶反应引起氧化应激,造成生物体内的脂质过氧化、蛋白质损伤、DNA表达改变、酶失活等,从而引发心血管疾病、风湿类疾病、感染及癌症等的发生。本文对环境污染物致氧化应激产生的原因、涉及的信号通路及酶反应、造成的危害,以及常见的基于细胞模型的氧化应激检测方法进行了综述,期望为评价环境污染物和检测氧化损伤提供参考。     

阿维菌素对中华绒螯蟹肝胰腺氧化胁迫效应和组织结构的影响

采用半静态染毒法,研究不同浓度(1.6、8.0、16.0μg·L-1)阿维菌素在胁迫中华绒螯蟹12、24、48、96 h时肝胰腺超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性和丙二醛(MDA)积累量等氧化胁迫相关指标的变化;并在胁迫60 d时,记录各实验组和对照组中华绒螯蟹肝胰腺颜色的变化并进行组织病理观察。3个阿维菌素浓度组为实验组,空白组和溶剂组为对照组。结果表明在整个实验过程中空白组和溶剂组各个时间点各项指标之间无显著差异(P>0.05);低浓度(1.6μg·L-1)组SOD和CAT活力变化不显著(P>0.05);中浓度(8.0μg·L-1)组SOD和CAT活力变化趋势一致,持续被诱导,SOD活力在24 h以后显著高于空白组(P<0.01),CAT活力在48 h以后显著高于空白组(P<0.01);高浓度(16.0μg·L-1)组SOD和CAT活力在12 h~24 h之间变化趋势一致,表现为显著升高(P<0.05),但是在48 h之后,SOD活力显著下降(P<0.05);96 h时,高浓度组SOD活力显著低于空白组(P<0.01),而CAT活力显著高于空白组(P<0.01);在整个实验过程中各实验组MDA积累量逐渐增加,高浓度组氧化胁迫指标的变化幅度大于低浓度组。胁迫60 d时,取样观察可见对照组中华绒螯蟹肝胰腺正常,各实验组中华绒螯蟹肝胰腺发生了不同程度的病变,肝胰腺颜色由最开始的橘黄色变成了淡黄色、黄白色甚至白色,高、中、低各浓度组肝胰腺白化所占的比例分别是66.6%、57.1%和25.0%。组织病理分析显示,淡黄色肝胰腺的病理变化主要是B细胞数量减少,肝胰腺上皮细胞部分肿大并出现空泡;黄白肝病理观察可见肝胰腺上皮细胞中空泡数量增多,体积增大,且空泡内出现内容物,细胞核固缩;白肝的病理表现主要是基膜增厚,上皮细胞大量脱落,散落在管腔中,空泡数量进一步增多,肝胰腺的生理功能受损。由此得出,阿维菌素会对中华绒螯蟹肝胰腺造成氧化胁迫和组织损伤,且阿维菌素和对肝胰腺的氧化胁迫效应和组织结构损伤程度有一定的剂量-效应关系。     

农药致慢性细胞毒性及基因毒性机制研究进展

大量流行病学研究和体内、体外检测分析表明,长期低剂量接触农药可以导致人体细胞和分子损伤,诱导细胞凋亡。农药致细胞及DNA损伤的机制主要与DNA加合物的形成、DNA单链和/或双链的断裂有关。此外,氧化应激参与农药致细胞及DNA损伤的过程,可能成为农药致细胞及DNA损伤的促发因素。从总体上看,其具体分子机制还不十分清楚,有待进一步研究。     

The impact of pesticides on oxidative stress level in human organism and their activity as an endocrine disruptor

Pesticides cause serious environmental and health problems both to humans and animals. The aim of this review is to discuss selected herbicides and fungicides regarding their mode of action and their influence on basic oxidative stress parameters and endocrine disruption properties tested in selected cell cultures in vitro. Because of numerous difficulties which animal studies are subject to, cell cultures are an excellent experimental model reflecting human exposure to different pesticides through all relevant routes. This experimental model can be used to monitor aggregate and cumulative pesticide exposures.     

铜、镉联合胁迫对羊角月牙藻的自由基氧化损伤影响研究

分析了铜和镉联合胁迫对羊角月牙藻(Selenastrum capricornutum)的影响,运用国内应用较少的新型技术——叶绿素荧光技术检测了胁迫下微藻的最大光能转化效率(Fv/Fm)受到的影响,并尝试通过膜脂过氧化损伤产物丙二醛(MDA)和其他指标在胁迫下的变化,对铜、镉联合胁迫机制进行初步探究。结果表明:(1)羊角月牙藻在铜、镉联合胁迫下生长受到抑制,表现出明显的浓度-效应关系。铜、镉的联合胁迫的相加指数为-1.63,表现为典型的拮抗作用。(2)通过叶绿素荧光技术的应用,探明Fv/Fm随毒性浓度的变化表现为浓度-效应关系,毒性浓度越大,羊角月牙藻的Fv/Fm越低,但在低毒性浓度刺激时随胁迫时间延长有回升迹象。(3)随毒性浓度的增加,羊角月牙藻的MDA增加,表现为显著的浓度-效应关系;可溶性蛋白质大体呈先升后降的趋势。(4)铜、镉联合胁迫下,MDA与羊角月牙藻生物量、Fv/Fm呈显著负相关。脂质过氧化是导致生物量下降和Fv/Fm受抑制的原因之一。(5)在微藻体内铜、镉发生拮抗作用的机制也可能与重金属的脂质过氧化作用由于拮抗受到抑制有关。     

Effect of prochloraz fungicide on biotransformation enzymes and oxidative stress parameters in three-spined stickleback (Gasterosteus aculeatus L.)

The aim of this study was to characterize biomarker responses in three-spined sticklebacks exposed to prochloraz (Pcz). For this purpose, adult sticklebacks were exposed for 2 weeks to prochloraz at 0, 10, 50, 100 and 500 μg/L prior to one week of depuration in clean water. At days 7, 14 and 21, several hepatic biomarkers were measured including 7-ethoxyresorufin-O-deethylase (EROD), glutathione-S-transferase (GST), glutathione peroxidase (GPx), catalase (CAT), total glutathione (GSH) content and thiobarbituric acid reactive substances (TBARS). Pcz induced a transient increase of antioxidant enzymes and a depletion of glutathione content during the first 7 days of exposure. This study showed that EROD activity and antioxidants were disrupted in a transient manner. GST was rapidly induced in a dose-dependent manner and this induction was persistent and observed also after depuration. GST appeared as a valuable biomarker to assess the exposure to Pcz.     

Corynebacterium glutamicum as an indicator for environmental cobalt and silver stress–A proteome analysis

Cobalt and silver are toxic for cells, but mechanisms of this toxicity are largely unknown. Analysis of Corynebacterium glutamicum proteome from cells grown in control and cobalt or silver enriched media was performed by two dimensional gel electrophoresis (2DE) followed by mass spectrometry. Our results indicate that the cell adapted to cobalt stress by inducing five defense mechanisms: Scavenging of free radicals, promotion of the generation of energy, reparation of DNA, reparation and biogenesis of Fe-S cluster proteins and supporting and reparation of cell wall. In response to the detoxification of Ag⁺ many proteins were up-regulated, which involved reparation of damaged DNA, minimizing the toxic effect of reactive oxygen species (ROS) and energy generation. Overexpression of proteins involved in cell wall biosynthesis (1,4-alpha-glucan branching enzyme and nucleoside-diphosphate-sugar epimerase) upon cobalt stress and induction of proteins involved in energy metabolism (2-methylcitrate dehydratase and 1, 2-methylcitrate synthase) upon silver demonstrate the potential of these enzymes as biomarkers of sub-lethal Ag⁺ and Co toxicity.