回火焊道焊接技术在焦炭塔修复中的应用

为了避免耗时长、费用高的焊后热处理或整体更换筒节,针对铬钼钢焦炭塔内壁环焊缝的裂纹和锥段内壁腐蚀缺陷,提出采用回火焊道焊接技术对内壁缺陷部位进行修复。结果表明,严格按照经评定合格的焊接工艺进行施焊,回火焊道焊接技术可以利用层道间的焊接热循环作用达到焊后热处理的效果,使焊接修复后铬钼钢焦炭塔的母材和复合层的冶金和力学性能满足要求。     

加轴压卸围压下含瓦斯煤岩损伤变形的能量演化机制

采动影响下含瓦斯煤岩的损伤变形是一个极其复杂的非线性过程,单纯依靠传统经典弹塑性力学无法准确分析其破坏机理。针对此情况,通过试验研究了不同初始围压条件下含瓦斯煤岩的损伤变形特征,并分析了损伤变形与能量演化规律之间的内在联系。研究表明:初始围压越高,煤样破坏时强度越大,脆性破坏特征越明显,瓦斯流量急剧增加幅度越大,煤样破坏时积累的总能量和弹性应变能越多,且初始围压与弹性能之间满足对数函数关系。采用累积耗散能定义了煤岩损伤变量,并分析了不同阶段损伤与渗透率之间的演化关系。     

重金属Cr(VI)、Pb及Cu胁迫对双齿围沙蚕体腔细胞的DNA损伤

为探讨重金属Cr(VI)、Pb以及Cu对沙蚕体腔细胞DNA的毒性效应,以双齿围沙蚕为受试动物,重金属按不同剂量水平,Cr(VI):10、100和200 mg·L~(-1),Pb:5、50和100 mg·L~(-1),Cu:1、10和20 mg·L~(-1),分别胁迫沙蚕24 h,以不加任何重金属离子的海水为对照,采用单细胞凝胶电泳技术,检测其体腔细胞DNA损伤程度。结果表明,与空白对照组相比,3种重金属离子的各浓度组都能引起沙蚕体腔细胞DNA损伤,且3种重金属胁迫浓度与细胞DNA损伤程度之间存在显著的剂量-效应关系。双齿围沙蚕可以作为单细胞凝胶电泳的实验材料用于重金属所致环境污染的生物监测指示生物。     

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。     

3种镉超富集植物毛状根体系对镉胁迫响应的比较

近年来,转基因毛状根组织被越来越多地应用于重金属和有机污染物的植物修复技术研究中,已成为进行污染物毒性响应机制研究的便捷的实验室工具。为了探究龙葵、油菜、芥菜3种镉(cadmium,Cd)超富集植物对Cd毒性胁迫响应的差异,以诱导出的3种植物毛状根为研究材料,从毛状根的生长状态、富集Cd的能力、根组织细胞的凋亡程度和抗氧化酶活性等方面进行了探讨。结果表明:Cd浓度为0~50μmol·L-1时,龙葵、油菜、芥菜毛状根受Cd毒害的影响都不明显;Cd浓度为75~100μmol·L-1时,龙葵、油菜、芥菜毛状根均表现出对Cd胁迫的防御响应。在较高的Cd浓度(100μmol·L-1)下,龙葵毛状根的生物量受Cd毒害的影响最小,芥菜次之,油菜受影响最大;同时龙葵毛状根富集的Cd含量最高(745.0μg·g-1),芥菜次之(681.4μg·g-1),油菜最差(505.2μg·g-1)。龙葵、油菜、芥菜毛状根在Cd胁迫下的细胞凋亡水平均随Cd浓度的升高而升高,当Cd浓度为100μmol·L-1时,龙葵毛状根比油菜和芥菜毛状根的细胞凋亡程度均低。同时3种植物毛状根在不同浓度Cd处理下抗氧化酶活性的变化有一定差异。从上述结果综合来看,龙葵毛状根受Cd毒害的影响最小、富集Cd的能力最好,是进一步开展Cd超富集植物转基因改造研究的较好的实验室载体。     

重金属Cr(Ⅵ)、Pb及Cu胁迫对双齿围沙蚕体腔细胞的DNA损伤

为探讨重金属Cr(Ⅵ)、Pb以及Cu对沙蚕体腔细胞DNA的毒性效应,以双齿围沙蚕为受试动物,重金属按不同剂量水平,Cr(Ⅵ):10、100和200 mg· L-1,Pb:5、50和100 mg·L-1,Cu:1、10和20 mg· L-1,分别胁迫沙蚕24 h,以不加任何重金属离子的海水为对照,采用单细胞凝胶电泳技术,检测其体腔细胞DNA损伤程度.结果表明,与空白对照组相比,3种重金属离子的各浓度组都能引起沙蚕体腔细胞DNA损伤,且3种重金属胁迫浓度与细胞DNA损伤程度之间存在显著的剂量-效应关系.双齿围沙蚕可以作为单细胞凝胶电泳的实验材料用于重金属所致环境污染的生物监测指示生物.     

Assessing stress response of Stylophora pistillata towards oil and phosphate pollution in the Gulf of Aqaba,using molecular and biochemical markers

Crude oil (from oil terminal) and raw phosphate (from phosphate port) pollution are responsible for the lowered health conditions of coral reefs at their vicinity in the Jordanian coast of the Gulf of Aqaba. Both in situ incubations and ex situ laboratory exposure experiments were used to study the effects of those pollutants on corals, by using molecular and biochemical biomarkers in the coral Stylophora pistillata. For ex situ part of the experiment, crude oil and raw phosphate were added to a final concentration of 500?ppm for both pollutants. The DNA damage was assessed by Comet assay, while biochemical stress markers were reassessed by lipid peroxidation (LPO) test. Although the corals looked healthy from outside, the use of stress biomarkers indicated that they are under high pressure at the cellular level. The corals incubated with oil and phosphate had more DNA damage and LPO in comparison with the control samples. The results obtained suggest that the use of stress biomarkers can be used as important prognostic tools for examining the sub-lethal stress on corals before their death.     

Urinary 8-oxo-7, 8-dihydro-2′-deoxyguanosine concentrations after frying of bacon,a pilot study

Cooking fumes contain compounds that may give rise to oxidative stress and mutations when inhaled. The aim of this study was to evaluate if cooking fumes from frying of bacon induce oxidative stress by measurement of urinary 8-oxo-7,8-dihydro-2 deoxyguanosine, a marker of oxidatively damaged DNA. Three non-smoking women fried bacon for 3 h. Urine samples were taken as early morning void at the same time on four days; the morning before frying, the morning after first frying, the morning after three days of frying and one week after first urine sample. 8-Oxo-7,8-dihydro-2 deoxyguanosine, 1-hydroxypyrene and 2-hydroxyphenanthrene, metabolites of polycyclic aromatic hydrocarbons, were measured by liquid chromatography-mass spectrometry/mass spectrometry (LC-MS/MS). 8-Oxo-7,8-dihydro-2 deoxyguanosine correlated weakly with concentrations of 1-hydroxypyrene (r = 0.31, p = 0.042), but it did not correlate with 2-hydroxyphenanthrene (r = ?0.074; p = 0.64). Average urinary 8-oxo-7,8-dihydro-2 deoxyguanosine concentrations increased from the day before frying (16.3 ± 4.2 nmol/L) to the third day of frying (26.2 ± 10.2 nmol/L), although not statistically significantly. Our pilot study shows that frying of bacon may result in increased oxidative stress which further emphasises the possible carcinogenic potential of cooking fumes.     

运用改进综合评分法筛选典型污染物的研究——以大武水源地地下水典型污染物筛选为例

结合潜在危害指数法和综合评分法筛选大武水源地地下水典型污染物。鉴于潜在危害指数法不考虑污染物的环境浓度,将潜在危害指数作为综合评分法的评价指标之一,同时引进污染物的检出频率、生物降解性、生物累积性、研究区是否有污染源检出、是否为环境激素、是否为美国环境保护署(EPA)优先有机污染物、是否为中国优先污染物、是否为持久性有机污染物等指标,计算不同污染物的综合得分,再通过聚类分析,筛选出典型污染物。研究结果表明,大武水源地地下水典型污染物为三氯甲烷、三氯乙烯、四氯乙烯、四氯化碳和苯。     

Evaluation of protective effects of sulforaphane on DNA damage caused by exposure to low levels of pesticide mixture using comet assay

The objective of the study was to evaluate the potential risk of DNA damage due to exposure to a mixture of the most widely used pesticides, namely endosulfan, chlorpyriphos and thiram at an environmentally relevant concentration (5 μM each) and the DNA protective capacity of sulforaphane (SFN) (10–30 μg/mL). DNA damage in human lymphocytes was ascertained with Single Cell Gel Electrophoresis (SCGE), also called Comet Assay. For positive control, H₂O₂ at 100 mM was used. The pesticide mixture produced DNA damage at the concentration used in the lymphocytes. SFN was able to offer a statistically significant (P < 0.01), concentration-dependant protection to DNA damage between 10–20 μg/mL in both the pre-incubation and co-incubation strategies. The results indicate that exposure to low levels of these pesticide mixtures can induce DNA damage, and the presence of SFN in diet may reduce the incidence of genetic damage, especially in farm workers. However, it is not clear whether SFN is involved in quenching of the free radicals generated by the pesticide mixture or it is involved in DNA repair mechanism.