水生态系统中微囊藻毒素的分布及其生态毒理效应研究进展

有毒蓝藻产生的蓝藻毒素对淡水生态系统构成了严重的全球性环境威胁,其中微囊藻毒素(MCs)是所有蓝藻毒素中分布最广、危害最大的一类肝毒素。MCs已对水生态系统的结构、功能和稳定性造成了不良影响,并对人类健康构成威胁。本文综述了当前MCs在水体、沉积物和水生动物体内的分布,以及MCs的生物毒性机制,在此基础上,总结了MCs对水生动物、水生植物及陆生植物的生态毒理效应,及其引发的人类健康风险,并关注了MCs的生物防治方法。最后,针对当前MCs相关研究领域中存在的不足提出展望,旨在为淡水水体中MCs的风险评估与治理管控提供参考。     

大田软海绵酸的遗传毒性

大田软海绵酸(okadaic acid, OA)是腹泻性贝类毒素中分布最广、危害最大的一种毒素。OA很容易在贝类(主要是双壳类软体动物)和鱼类体内累积,一旦被人类食用,将导致消化道中毒从而引起胃肠道症状。许多研究表明,OA可以诱导细胞毒性、神经毒性、免疫毒性、胚胎毒性、遗传毒性和促癌作用。随着有关OA中毒的报道数量的增加,这种毒素逐渐引起了公众的关注,所以研究该毒素的作用机制及毒理作用意义重大。本文主要针对大田软海绵酸的遗传毒性展开综述。     

可食植物中砷赋存形态研究进展

砷是环境中普遍存在的一种化学元素,近年来日益严重的砷污染问题在世界范围内受到高度重视,我国目前已经成为世界卫生组织(WHO)列出的砷污染最严重的国家和地区之一.经口摄入是外界砷进入人体并累积产生生物毒性的主要途径.可食植物是人类饮食结构中不可缺少的部分,食品总砷含量并不能完全决定其毒性大小,砷的赋存形态与其生物毒性密切相关,无机砷已被确认为致癌物质.本文主要综述了不同种类可食植物中砷形态的分析方法,以及砷的主要赋存形态及其生物毒性.     

应用环境微生物治理淡水湖泊微囊藻毒素污染的研究进展

近年来,随着水体富营养化程度的加剧,蓝藻水华现象时有发生,蓝藻及其释放的藻毒素对生态环境和人类健康构成严重威胁。在各种藻毒素中,以微囊藻毒素(Microcystins,MCs)毒性最强,对人类危害也最大,微囊藻毒素的化学性质相对稳定且难以通过常规水处理方法消除,因此如何有效去除环境中的MCs是国内外普遍关注的难题。研究发现自然界中的微生物能够有效降解和消除MCs污染,由此产生的环保技术极具应用价值。本文主要概述了微囊藻毒素的产生机理、化学结构以及毒性危害,总结了微囊藻毒素的自然分解过程以及微生物群落对微囊藻毒素的响应机制,重点分析了微生物群落在微囊藻毒素污染控制技术中的潜在应用,并对应用微生物技术治理微囊藻毒素污染的技术瓶颈提出了建议,以期加速微囊藻毒素微生物降解技术的完善和应用。     

微囊藻毒素对鱼类的毒性效应

湖泊富营养化导致的蓝藻水华已成为国内外普遍关注的环境问题,它所带来的主要危害之一是产生的藻毒素对鱼类的影响。在已发现的藻毒素中,微囊藻毒素(microcystins,MCs)的分布广、毒性大、危害严重,而备受关注。阐述了MCs对鱼类的影响。微囊藻毒素能干扰胚胎的发育,降低孵化率,增加畸形率,影响存活率,胚胎孵化受微囊藻毒素影响还具有剂量依赖效应;野外室内实验均表明鱼类暴露于微囊藻毒素后不仅可在肝脏中富集还可在肌肉、肠道等组织器官中快速积累;对鱼类进行组织病理检测发现MCs可导致肝脏、肾脏、心脏、脑、鳃等组织受损;MCs在鱼体中的解毒过程可能开始于由谷胱甘肽S-转移酶催化的还原型谷胱甘肽的结合反应;MCs还可影响鱼类的生长、行为和血清生化指标,此外,还具有一定的免疫毒性。MCs的转运机制和分子作用机制以及在食物链中传递过程中对人类造成的潜在影响可能成为今后研究重点。     

微囊藻毒素LR影响人肝细胞HL7702的ERK及JNK的蛋白磷酸化

微囊藻毒素(Microcystin,MCYST)是蓝藻的一些属产生的次级代谢产物,在发生水华的水体中普遍存在。微囊藻毒素LR(MCLR)是微囊藻毒素中存在最为普遍且毒性作用最强的一种。已有研究表明,微囊藻毒素可以诱发肝毒性并且与人群中的肝癌发生密切相关1,2,因此进一步阐明其致毒机理具有重要的意义。       

节球藻毒素研究进展

节球藻毒素(Nodularin)是由泡沫节球藻(Nodularia spumigena)产生的一种环状五肽肝毒素。节球藻毒素对陆生动物和人体均具有毒性和致癌作用,还会影响水生生态系统的结构和功能,对许多陆生植物、水生动物的生长繁殖具有一定的威胁,受到了社会的广泛关注。综述了节球藻毒素的分子结构、检测方法和产生途径,深入讨论了节球藻毒素的环境归趋和毒性效应的研究进展,并对其重要的研究领域提出进一步的展望。     

金属型纳米颗粒对植物的生态毒理效应研究进展

纳米技术的高速发展和人工纳米颗粒(NPs)的广泛应用带来的潜在环境风险已经引起国内外的广泛关注.金属型纳米颗粒(MB NPs)具有金属毒性和纳米毒性的双重效应,其生物毒性和生态风险已成为纳米毒理学的研究热点之一.植物作为生态系统中的重要组分,是NPs生物累积并进入食物链的潜在途径.本文论述了MB NPs在植物中的吸收、转运和累积过程,总结了MB NPs对植物的毒性效应及其机制,探讨了MB NPs植物毒性的影响因素,综合评述了近年来关于MB NPs对植物特别是农作物的生态毒理效应的研究进展,同时分析了目前研究中存在的问题,对今后的研究方向进行了展望.     

环境因子对小麦体内镉的生物毒性和植物络合素合成的影响

采用水培方式,研究了不同环境因子对小麦体内Cd的生物毒性与植物络合素(PCs)合成的影响.结果表明,Cd胁迫对小麦产生明显的毒害效应,并显著诱导根合成PCs;pH、Ca和S对小麦体内Cd的吸收和生物毒性具有不同程度的影响,根中PCs的诱导量与Cd的生物毒性变化表现一致;供磷减轻了Cd胁迫的生物毒性,根中PCs的诱导量也显著降低;镁对Cd胁迫的生物毒性影响甚微,根中PCs的诱导量和Cd的吸收量均未见明显变化.本实验结果证明Cd对PCs的诱导能力与植物体内Cd的毒性之间存在一定的相关关系,可将PCs作为Cd胁迫的生物标记物.     

有机酸在植物对重金属耐性和解毒机制中的作用

植物对重金属的耐受和解毒机制可分为外部排斥和内部耐受两大类。该文综述了有机酸作为一类金属配位体, 在植物对重金属的这两大类机制中的重要作用。在重金属的外部排斥过程中, 植物根系分泌有机酸, 与金属离子形成稳定的金属配位体复合物, 改变重金属的移动性和生物可利用性, 阻止金属离子进入植物体内或避免其在根部敏感位点累积。此外, 有机酸还可与进入植物体内的金属离子螯合, 使其转化为无毒或毒性较小的结合形态, 缓解重金属的毒害效应, 实现植物对重金属的内部耐受。     

Microcystin-Degrading Activity of an Indigenous Bacterial Strain Stenotrophomonas acidaminiphila MC-LTH2 Isolated from Lake Taihu

Microcystin-LR (MC-LR) and microcystin-RR (MC-RR) produced by harmful cyanobacterial blooms (HCBs) pose substantial threats to the ecosystem and public health due to their potential hepatotoxicity. Degradation of microcystins (MCs) by indigenous bacteria represents a promising method for removing MCs from fresh water without harming the aquatic environment, but only a few microcystin (MC)-degrading bacteria have been isolated and had their mechanisms reported. This study aimed to isolate indigenous bacteria from Lake Taihu, and investigate the capability and mechanism of MC degradation by these bacteria. During a Microcystis bloom, an indigenous MC-degrading bacterium designated MC-LTH2 was successfully isolated from Lake Taihu, and identified as Stenotrophomonas acidaminiphila based on phylogenetic analysis. In the presence of MC-LR together with MC-RR, the strain MC-LTH2 was capable of totally degrading both simultaneously in 8 days, at rates of 3.0 mg/(L⋅d) and 5.6 mg/(L⋅d), respectively. The degradation rates of MCs were dependent on temperature, pH, and initial MC concentration. Adda (3-amino-9-methoxy-2, 6, 8-trimethyl-10-phenyldeca-4, 6-dienoic acid) was detected as an intermediate degradation product of MCs using high performance liquid chromatography coupled with time-of-flight mass spectrometry (HPLC-TOF-MS). To the best of our knowledge, this is the first report of Stenotrophomonas acidaminiphila capable of degrading two MC analogues and other compounds containing Adda residue completely under various conditions, although the mlrA gene in the strain was not detected. These results indicate the Stenotrophomonas acidaminiphila strain MC-LTH2 possesses a significant potential to be used in bioremediation of water bodies contaminated by MC-LR and MC-RR, and is potentially involved in the degradation of MCs during the disappearance of the HCBs in Lake Taihu.     

Microcystins -LA, -YR, and -LR action on neutrophil migration

Microcystins (MCs) produced by some freshwater cyanobacterial species possess potent liver toxicity as evidenced by acute neutrophil infiltration. Here, we investigate the ability of three structurally distinct toxins (MC-LA, MC-LR, and MC-YR) to evoke neutrophil recruitment per se and their effects on migration pathways. Intravital microscopic studies showed that topical application of only MC-LR enhanced the numbers of rolling and adhered leukocytes in the endothelium of postcapillary mesenteric venules. The latter effects may be dependent upon induction of the synthesis and expression of l-selectin and β2-integrin in neutrophils, as assessed by flow cytometry and RT-PCR, respectively. Conversely, the three toxins promoted direct locomotion of neutrophils and enhanced their migration in response to fMLP, as measured by Boyden chamber assays, and increased intracellular calcium, a messenger in the chemotaxic process. In conclusion, our results show that MCs act on specific pathways of neutrophil recruitment, indicating their potential effect on neutrophils activation.     

Turbulence increases the risk of microcystin exposure in a eutrophic lake (Lake Taihu) during cyanobacterial bloom periods

Toxic cyanobacterial harmful algal blooms (CyanoHABs) have posed serious water use and public health threats because of the toxins they produce, such as the microcystins (MCs). The direct physical effects of turbulence on MCs, however, have not yet been addressed and is still poorly elucidated. In this study, a 6-day mesocosm experiment was carried out to evaluate the effects of wind wave turbulence on the competition of toxic Microcystis and MCs production in highly eutrophicated and turbulent Lake Taihu, China. Under turbulent conditions, MCs concentrations (both total and extracellular) significantly increased and reached a maximum level 3.4 times higher than in calm water. Specifically, short term (∼3 days) turbulence favored the growth of toxic Microcystis species, allowing for the accumulation of biomass which also triggered the increase in MCs toxicity. Moreover, intense turbulence raises the shear stress and could cause cell mechanical damage or cellular lysis resulting in cell breakage and leakage of intracellular materials including the toxins. The results indicate that short term (∼3 days) turbulence is beneficial for MCs production and release, which increase the potential exposure of aquatic organisms and humans. This study suggests that the importance of water turbulence in the competition of toxic Microcystis and MCs production, and provides new perspectives for control of toxin in CyanoHABs-infested lakes.     

Genotoxicity and potential carcinogenicity of cyanobacterial toxins – a review

The occurrence of cyanobacterial blooms has increased significantly in many regions of the world in the last century due to water eutrophication. These blooms are hazardous to humans, animals, and plants due to the production of cyanotoxins, which can be classified in five different groups: hepatotoxins, neurotoxins, cytotoxins, dermatotoxins, and irritant toxins (lipopolysaccharides). There is evidence that certain cyanobacterial toxins are genotoxic and carcinogenic; however, the mechanisms of their potential carcinogenicity are not well understood. The most frequently occurring and widespread cyanotoxins in brackish and freshwater blooms are the cyclic heptapeptides, i.e., microcystins (MCs), and the pentapeptides, i.e., nodularins (NODs). The main mechanism associated with potential carcinogenic activity of MCs and NOD is the inhibition of protein phosphatases, which leads to the hyperphosphorylation of cellular proteins, which is considered to be associated with their tumor-promoting activity. Apart from this, MCs and NOD induce increased formation of reactive oxygen species and, consequently, oxidative DNA damage. There is also evidence that MCs and NOD induce micronuclei, and NOD was shown to have aneugenic activity. Both cyanotoxins interfere with DNA damage repair pathways, which, along with DNA damage, is an important factor involved in the carcinogenicity of these agents. Furthermore, these toxins increase the expression of TNF-α and early-response genes, including proto-oncogenes, genes involved in the response to DNA damage, cell cycle arrest, and apoptosis. Rodent studies indicate that MCs and NOD are tumor promotors, whereas NOD is thought to have also tumor-initiating activity. Another cyanobacterial toxin, cylindrospermopsin (CYN), which has been neglected for a long time, is lately being increasingly found in the freshwater environment. The principal mechanism of its toxicity is the irreversible inhibition of protein synthesis. It is pro-genotoxic, and metabolic activation by cytochrome P-450 enzymes is needed for its genotoxic activity. In metabolically competent cells, it induces DNA strand breaks and exerts clastogenic and aneugenic activity. In addition, CYN increased the expression of p53 regulated genes involved in cell cycle arrest, DNA damage repair, and apoptosis. It also has cell transforming potential, and limited preliminary rodent studies indicate that CYN could have tumor-initiating activity. In 2010, the International Agency for Research on Cancer (IARC) classified MCLR as possible human carcinogen (Group 2B). Although there is not enough available information for the classification of other cyanobacterial toxins, the existing data from in vitro and in vivo studies indicate that NOD and especially CYN may be even more hazardous than MCLR to human and animal health. In addition in the environment, cyanobacterial toxins occur in complex mixtures as well as together with other anthropogenic contaminants, and numerous studies showed that the toxic/genotoxic potential of the extracts from cyanobacterial scums is higher than that of purified toxins. This means that the mixtures of toxins to which humans are exposed may pose higher health risks than estimated from the toxicological data of a single toxin. Future research efforts should focus on the elucidation of the carcinogenic potential of NOD, CYN, and the mixture of cyanobacterial extracts, as well as on the identification of possible novel toxins.     

Ecological Dynamics of Toxic Microcystis spp. and Microcystin-Degrading Bacteria in Dianchi Lake,China

Toxic cyanobacterial blooms directly threaten both human safety and the ecosystem of surface waters. The widespread occurrence of these organisms, coupled with the tumor-promoting properties of the microcystin toxins that they produce, demands action to mitigate their potential impacts and, thus, a robust understanding of their ecological dynamics. In the present work, the abundance of toxic Microcystis spp. and microcystin (MC)-degrading bacteria in Dianchi Lake, located in Yunnan Province, China, was studied using quantitative PCR. Samples were taken at monthly intervals from June 2010 to December 2011 at three sampling stations within this freshwater lake. Results revealed that variation in the abundance of both total Microcystis spp. and toxic Microcystis spp. exhibited similar trends during the period of the algal bloom, including the reinvasion, pelagic growth, sedimentation, and overwintering periods, and that the proportion of toxic Microcystis was highest during the bloom and lowest in winter. Importantly, we observed that peaks in mlrA gene copy numbers of MC-degrading bacteria occurred in the months following observed peaks in MC concentrations. To understand this phenomenon, we added MCs to the MC-degrading bacteria (designated strains HW and SW in this study) and found that MCs significantly enhanced mlrA gene copy numbers over the number for the control by a factor of 5.2 for the microcystin-RR treatment and a factor of 3.7 for the microcystin-LR treatment. These results indicate that toxic Microcystis and MC-degrading bacteria exert both direct and indirect effects on each other and that MC-degrading bacteria also mediate a shift from toxic to nontoxic populations of Microcystis.     

Genotoxicity and potential carcinogenicity of cyanobacterial toxins - a review

The occurrence of cyanobacterial blooms has increased significantly in many regions of the world in the last century due to water eutrophication. These blooms are hazardous to humans, animals, and plants due to the production of cyanotoxins, which can be classified in five different groups: hepatotoxins, neurotoxins, cytotoxins, dermatotoxins, and irritant toxins (lipopolysaccharides). There is evidence that certain cyanobacterial toxins are genotoxic and carcinogenic; however, the mechanisms of their potential carcinogenicity are not well understood. The most frequently occurring and widespread cyanotoxins in brackish and freshwater blooms are the cyclic heptapeptides, i.e., microcystins (MCs), and the pentapeptides, i.e., nodularins (NODs). The main mechanism associated with potential carcinogenic activity of MCs and NOD is the inhibition of protein phosphatases, which leads to the hyperphosphorylation of cellular proteins, which is considered to be associated with their tumor-promoting activity. Apart from this, MCs and NOD induce increased formation of reactive oxygen species and, consequently, oxidative DNA damage. There is also evidence that MCs and NOD induce micronuclei, and NOD was shown to have aneugenic activity. Both cyanotoxins interfere with DNA damage repair pathways, which, along with DNA damage, is an important factor involved in the carcinogenicity of these agents. Furthermore, these toxins increase the expression of TNF-α and early-response genes, including proto-oncogenes, genes involved in the response to DNA damage, cell cycle arrest, and apoptosis. Rodent studies indicate that MCs and NOD are tumor promotors, whereas NOD is thought to have also tumor-initiating activity. Another cyanobacterial toxin, cylindrospermopsin (CYN), which has been neglected for a long time, is lately being increasingly found in the freshwater environment. The principal mechanism of its toxicity is the irreversible inhibition of protein synthesis. It is pro-genotoxic, and metabolic activation by cytochrome P-450 enzymes is needed for its genotoxic activity. In metabolically competent cells, it induces DNA strand breaks and exerts clastogenic and aneugenic activity. In addition, CYN increased the expression of p53 regulated genes involved in cell cycle arrest, DNA damage repair, and apoptosis. It also has cell transforming potential, and limited preliminary rodent studies indicate that CYN could have tumor-initiating activity. In 2010, the International Agency for Research on Cancer (IARC) classified MCLR as possible human carcinogen (Group 2B). Although there is not enough available information for the classification of other cyanobacterial toxins, the existing data from in vitro and in vivo studies indicate that NOD and especially CYN may be even more hazardous than MCLR to human and animal health. In addition in the environment, cyanobacterial toxins occur in complex mixtures as well as together with other anthropogenic contaminants, and numerous studies showed that the toxic/genotoxic potential of the extracts from cyanobacterial scums is higher than that of purified toxins. This means that the mixtures of toxins to which humans are exposed may pose higher health risks than estimated from the toxicological data of a single toxin. Future research efforts should focus on the elucidation of the carcinogenic potential of NOD, CYN, and the mixture of cyanobacterial extracts, as well as on the identification of possible novel toxins.     

水华蓝藻对鱼类的营养毒理学效应

水体富营养化导致蓝藻水华的发生已成为全球关注的水环境问题,很多鱼类处于水生态系统食物链的最高级,蓝藻水华的主要次级代谢产物-微囊藻毒素可通过鱼类的摄食活动或生物富集作用在鱼体组织中累积,并通过食物链危及人类健康。近年来,微囊藻毒素对鱼类的毒性效应引起众多科学家的关注。在天然水体中不少鱼类可以主动摄食蓝藻,所以,水华蓝藻对鱼类来说既具有营养物作用、也具有潜在的毒性作用。鉴于目前机械收获的水华蓝藻生物量资源化利用问题以及水产饲料业亟需大力开发鱼粉替代蛋白源的需要,从营养学和毒理学这两个角度来研究水华蓝藻对鱼类的营养作用和毒性效应具有较高的理论和现实意义。主要概述了蓝藻粉、蓝藻细胞对鱼类的营养学和毒理学效应,以期拓展水华蓝藻对鱼类毒性效应的研究视野,同时也为水华蓝藻的资源化利用提供新的思路。     

蓝藻水华堆积处理池中微囊藻毒素降解细菌的分离及降解特性

微囊藻毒素(microcystins, MCs)近年来由于蓝藻水华在世界范围内频发而受到广泛关注。从太湖北部蓝藻水华堆积处理池中分离出一株微囊藻毒素降解细菌SW1, 经16S rDNA序列分析鉴定为鞘氨醇单胞菌(Sphingopyxis sp.)。SW1的生长最适pH为中性(pH 6-8), 但也能生长于pH 10条件下。SW1对MCs的两种异构体MC-LR和MC-RR具有高降解活性, 并表现出一级反应动力学特征, 其降解速率常数分别为0.35/h和0.28/h。温度和pH对SW1降解活性有很强影响: 在温度为22-37℃, pH中性或弱碱性条件下(MC-LR, pH 6-9; MC-RR, pH 7-8), SW1具有高降解活性; 而在低温和强碱性条件下其降解活性受到强烈抑制。聚合酶链式反应(PCR)表明SW1及蓝藻水华堆积处理池均含有mlrA的同源基因, 表明处理池中存在MCs的生物 降解。