芦苇化感物质EMA对铜绿微囊藻生长及藻毒素产生和释放的影响

研究了芦苇化感物质2-甲基乙酰乙酸乙酯（ethyl-2-methylacetoacetate,EMA）对铜绿微囊藻PCC7806的生长抑制特性以及对微囊藻毒素MC-LR产生和释放的影响.结果表明,EMA在培养1周内对铜绿微囊藻PCC7806具有较强的抑制作用,EC_50,7d值为2.0 mg·L^-1,但EMA的抑制效果随时间的延长而减弱.整个培养期间,EMA对MC-LR的胞外释放无显著影响.培养7　d后,单位藻细胞内MC-LR的含量随EMA浓度的增加而升高,EMA投加浓度为1.5　mg·L^-1时,单位藻细胞MC-LR的含量为25 ng·(10⁶个)^-1,比对照组增加了39%.但单位体积培养液中MC-LR总量（胞内和胞外的总和）随EMA浓度增加先略微升高后显著降低,EMA投加浓度为3 mg·L^-1时,培养液中MC-LR胞内胞外总量为28 μg·L^-1,约为对照组的一半;16　d后,EMA对单个细胞内MC-LR的含量以及MC-LR总量均无显著影响.     

活性炭纤维对水中微囊藻毒素的吸附性能

利用活性炭纤维对水中微囊藻毒素MC—LR的吸附，研究了吸附过程的热力学与动力学特性。结果表明，活性炭纤维对MC—LR的平衡吸附量在相同温度下随MC-LR初始浓度的增加而显著增大，并随着温度升高而增加，最大吸附量达246μg／g。不同温度条件下，活性炭纤维对MC-LR的吸附均较好地符合Langmuir等温吸附模型。通过热力学分析发现，△H=15．7kJ／mol、△G〈0、△S〉0，表明该吸附是自发的、吸热的过程，温度升高有利于吸附反应。动力学研究表明，该过程符合一级动力学方程。吸附反应速率受颗粒内扩散和液膜扩散共同影响。活性炭纤维经再生后，平衡吸附量变化较小，具有良好的重复使用性能。     

Role of nitric oxide in the genotoxic response to chronic microcystin-LR exposure in human–hamster hybrid cells

Microcystin-LR(MC-LR) is the most abundant and toxic microcystin congener and has been classified as a potential human carcinogen(Group 2B) by the International Agency for Research on Cancer. However, the mechanisms underlying the genotoxic effects of MC-LR during chronic exposure are still poorly understood. In the present study, human–hamster hybrid(AL) cells were exposed to MC-LR for varying lengths of time to investigate the role of nitrogen radicals in MC-LR-induced genotoxicity. The mutagenic potential at the CD59 locus was more than 2-fold higher(p 0.01) in ALcells exposed to a cytotoxic concentration(1 μmol/L) of MC-LR for 30 days than in untreated control cells, which was consistent with the formation of micronucleus. MC-LR caused a dose-dependent increase in nitric oxide(NO) production in treated cells. Moreover, this was blocked by concurrent treatment with the NO synthase inhibitor NG-methyl-L-arginine(L-NMMA), which suppressed MC-LRinduced mutations as well. The survival of mitochondrial DNA-depleted(ρ0) ALcells was markedly decreased by MC-LR treatment compared to that in ALcells, while the CD59 mutant fraction was unaltered. These results provided clear evidence that the genotoxicity associated with chronic MC-LR exposure in mammalian cells was mediated by NO and might be considered as a basis for the development of therapeutics that prevent carcinogenesis.     

Induction of chemotaxis to sodium chloride and diacetyl and thermotaxis defects by microcystin-LR exposure in nematode Caenorhabditis elegans

Apart from the liver disruption, embryotoxicity and genotoxicity, microcystin (MC)-LR also could cause neurotoxicity. Nematode Caenorhabditis elegans was explored as a model to study the neurotoxicity. In the present study, we provided evidence to indicate the neurotoxicity on chemotaxis to NaCl and diacetyl, and thermotaxis from MC-LR exposure to C. elegans. As a result, higher concentrations of MC-LR caused significantly severe defects of chemotaxis to NaC1 and diacetyl, and thermotaxis. The neurotoxicity on chemotaxis to NaCl and diacetyl, and thennotaxis from MC-LR exposure might be largely mediated by the damage on the corresponding sensory neurons (ASE, AWA, and AFD) and interneuron AIY. The expression levels of che-1 and odr-7 were significantly decreased (P<0.01) in animals exposed to MC-LR at concentrations lower than 10 μg/L, whereas the expression levels of ttx-1 and ttx-3 could be significantly (P<0.01) lowered in animals even exposed to 1 μg/L of MC-LR. Moreover, both the chemotaxis to NaCl and diacetyl and the thermotaxis were more significantly reduced m MC-LR exposed mutants of che-1(p674), odr-7(ky4), ttx-1(p767), and ttx-3(ks5) than those in exposed wild-type N2 animals at the same concentrations.     

UV/H2O2工艺降解微囊藻毒素-LR

采用UV/H₂O₂联合工艺,研究了光强、初始浓度、H₂O₂投加量、pH及阴离子对微囊藻毒素-LR (MC-LR)去除率的影响.结果表明,单独H₂O₂对MC-LR基本无去除效果;单独UV工艺可以一定程度上降解MC-LR;而UV/H₂O₂联合工艺由于发生协同作用明显提高降解效率.试验发现,随着光强的增大,MC-LR的去除率不断提高;随着MC-LR初始浓度的增大,其去除率不断降低;随着H₂O₂投加量的增大,降解速率常数逐渐增大,当H₂O₂投加量由1 mmol/L增大到3 mmol/L时,降解速率常数由0.084 4上升到0.166 4;当pH为3.13时,在相同条件下MC-LR的去除效果最好;阴离子的投加不利于MC-LR的降解,其中CO^2-₃、NO^-₃影响最大.     

微囊藻毒素-LR的臭氧降解研究

采用不同的臭氧投加量,考察了微囊藻毒素-LR(MC-LR)的降解效果,并通过对臭氧氧化过程中产生的8种主要降解产物的相对分子质量分析,推测其降解途径.结果表明,臭氧氧化降解MC-LR主要通过Adda途径和Mdha途径来完成对MC-LR的降解和脱毒作用.臭氧氧化的Adda途径是通过对MC-LR上Adda侧链的进攻,断开具有活性的Adda支链,而达到脱毒的目的;臭氧氧化的Mdha途径是通过对MCs肽环上面Mdha和Ala的断键,打开环状肽链,使藻毒素失去活性,在整个过程中Adda途径占主导地位.在O3∶MC为6时,MC-LR的去除率最高可达到92%.     

假单胞菌M-6菌株对微囊藻毒素MC-LR的降解机理初探

研究了以假单胞菌M--6菌株对藻毒素MC—LR的降解机理。结果表明M-6菌株的胞外物质提取波对MC—LR没有降解能力,而胞内物质提取液60min能将15mg／mL的MC--LR降解92％。SDS--PAGE电泳发现经MC—LR诱导后M-6菌株胞内有三种蛋白的表达量增加,HPLC图谱显示在降解过程中产生了两种中间产物和两种终产物。     

黄铁矿光化学氧化降解微囊藻毒素-LR的机制

在可见光(λ420 nm)照射和中性条件(p H=6.8)下,采用天然黄铁矿降解微囊藻毒素MC-LR,XRD和SEM检测表明黄铁矿为层状结构,反应前后黄铁矿表面XPS的表征说明矿物表面存在着S缺陷和缺陷位点Fe(Ⅱ)到Fe(Ⅲ)的转化过程.ESR检测显示黄铁矿光化学反应体系涉及·OH机制.HPLC和LC-MS结果显示可见光照射能有效活化黄铁矿降解MC-LR,反应10 h时能完全降解MC-LR,20 h时对MC-LR矿化率达到约60%,据实验结果推测出黄铁矿光化学氧化MC-LR的两条反应途径.     

磷酸改性水生植物生物炭吸附微囊藻毒素-LR及其影响因素

将水生植物制成生物炭是水生植物资源化利用的新方式,本研究将两种水生植物苦草和狐尾藻在不同温度下热解制备生物炭并用磷酸进行改性,探究了生物炭对水中微囊藻毒素（以MC-LR为例）去除的影响,并研究了其对MC-LR的吸附动力学及影响因素.同时,采用扫描电镜、元素分析、比表面及孔径分析、FTIR和XPS对生物炭进行表征.结果表明,生物炭表面含有丰富的含氧官能团,更高热解温度制备的生物炭具有更丰富的孔隙,对MC-LR的去除率也更高.生物炭对MC-LR的吸附符合准一级动力学、准二级动力学和颗粒内扩散模型.离子强度对生物炭吸附的影响较小,而较高的pH、较大分子量的DOM会抑制吸附.磷酸改性能提高生物炭的吸附性能,并且减弱pH和DOM对生物炭吸附效果的影响.综上,利用水生植物制备的改性生物炭可用于吸附MC-LR,为控制水体中的微囊藻毒素污染提供了新的思路和理论依据.     

Role of nitric oxide in the genotoxic response to chronic microcystin-LR exposure in human-hamster hybrid cells

Microcystin-LR (MC-LR) is the most abundant and toxic microcystin congener and has been classified as a potential human carcinogen (Group 2B) by the International Agency for Research on Cancer. However, the mechanisms underlying the genotoxic effects of MC-LR during chronic exposure are still poorly understood. In the present study, human-hamster hybrid (A_L) cells were exposed to MC-LR for varying lengths of time to investigate the role of nitrogen radicals in MC-LR-induced genotoxicity. The mutagenic potential at the CD59 locus was more than 2-fold higher (p < 0.01) in A_L cells exposed to a cytotoxic concentration (1 μmol/L) of MC-LR for 30 days than in untreated control cells, which was consistent with the formation of micronucleus. MC-LR caused a dose-dependent increase in nitric oxide (NO) production in treated cells. Moreover, this was blocked by concurrent treatment with the NO synthase inhibitor N^G-methyl-_L-arginine (L-NMMA), which suppressed MC-LRinduced mutations as well. The survival of mitochondrial DNA-depleted (ρ⁰) A_L cells was markedly decreased by MC-LR treatment compared to that in A_L cells, while the CD59 mutant fraction was unaltered. These results provided clear evidence that the genotoxicity associated with chronic MC-LR exposure in mammalian cells was mediated by NO and might be considered as a basis for the development of therapeutics that prevent carcinogenesis.