古夫河着生藻类优势种体积与水质因子的相关性研究

通过研究长江三峡库区古夫河着生藻类优势种体积的变化,探索影响其体积的主要水质因子,为河流水质评价提供依据.于2010年12月至2012年2月,对古夫河着生藻类和地表水采样11次,共鉴定着生藻类197种,检测水质指标10项.选取Mcnaughton优势度指数(Y)>0.02的着生藻类(共30种)作为优势种并计算体积;利用主成分分析(PCA)分析优势种藻类在不同月份的体积变化.结果显示,硅藻门对冷暖季的变化较为敏感.将水质因子与优势种藻类体积进行典范对应分析(CCA),结果显示水质因子与藻类体积相关性大小为:溶解氧>氨氮>叶绿素a>酸碱度>硝态氮>总磷>水温>总氮>总有机碳>化学需氧量.Monte Carlo显著性检验结果为溶解氧和氨氮对着生藻类体积的影响最大,其次为叶绿素a、酸碱度和硝态氮.硅藻门藻类体积的变化可以判断古夫河水体中溶解氧、氨氮、叶绿素a、酸碱度、硝态氮的含量与变化.     

铜绿微囊藻与藻际细菌Ma-B1菌株的相互作用

藻与细菌通常共生于淡水生境,形成藻-菌共生体系,藻际细菌是水体生态系统中的重要组成部分,对藻的消长起重要的调控作用,但有关藻际微环境中藻与细菌的互作机制还不清楚. 采用传统的细菌平板培养方法,从太湖优势水华藻——铜绿微囊藻(Microcystis aeruginosa)细胞表面分离出一株藻际细菌Ma-B1,基于生理、生化试验和16S rRNA基因序列分析,初步鉴定为甲基营养芽孢杆菌(Bacillus methylotrophicus). 通过测定细胞生长,分析藻-菌相互作用机理. 结果表明:一定浓度(＞60 μg/mL)的Ma-B1的胞外代谢物可显著抑制铜绿微囊藻的生长(培养基为BG11,28 ℃/日,22 ℃/夜,3 000 lx,光暗比为14 h∶10 h);铜绿微囊藻的胞外滤液(500 μL/mL)对Ma-B1的生长有一定的促进作用,但其总滤液(500 μL/mL)显著促进Ma-B1的生长;Ma-B1细胞对铜绿微囊藻的生长没有显著影响,而高浓度(藻菌比10∶1)的铜绿微囊藻细胞则可显著抑制Ma-B1的生长. 铜绿微囊藻与Ma-B1之间存在复杂的相互抑制或促进关系,共同影响着藻、菌在自然水体生态系统中的消长.      

羊角月牙藻在制药废水毒性评价中的应用

以羊角月牙藻(FACHB-271 Selenastrum capricornutum)作为测试生物,分别采用EC₅₀(半数抑制浓度)、TU_a(急性毒性单位)和LID(最低无效应稀释度)指标对某制药厂污水处理站4个工艺节点和总出水排放口的水样进行急性毒性效应评价. 结果表明:地下调节池(工艺节点①)水样EC₅₀为15.12%±3.82%,TU_a为6.6,LID为16,为极毒/中毒废水;地上调节池(工艺节点②)水样EC₅₀为15.81%±1.04%,TU_a为6.3,LID为16,为极毒/中毒废水;中间沉淀池(工艺节点③)水样EC₅₀为62.12%±3.83%,TU_a为1.6,LID为8,为中毒/低毒废水;二级沉淀池(工艺节点④)水样EC₅₀为89.10%±1.43%,TU_a为1.1,LID为4,为低毒废水;总出水排放口水样EC₅₀＞100%,TU_a＜1,LID为1,为无毒或微毒废水. 经过各污水处理工艺节点后,制药废水对羊角月牙藻的急性毒性逐级减弱,并且毒性指标与ρ(COD_Cr)具有较好的线性关系. 研究还发现,采用毒性指标LID表征该制药废水的生物毒性,对废水样品的毒性分辨能力更强.      

厦门汀溪水库溶解有机氮对有毒藻种的生物有效性及其化学本质

为探究厦门汀溪水库溶解有机氮(DON)对有毒藻种的生物有效性及其化学本质,采用水样分子质量和极性分级技术,进行铜绿微囊藻 (Microcystis aeruginosa)培养实验.结果表明,汀溪水库中DON含量呈季节性差异,在枯水期比较高,而丰水期比较低.汀溪水库DON在不同季节中的主要成分都是疏水组分和>3kDa组分.汀溪水库DON的生物有效性为65.20%.较疏水组分和>3kDa组分而言,亲水组分和￡3kDa组分DON更易被铜绿微囊藻利用.从水环境和水源保护角度出发,应首先考虑消除DON中的亲水性组分和小分子质量组分.     

Royal jelly inhibited N-acetylation and metabolism of 2-aminofluorene in human liver tumor cells (J5)

The present study was carried out to evaluate the question of whether or not royal jelly affects N-acetylation and metabolism of 2-aminofluorene (2-AF) in the human liver tumor cell line (J 5). N-acetylation and metabolism of 2-AF in intact J5 cells was determined by using high performance liquid chromatography for the amounts of acetylated and nonacetylated 2-AF and profile of 2-AF metabolism. The results indicated that royal jelly displayed a dose-dependent inhibition of N-acetylation of 2-AF in J5 cells. Royal jelly also decreased the profile of 2-AF metabolites in J5 cells. This report is the first demonstration which showed that royal jelly affects N-acetylation of 2-AF in human liver tumor cells (J5).     

Determination of F2-isoprostanes in cultured human lung epithelial cells after exposure to metal oxide and silica nanoparticles by high-performance liquid chromatography/tandem mass spectrometry

The environmental impact of nanotechnology has caused a great concern. Many in vitro studies showed that many types of nanoparticles were cytotoxic. However, whether these nanoparticles caused cell membrane damage was not well studied. F₂-isoprostanes are specific products of arachidonic acid peroxidation by nonenzymatic reactive oxygen species and are considered as reliable biomarkers of oxidative stress and lipid peroxidation. In this article, we investigated the cytotoxicity of different nanoparticles and the degree of cellular membrane damage by using F₂-isoprostanes as biomarkers after exposure to nanoparticles. The human lung epithelial cell line A549 was exposed to four silica and metal oxide nanoparticles: SiO₂ (15 nm), CeO₂ (20 nm), Fe₂O₃ (30 nm), and ZnO (70 nm). The levels of F₂-isoprostanes were determined by using high-performance liquid chromatography/mass spectrometry. The F₂-isoprostanes’ peak was identified by retention time and molecular ion m/z at 353. Oasis HLB cartridge was used to extract F₂-isoprostanes from cell medium. The results showed that SiO₂, CeO₂, and ZnO nanoparticles increased F₂-isoprostanes levels significantly in A549 cells. Fe₂O₃ nanoparticle also increased F₂-isoprostanes level, but was not significant. This implied that SiO₂, CeO₂, ZnO, and Fe₂O₃ nanoparticles can cause cell membrane damage due to the lipid peroxidation. To the best of our knowledge, this is the first report on the investigation of effects of cellular exposure to metal oxide and silica nanoparticles on the cellular F₂-isoprostanes levels.     

Protective role of epigallocatechin 3-gallate against lead-induced toxicity in human neuroblastoma cells

Lead (Pb) is a heavy metal, known to induce oxidative stress and produce damage to the antioxidant defence system ultimately leading to cell death. Antioxidants such as epigallocatechin 3-gallate (EGCG), a green tea polyphenol, was shown to play a protective role during Pb-exposure. In this study, human SH-SY5Y neuroblastoma cells were exposed to different concentrations (0.01–10?µM) of Pb for 48?h to determine effects on the viability of cells. It was observed that IC₅₀ was at 5?µM and at this concentration the cells exhibited a significant increase in caspase-3 activity, an indicator of apoptosis at least by 10-fold and the decrease of 59.4% in glutathione (GSH) content. The total cellular prostaglandin-E₂ (PGE₂) level was found to be elevated at least 10-fold upon Pb exposure. However, the effects of Pb on cells pre-incubated with 50?µM EGCG followed by 5?µM Pb showed 40% inhibition in cell viability, 17.3% decrease in caspase-3 activity, 23% increase in GSH content, and 11.4% fall in PGE₂ levels when compared with cells exposed to Pb only. Data suggest that EGCG exerted a significant protection to cell viability in preventing cell death and elevation in levels of GSH in cells exposed to Pb. However, EGCG did not elicit any significant effect on release of PGE₂ indicating the nature of EGCG as an effective anti-apoptotic, antioxidant, and anti-inflammatory agent.     

Cadmium accumulation by green algae Cladophora glomerata (L.) Kutz. (Chlorophyta) in presence of Nile tilapia Oreochromis niloticus (L.)

Accumulation of metals by aquatic organisms is mostly affected by other biological components in environments. In this study, cadmium (Cd) accumulation in green algae, Cladophora glomerata (L.) Kutz., exposed to 0.1 and 1.0 mg L^?1 of Cd for 15 and 30 days was examined in laboratory conditions in the presence of Nile tilapia Oreochromis niloticus (L.). The green algae C. glomerata accumulated Cd concentrations as 690 ± 70 and 3430 ± 470 mg kg^?1 on day 15, and 1130 ± 180 and 6830 ± 1540 mg kg^?1 on day 30. There were significant increases (p < 0.05) in metal accumulation by green algae as the exposure time and metal concentration increased. The results also indicated that the presence of Nile tilapia in the medium led to a significant Cd accumulation in the green algae compared to control (p < 0.05).     

Single walled carbon nanotubes induce cytotoxicity and oxidative stress in HEK293 cells

The aim of the present study was to evaluate the potential toxicity and general mechanisms involved in single walled carbon nanotubes (SWCNTs)-induced cytotoxicity using human embryonic kidney cell line (HEK293) cells. Carbon nanotubes (coded as CNT) used in this study were synthesized by the chemical vapor deposition method. To elucidate the possible mechanisms underlying SWCNT-induced cytotoxicity, cell viability, cell membrane damage (lactate dehydrogenase activity (LDH) assay), reduced glutathione (GSH), interleukin-8 (IL-8) and lipid peroxidation products levels were quantitatively assessed following SWCNT exposure for 48 hr using HEK293 cells. Exposure of cells to SWCNT at 3–300 μg/ml produced significant reduction in cell viability in a concentration-dependent manner. The IC₅₀ value of SWCNT was found to be 87.58 μg/ml. Exposure of HEK cells to SWCNT at 10–100 μg/ml resulted in concentration-dependent cell membrane damage, increased production of IL-8, elevated levels of thiobarbituric acid reactive substances like malondialdehyde and decreased intracellular GSH levels. In summary, exposure to SWCNT resulted in a concentration-dependent cytotoxicity in cultured HEK293 cells that was associated with increased oxidative stress.     

Model reactions of chromium compounds with mammalian and bacterial cells†

Chromate uptake, reduction, cytotoxicity and mutagenicity were studied with human red blood cells, Chinese hamster ovary (CHO) cells and/or Salmonella typhimurium mutant cells. All cell types rapidly took up chromates whereas chromium(III) salts were excluded under the experimental conditions. Red blood cells reduced and accumulated chromium from chromate. At concentrations above 0.1 mM, chromate inactivated the red cell chromate carrier. Chromate above 0.01 mM inhibited CHO cell proliferation irrespective of the cations present. Chromate and two chromium(III) complexes were mutagenic with Salmonella mutants in the Ames’ assay. A model for chromate metabolism and genotoxicity is proposed.