Radical Scavenging and Antimicrobial Activities of Methanol Extracts of Two Kinds of Formicary

对两种不同的蚂蚁窝进行甲醇提取,并对提取物进行了急性毒性、抗自由基,酚含量、还原能力和抗菌活性的检测。二苯基三硝基肼(1,1-diphenyl-2-picrylhydrazyl,DPPH)自由基的清除能力的检测表明:两种蚂蚁窝甲醇提取物都具有显著的自由基清除能力,并呈现出剂量依赖性,而且,在高浓度时(5~10mg·mL-1),它们的自由基清除能力甚至显著地高于二丁基羟基甲苯(butylated hydroxyl toluene,BHT)。酚的含量和还原能力分别用福林酚试剂和铁氰化钾还原反应来测定,统计分析显示两种蚂蚁窝的抗氧化能力和其酚含量、还原能力都存在着正相关。两种蚂蚁窝甲醇提取物都具有抗革兰氏阴性菌和革兰氏阳性菌的活性,但它们却对真菌没有作用。

微囊藻毒素对人类健康影响相关研究的回顾

本文回顾了微囊藻毒素(MC,一种最常见而重要的蓝藻毒素)对人类健康影响相关的研究.迄今为止的一些重要历史事件包括:(1)1990年,科学家首次发现,MC进入肝细胞后,能强烈地抑制蛋白磷酸酶(PP1、PP2A)的活性,这是MC致毒的最重要的分子基础;(2)1996年,在巴西发生了肾透析用水被MC(-LR、-YR和-AR)污染导致52人死亡的严重事件;(3)中国南方原发性肝癌的高发病率被认为与饮水中的MC污染有关;(4)1998年,世界卫生组织提出了饮用水中MC-LR含量的临时指导值为1μg/L;(5)从巢湖......

微囊藻毒素对束丝藻细胞生长和抗氧化系统的影响

为从活性氧(ROS)角度探讨微囊藻毒素(MC)导致藻类细胞死亡的机理及揭示藻细胞对MC诱发的氧化胁迫的响应机制,采用50和500μg·L-1的微囊藻毒素LR(MC-LR)处理束丝藻(Aphanizomenon sp. DC01)细胞,测定了细胞生长、细胞内活性氧(ROS)含量及抗氧化系统的变化.结果表明,50μg·L-1的MC-LR处理对藻细胞的生长无显著影响,而500μg·L-1的MC-LR处理可诱导藻细胞死亡.50μg·L-1的MC-LR处理的藻细胞ROS含量在处理第2d显著高于对照;但藻细胞能通过还

重庆市涪陵区城乡饮用水中微囊藻毒素的污染

目的探讨重庆市涪陵区城乡居民饮用水中微囊藻毒素LR(MC-LR)污染现状。方法在涪陵区市政水源水(长江水)、管网水、二次供水系统设立采样点;同时,抽取水源和水处理工艺完全相同的4个乡镇水厂,选择其水源水、管网水;在上述4个乡镇分别选择3～4个农村居民饮用水井。于2004年6—11月,采集各采样点水样。采用酶联免疫试剂盒测定MC-LR含量,采用氯化亚锡分光光度法测定水样中总磷含量,采用紫外分光光度法测定水样中总氮含量。结果6—11月市政水源水(长江水)、管网水以及6月市政二次供水、乡镇水厂水源水、管网水、农

微囊藻毒素与自然水体中细菌VIVIFORM状态的相关性

细菌VIVIFORM状态是直接关系到自然水体水质评价和环境保护的生态现象 ,其形成机理相当复杂 ,但环境胁迫是主要诱因。通过人为改变湖水中的微囊藻毒素 (MC LR)水平 ,对水体中蓝藻毒素与细菌VIVIFORM状态之间的相关性进行了分析。结果表明 ,较高的毒素水平对水体中细菌种群总量没有明显的影响 ,但能刺激VIVIFORM细菌转化成可培养状态 ,从而证实了自然水体中蓝藻毒素与水细菌VIVIFORM状态之间存在直接的相关性。

天然水体中痕量微囊藻毒素的高效液相色谱测定方法优化

以微囊藻毒素LR(MC-LR)和微囊藻毒素RR(MC-RR)为材料,主要通过调节杂质淋洗液和毒素洗脱液中甲醇、水和三氟乙酸(TFA)的配比来改变极性和PH值,对高效液相色谱(HPLC)法分析MC环境样品的方法进行了优化。结果表明,含0.1%TFA的40%~45%的甲醇水溶液可以取得较好的杂质淋洗效果;含0.1%TFA的70%的甲醇水溶液可以将固相萃取柱(SPE)上的MC完全洗下。因此,建议在分析杂质较多的环境样品时,使用含0.1%TFA的40%~45%的甲醇水溶液对杂质进行淋洗,然后用含0.1%TFA的7

武汉莲花湖微囊藻毒素含量变化特征及其影响因素的研究

采用现场采样及室内测试方法,研究了武汉莲花湖水华消亡过程中微囊藻毒素和环境生态因子的变化规律,并探讨了环境生态因子对微囊藻毒素产生的影响。结果表明,莲花湖微囊藻毒素含量以MC-LR为主,在水华消亡时大量释放到水体中,且较高的藻毒素含量能持续数天。对环境因子的相关分析表明,水体中的微囊藻毒素含量与铵氮、总磷显著正相关,与氮磷比显著负相关(P<0.05)。根据多元逐步回归统计进一步分析,筛选出相对重要的影响因子及合并共线形因子。经显著性检验,逐步回归统计结果为MC=13.62+5.77×NH4+-0.48×T

铜锈微囊藻两种表型的生长生理特性及毒素组成比较分析

从滇池蓝藻水华中分离得到的铜锈微囊藻群体在实验室无机营养中解聚成单细胞 ,结果表明 ,群体微囊藻的生长速度明显低于单细胞微囊藻 ;前者具明显可见的胞外酸性多糖胶鞘 ,而单细胞则几乎没有 ;按常规方法分析比较两种细胞形态的毒性大小和毒素组成 ,发现群体微囊藻主要含有三种微囊藻毒素的异构体 ,而单细胞以MC LR为主 ;且单细胞微囊藻的毒性约为群体的 1 0倍。二者的LDH和PGM同工酶酶谱也有差异。本研究为解释毒素的合成和调控机理提供了新的证据

固相萃取高效液相色谱法测定水中痕量微囊藻毒素

微囊藻毒素是有害的蓝藻水华释放的有毒代谢物 ,对人类及环境具有很大危害性。建立了固相萃取 高效液相色谱测定水中痕量藻毒素的方法。该法对两种常见微囊藻毒素MC LR、MC RR的检测限为 0 .0 2～ 0 .0 5 μg/L ,线性定量范围为 0 .1～ 5 0 μg/L。应用该法分析了天然水样 ,表明方法具有实用性

滇池水华蓝藻铜锈微囊藻和绿色微囊藻的生长生理特性及毒素分析

从滇池分离纯化了两种常见水华微囊藻即铜锈微囊藻和绿色微囊藻．在常规培养条件下，两种藻类在对数生长期的生长速率μ值分别为0．61和0.63;早期生长的抑制光强不大于100μmolm-2s-1.铜锈微囊藻主要产生3种微囊藻毒素：MYCST-RR,MYCST-YR和MYCST－LR绿色微囊藻产生的主要微囊藻毒素为[Dha7]－MYCST－RR和[Dha7]MYCST．LR，另含有少量的[Dha7]－MYCST-YR．在低光强15μEm-2s－1时，毒素含量每毫克于重细胞达到3．127μg微囊藻毒素，当光强达到1

有毒铜绿微囊藻对鱼和溞的毒性

用有毒铜绿微囊藻细胞及其从毒细胞中提取的毒素喂养和腹腔注射鱼类，结果表明：（1）微囊藻毒素MCYST－LR对所有实验过的鱼有毒害作用（LD_(50)为110－500μg／kg）．注射毒素24h后，鱼肝电镜超微结构观察均表现出肝损伤．（2）在受控条件下，当用有毒铜绿微囊藻作为食物喂养日鲢和罗非鱼时，鱼类能在以毒藻为唯一食物的环境中生活20d以上．白鲢和罗非鱼粪便的毒性比喂食藻类的毒性分别降低约2—4．5倍，其肝的超微结构现察仍有轻度损伤．（3）在培养液中加入15μg／mLMCYST－LR和用实验室纯培养的铜

Mechanism study on the frequent variations of cell-bound microcystins in cyanobacterial blooms in Lake Taihu: Implications for water quality monitoring and assessments

Although Microcystis-based toxins have been intensively studied, previous studies using laboratory cultures of Microcystis strains are difficult to explain the phenomenon that microcystin concentrations and toxin variants in natural blooms differ widely and frequently within a short-term period. The present study was designed to unravel the mechanisms for the frequent variations of intracellular toxins related to the differences in cyanobacterial colonies during bloom seasons in Lake Taihu, China. Monitoring of Microcystis colonies during warm seasons indicated that the variations in microcystins in both concentrations and toxin species were associated with the frequent alteration of Microcystis colonies in Lake Taihu. High concentration of microcystins in the blooms was always associated with two Microcystis colonies, Microcystis flos-aquae and Microcystis aeruginosa, whereas when Microcystis wesenbergii was the dominant colonial type, the toxin production of the blooms was low. Additionally, environmental factors such as temperature and nutrition were also shown to have an effect on the toxin production of the blooms, and may also potentially influence the Microcystis species present. The results of the present study provides insight into a new consideration for quick water quality monitoring, assessment and risk alert in cyanobacterium- and toxin-contaminated freshwaters, which will be beneficial not only for water agencies but also for public health. (C) 2009 Elsevier Ltd. All rights reserved.

Physiological Responses of Microcystis aeruginosa PCC7806 to Nonanoic Acid Stress

A recent study has shown that nonanoic acid (NA) is one of the strongest allelochemicals to a cyanobacterium Microcystis aeruginosa, but the physiological responses of M. aeruginosa to NA stress remain unknown. In this study, physiological characters such as the growth rate, photosynthetic processes, phosphorus and nitrogen uptake kinetics, and the contents of intracellular microcystin of M. aeruginosa PCC7806 were studied under the NA stress. The results showed that the growth rates of M. aeruginosa PCC 7806 were significantly inhibited in all NA stress treatments during first 3 days after exposure, and the growth rate was recovered after 5-day exposure. After 2-day exposure, the contents of both phycocyanin and allophycocyanin per cell decreased at NA concentration of 4 mg L-1, and oxygen evolution was inhibited even at the concentration of 0.5 mg L-1, but carotenoid content per cell was slightly boosted in NA stress. Physiological recovery of M. aeruginosa PCC7806 was observed after 7-day exposure to NA. It was shown that NA stress had no effect on uptake of nitrogen, but could stimulate the uptake of phosphorus. The contents of intracellular microcystin have not been affected in all NA treatments in contrast with the control. (C) 2008 Wiley Periodicals, Inc. Environ Toxicol 24: 610-617, 2009.