The cytotoxicity of nici2 for mammalian cells in culture†

The effects of NiCl₂ were studied in two human cell lines, HeLa and diploid embryonic fibroblasts as well as in V79 Chinese hamster cells and in L‐A mouse fibroblasts. NiCl₂ produces a dose‐dependent depression of proliferation, mitotic rate, and viability, accompanied by an increasing release of lactic dehydrogenase and stimulation of lactic acid production. The plating efficiency is reduced, as are DNA and protein synthesis and, to a lesser degree, RNA synthesis.

The cytotoxicity of NiCl₂ is comparable in degree to those of PbCl₂ and MnCl₂, but is weaker than those of HgCl₂ and CdCl₂. However, the different sensitivities of different cell lines must also be considered.

NiCl₂ effects are more severe in serum‐free medium than in medium containing serum or serum albumin indicating that serum constituents, notably albumin, bind the metal effectively and inhibit cellular uptake; this confirms earlier reports on the serum binding and slow uptake of NiCl₂.

Synchronized cells are most sensitive in the Gl and early S phases of the cell cycle. In the Painter test the depression of DNA synthesis persists following cessation of exposure to NiCI₂. These findings contribute an explanation for the known genotoxic effects of nickel.     

Genetic toxicology of metal compounds: An examination of appropriate cellular models †

Bacterial systems have not had success predicting metal carcinogenicity. Hypotheses explaining this failure are examined. Using a broad genetic endpoint, λ prophage induction, under sub‐toxic growing conditions, genotoxicity is seen for compounds of chromium, manganese, lead, molybdenum and tungsten. Copper, manganese, arsenic and molybdenum compounds enhanced UV mutagenesis in E. coli WP2.

The toxicity of metal compounds to cultured mammalian cells correlates well with rat oral LD₅₀ values. Whereas insolubility can present problems in bacterial studies, concentrations of metal compounds toxic to mammalian cells can be determined even in the presence of precipitate, and sometimes [Pb(NO₃)₂, BaCl₂ and BeCl₂] occurs only in its presence. PbS and MnS, which are insoluble, are much more toxic than the more soluble compounds Pb(NO₃)₂ and MnCl₂. These results demonstrate the importance of cellular phagocytosis of insoluble metal compounds as a factor in studying the toxicity and genotoxicity of metal compounds.     

桉树叶水浸出液对2种海洋微藻生长和叶绿素荧光特性的影响

运用水样叶绿素荧光仪(Water-PAM)研究了桉树叶水浸出液胁迫下湛江叉鞭金藻(Dicrateria zhanjiangensis)和纤细角毛藻(Chaetoceros gracilis)2种海洋微藻叶绿素荧光特性〔包括PS(光系统)Ⅱ的F_v/F₀(潜在活性)、F_v/F_m(最大光能转化效率)、Yield(实际光能转化效率)、ETR(电子传递效率),其中F_m和F₀分别为最大荧光和基础荧光〕的变化,同时监测微藻的生长情况,以研究桉树叶水浸出液对海洋微藻的影响,从而为探讨华南沿海大量种植桉树所造成潜在的海洋生态问题提供一些依据. 结果表明:①低浓度(以φ计,0.4、0.8、1.2mL/L)胁迫在96h内对湛江叉鞭金藻的上述4项荧光参数均无显著影响(P>0.05);高浓度(2.0mL/L)胁迫下,24h时湛江叉鞭金藻的4项荧光参数都处于最低值,48h时处于次低值. 表明高浓度在胁迫早期(48h内)对湛江叉鞭金藻4项荧光参数有抑制作用,而后期(72、96h)这4项荧光参数又恢复到正常水平,抑制作用解除. ②低浓度(0.4、0.8mL/L)胁迫下纤细角毛藻的4项荧光参数在24、48h内均得到促进,而高浓度(2.0mL/L)胁迫下F_v/F_m在24h时为最小值,表现抑制作用;另外3项荧光参数则未受显著影响. 在胁迫后期(72、96h),纤细角毛藻的4项荧光参数均随着胁迫浓度的增大而增加,表现为促进作用. ③就生长情况而言,随着胁迫浓度的增大,2种海洋微藻细胞密度的增长明显变缓. 表明桉树叶水浸出液对2种海洋微藻的生长以及叶绿素荧光特性都有影响,从而将会对整个海洋生态系统产生影响.      

Detection of polychlorinated biphenyls employing chemical dechlorination followed by biphenyl whole cell sensing system

Polychlorinated biphenyls (PCBs) are a mixture of 209 individual chlorinated compounds commonly known as PCB congeners. These compounds are hydrophobic and are persistent in the environment. Their use was banned in the US a few decades ago because of harmful health effects. Therefore, detection of PCBs in environmental samples is increasingly important. To that end, we have developed a two-step simple and sensitive method for the detection of total PCBs. Specifically, our method involves dechlorination of PCBs to biphenyl followed by detection of biphenyl using a whole cell sensing system as the detection system. The whole cell sensing system consists of cells of the strain Pseudomonas pseudoalcaligenes KF707 harboring plasmid pSD7000. Plasmid pSD7000 contains the gene of lacZ, a reporter protein under the control of the bph operon. The detection is achieved through the emission of light afforded by the expression of reporter protein triggered by the presence of biphenyl. Due to the fact that this operon is activated only by few PCB congeners, a chemical dechlorination method was employed to convert all PCBs to biphenyl, and thus all the PCBs present in a given sample are able to be detected. The results showed that PCB congeners were rapidly (30?min) and efficiently (>98.5%) dechlorinated to biphenyl using a Mg/K₂PdCl₆ catalyst, and the biphenyl could be subsequently quantified using the whole cell sensing system. This hybrid analytical method that combines classical dechlorination with novel biosensing methods may find applications in the on-site monitoring of PCBs contamination levels.     

活性氧参与多壁碳纳米管诱导的RAW264.7细胞毒性

碳纳米管以其独特的结构和性能,在生物医药和电子等领域广泛应用,而其生态安全性也成为科学界关注的焦点。为探究多壁碳纳米管(MWCNTs)诱导的细胞毒性机制,将小鼠肺泡巨噬细胞(RAW264.7)暴露于6个浓度梯度(0、25、50、100、150和200μg.mL-1)的MWCNTs中,应用噻唑蓝(MTT)法测定细胞存活率,用2’,7’-二氯荧光素二乙酸(DCFH-DA)荧光染色法测定细胞内活性氧的生产量,用流式细胞方法测定MWCNTs对细胞周期的影响。同时使用抗氧化剂氮乙酰半胱氨酸(NAC)验证MWCNTs诱导的细胞氧化损伤的作用机理。结果显示,MWCNTs对RAW264.7的细胞毒性呈剂量依赖性。暴露于不同浓度的MWCNTs(25、50、100、150和200μg.mL-1)下24h后,细胞活力分别为对照的74%、62%、59%、51%和45%。MWCNTs对RAW264.7的周期阻滞作用主要发生在G0/G1期。200μg.mL-1的MWCNTs处理3h后活性氧较对照组上升6.6倍。NAC对MWCNTs细胞毒作用有明显的抑制作用,且NAC能减弱MWCNTs对RAW264.7的细胞周期阻滞作用。研究表明,活性氧能够介导MWCNTs对小鼠巨噬细胞RAW264.7的损伤,并且MWCNTS通过细胞周期G0/G1期的阻滞,诱导细胞凋亡。     

不对称还原丙酮酸乙酯菌株的筛选及鉴定

以丙酮酸乙酯为底物,从成都某化工厂污水池及其附近土壤中分离到36株可将丙酮酸乙酯不对称还原成(S)-乳酸乙酯的菌株.经过多次复筛,最终获得了一株具有较高催化活性的酵母菌BTY18-6.在以该菌株静息细胞为催化剂,催化不对称还原丙酮酸乙酯合成(S)-乳酸乙酯的反应中,底物浓度为60 mmol/L时,底物转化率为86.9%,产物(S)-乳酸乙酯的ee值为88.7%.通过对其形态学、生理生化特征及其26S rDNA Dl/D2区域的分析表明,BTY18-6为胶红酵母.     

反硝化微生物燃料电池的基础研究

在启动双室型反硝化微生物燃料电池的基础上,研究了阴极溶解氧及外电阻对其产电性能和污染物去除效果的影响.结果表明,以乙酸钠为阳极电子供体,硝酸钠为阴极电子受体,在25℃的环境温度下,采用先间歇后连续培养的方式,42d内成功启动了反硝化微生物燃料电池.在阴极进水含氧的情况下,氧和硝酸盐可共同用作阴极电子受体.在较小电流密度区域内,氧是阴极的主要电子受体,相应的最大功率密度为26.0W/m3NC;电流密度增加到一定程度后,硝酸盐逐步变为阴极的主要电子受体,相应的最大功率密度为20.9W/m3NC.外阻变化对COD去除及反硝化程度影响较小,阳极COD去除负荷维持在1.2kg/(m3NC·d)左右,出水NO-2-N保持在0.05mg/L以下;但外阻减小有利于提高阴极脱氮效果,外阻为5 Ω时NO-3-N去除负荷达0.111kg/(m3NC·d).     

污泥为燃料的微生物燃料电池运行特性研究

实验采用单室无膜悬浮阴极微生物燃料电池(MFC),考察了运行特性对污泥为燃料的MFC(SMFC)的影响.研究表明,相对于未搅拌情况,搅拌时SMFC最大输出功率由45.94mW/m2分别增加到124.03mW/m2(1300r/min)和136.5mW/m2(2600 r/min),主要是由于搅拌有利于改善SMFC内物质的传递. 温度对SMFC的产电特性影响较明显,但在一定区间内(如20~25℃;30~40℃;45~50℃)变化不明显,说明产电微生物有一定的温度适应范围,这也可能是在不同温度下产电微生物不同导致.相对于采用未经处理的剩余污泥为燃料,微波处理后的污泥和微波处理过滤后的上清液做燃料时SMFC输出功率迅速增加,这主要是由于污泥中的微生物竞争作用引起.阴极面积的增加有利于降低阴极电势,降低SMFC内阻,从而促进功率密度的增加.     

离子液体1-丁基-3-甲基咪唑氯盐对斜生栅藻的毒性效应

按照毒性试验标准方法研究了不同浓度离子液体1-丁基-3-甲基咪唑氯盐([BMIM]Cl)对斜生栅藻的影响,测定了半数抑制浓度(IC50)、叶绿素含量、超氧化物歧化酶(SOD)活性、过氧化氢酶(CAT)活性以及藻细胞通透性的变化,观察了80mg/L[BMIM]Cl处理96h对藻细胞的影响.结果表明:[BMIM]Cl对斜生栅藻生长具有抑制作用,随着浓度的增大抑制率增加,叶绿素含量下降, 48h IC50、72h IC50和96h IC50分别为103.77、76.44和68.49mg/L.藻细胞对[BMIM]Cl有一定的氧化应激反应,CAT和SOD活性随[BMIM]Cl浓度升高而降低.[BMIM]Cl对藻细胞的细胞膜有一定程度的破坏作用,藻细胞通透性随浓度升高而增大,同时藻细胞的超微结构受到了[BMIM]Cl的影响,造成质壁分离,叶绿体片层断裂,线粒体嵴数量减少.     

Oxidative and genotoxic effects of bisphenol A on primary gill cell culture of Lake Van Fish (Alburnus tarichi Güldenstädt, 1814)

Lake Van is the largest lake in Turkey. The lake limits lifespan due to its high pH and brackish water. For this reason, only a single species of fish (Van Fish) is living in the lake that has been adapted to these conditions. In the present study, we investigated the total oxidant status (TOS), total antioxidant status (TAS), malondialdehyde (MDA) level and DNA damage effect of bisphenol A (BPA) (10^?7, 10^?6 and 10^?5?M) on primary gill cell culture of Van Fish for 24 and 48?h of incubation periods. TAS levels were not changed when compared to those of the control group, but TOS levels were decreased in both 24 and 48?h. The MDA level increased only at the highest concentration (10^?5) at the end of 12 and 24?h (p?.05). DNA damage increased only at the 10^?5?M concentration after 48?h. At the end of the experiment, BPA exposure caused lipid peroxidation and genotoxic effect. These results indicate that high levels of BPA exposure induced oxidative stress and DNA damage by time- and concentration-dependent fashion in the gill cell culture of Van Fish. Gill cell culture is a useful model for the rapid identification of the harmful effects of chemicals in the aquatic environment.