北京市大气细颗粒物的遗传和非遗传毒性研究

用胞质阻断微核试验与单细胞凝胶电泳法检测北京市大气PM_2.5无机提取物与有机提取物对Balb/c 3T3细胞微核形成与DNA链断裂的影响;通过划痕染料示踪技术(SL/DT)观察PM_2.5无机提取物与有机提取物对Balb/c3T3细胞间通讯的影响.发现PM_2.5有机提取物可引起双核微核细胞率显著增加(P<0.01)及导致慧星细胞率和DNA迁移长度显著增加(P<0.01);PM_2.5有机提取物引起细胞间通讯的抑制; PM_2.5无机提取物未见明显毒作用.结果表明,PM_2.5可引起染色体损伤和原发性DNA损伤,抑制细胞间通讯,其毒作用主要由其有机成分引起.     

微生物燃料电池-人工湿地耦合系统研究进展

微生物燃料电池-人工湿地耦合系统(CW-MFC)是一种新型污水处理工艺,该系统在增强污水处理效果的同时提高了产电性能,具有广阔的应用前景。综述了CW-MFC系统的研究现状,并将影响CW-MFC系统处理效果和产电效率的因素概括为组成要素、结构特点和运行参数3个方面。论文最后总结了系统当前存在的问题,并对未来的研究方向进行展望。     

微生物固定化技术在污水生物脱氮中的应用

综述了微生物固定化技术在污水硝化、生物脱氮中的应用,包括固定化材料与固定化工艺;国内外研究与应用现状;以及在较大规模污水处理中的实际应用;对该项技术目前存在的问题及其解决途径、发展前景和趋势进行了评述。     

微生物燃料电池恒电流预培养阳极生物膜分析表征

阳极性能是影响微生物燃料电池(Microbial Fuel Cells,MFCs)性能的关键因素之一,同时阳极的接种挂膜过程是影响微生物燃料电池启动效率的关键因素.因此,本课题组提出了预培养阳极作为微生物燃料电池的一种新型阳极的概念,在三电极体系下,通过外加恒定电流预培养阳极,在不同条件下对阳极表面进行电化学选择和生物膜驯化以丰富生物膜结构和厚度.结果表明,阳极的性能与预培养电流大小密切相关,预培养阳极CF-4i(外加4 A·m-2电流密度)通过循环伏安法、塔菲尔曲线、电化学阻抗谱测试,性能好于其他测试组及对照组,装配阳极CF-4i的微生物燃料电池能实现最大功率密度968.20 m W·m-2,是对照组的2.53倍.同时,通过共聚焦显微镜观察发现,生物膜大体分两层,外层的活细胞及内层的死细胞,外层活细胞长在内层死细胞之上.这种结构分布表明,阳极生物膜中的活细胞部分绝大多数都分布于生物膜的外侧,而不是均布于整个阳极生物膜中;同时这也表明不是整个阳极生物膜都具有新陈代谢活性,但死亡的细胞可以继续积累在电极表面附近,活的外层膜负责电流的产生,而内层的死细胞作为一种导电基质.     

东亚钳蝎抑制型神经毒素基因在昆虫细胞中的表达及活性鉴定

基因BmKIT3R 是根据东亚钳蝎 (ButhusmartensiiKarsch)抑制型神经毒素基因BmKIT3 优化而得的 .将优化过的蝎毒素基因BmKIT3R 通过Bac to Bac操作技术 ,使重组杆状病毒基因组DNA转染到草地粘虫sf2 1细胞中对IT3R 基因进行表达 ,经SDS PAGE检测在 8.7× 10 3 处有一表达条带 .表达产物经生物鉴定 ,证明具有很高的活性 ,它对昆虫具有非常明显的致死作用 .图 3参 5     

基于pH值调控的沉积型微生物燃料电池（SMFC）运行特性

以蓝藻发酵液为处理对象,分别研究两极区pH值对沉积型微生物燃料电池（Sediment Microbial FuelCell,SMFC）运行特性的影响.结果表明,阳极碱性（pH=8.5）阴极酸性（pH=5.5）时,SMFC输出功率最高（83.55 mW·m-2）,COD去除率（63%）仅次于阴、阳极中性（阴、阳极pH值均...     

Liver and renal lesions in mercury-contaminated narwhals (Monodon monoceros) from North West Greenland

Narwhals (Monodon monoceros) from North West Greenland are known to bioaccumulate mercury (Hg) in tissues and internal organs. This is postulated to be a health concern and therefore studies were undertaken to conduct a screening study of Hg concentrations and histopathology of liver and renal tissues in a total of 12 specimens. The sample consisted of two sub-adults (one male, one female) and 10 adult (six males, four females) collected in Qaanaaq (Thule) 2010. In liver, Hg mean ± SD was 11.88 ± 10.47 μg/g ww (range: 0.39?31.8 μg/g ww) while the concentrations in kidneys were 1.85 ± 1.20 μg/g ww (range: 0.41?4.03 μg/g ww). There was no marked difference in Hg concentrations between males and females while sub-adults had significantly lower concentrations. The histological examinations of renal tissue showed glomerular capillary dilatation and basement membrane thickening, dilatation, and hyalinization of Bowman's space/capsule and tubular lesions with hyaline casts accompanied by interstitial fibrosis in the kidneys. In liver tissue, portal cell infiltrates and fibrosis, bile duct proliferation, lipid-filled Ito cells, and steatosis were found. There was no marked difference in histological prevalence between males and females and in Hg concentrations in individuals with or without lesions. Four of seven renal lesions and one liver lesion were found in the two sub-adult whales. Based upon these findings, as well as the nature of the lesions, evidence suggests that histopathological alterations were a result of age but that Hg might be an aggravating co-factor in development of renal lesions in particular.     

Thimerosal in childhood vaccines contributes to accumulating mercury toxicity in the kidney

Mercury (Hg) is a hazardous chemical that accumulates in many cells and tissues, thereby producing toxicity. The kidney is a key target organ for Hg accumulation and toxicity. The contributing factors to Hg accumulation in humans include: (1) elemental and inorganic Hg exposure, often occurring by inhalation of Hg vapors; (2) exposure to methyl Hg (meHg), for example, through contaminated seafood; and (3) exposure to ethyl mercury (etHg) via thimerosal-containing vaccines. Systematic investigations on the toxic effects of etHg/thimerosal on the nervous system were carried out, and etHg/thimerosal emerged as a possible risk factor for autism and other neurodevelopmental disorders. There is, however, little known about the mechanisms and molecular interactions underlying toxicity of etHg/thimerosal in the kidney, which is the focus of the current review. Susceptible populations such as infants, pregnant women, and the elderly are exposed to etHg through thimerosal-containing vaccines, and in-depth study of the potential adverse effects on the kidney is needed. In general, toxicity occurring in association with different forms of Hg is related to: intracellular thiol metabolism and oxidative stress reactions; mitochondrial function; intracellular distribution and build-up of calcium; apoptosis; expression of stress proteins; and also interaction with the cytoskeleton. Available evidence for the etHg-induced toxicity in the kidney was examined, and the main mechanisms and molecular interactions of cytotoxicity of etHg/thimerosal exposure in kidney described. Such accumulating knowledge may help to indicate molecular pathways that, if modulated, may better handle Hg-mediated toxicity.     

Biochemical speciation in chromium genotoxicity

The biochemical speciation of chromium compounds in mammalian cells is discussed with respect to uptake, metabolism, DNA binding and damaging. Whereas soluble hexavalent chromium is taken up rapidly and accumulated intracellularly after its reduction, compounds of trivalent chromium penetrate biomembranes about three orders of magnitude slower. Cr(VI) after its uptake is metabolised by electron donating compounds via Cr(V) to Cr(III) compounds. Chromium from various Cr(III) compounds, but not chromate, binds to chromatin in isolated cell nuclei. The DNA‐protein crosslinks and DNA strand breaks observed in rat liver and kidney after chromate administration are also found in vitro, when Cr(III) compounds (but not chromate) interacts with isolated nuclei. In the Chinese Hamster cell HGPRT mutation assay, three out of four tested Cr(III) complexes were found to be mutagenic. In a direct DNA strand break assay with supercoiled bacteriophage PM 2 DNA, neither chromate nor the four Cr(III) compounds tested caused nicks. However, the combined action of chromate plus glutathione as well as the isolated complex of pentavalent chromium, Na₄Cr(glutathione)₄, did cause DNA breaks. Reactive oxygen species are inferred to be the ultimate DNA nicking agents in this assay. In conclusion there appear to be two mechanisms of chromate genotoxicity; one with direct DNA damage caused by Cr(V) species and one via DNA‐protein crosslinks formed with Cr(III), the final reduction state of chromate.