生物毒素的研究进展

本文对动物毒素、植物毒素和微生物毒素等生物毒素的种类、功能和危害做了简要介绍,概括了生物毒素在生物学、医药学、农药中的应用及进展,并对生物毒素目前的研究发展趋势进行了分析,指出了生物毒素研究的热点。     

淡水水体中的蓝藻毒素研究进展（综述）

概述了蓝藻毒素的结构,毒性机理以及蓝藻毒素的危害,并简要介绍了蓝藻毒素的环境行为,对蓝藻毒素的危险评价和监测。     

微囊藻毒素的危害及其分析方法研究进展

微囊藻毒素在蓝藻水华污染中是出现频率高、产量大、危害最为严重的蓝藻毒素,其污染已成为亟待解决的全球性环境问题.本文结合国内外最新相关文献,综述了微囊藻毒素的产生机理、理化性质,并详细介绍了微囊藻毒素对生物体(动物、植物、微生物及人类)的危害及微囊藻毒素测定方法的研究进展,最后对微囊藻毒素的测定分析技术和污染防治的发展方向进行了展望.     

蓝藻毒素及其分析方法(英文)

鉴于蓝藻毒素的安全性问题 ,对蓝藻毒素及其分析方法进行了综述 ,首先阐述了蓝藻毒素的分类及各自产生的主要藻种、毒素的作用机理、半致死剂量等 ,然后从生物法、生物化学法、化学法三个方面介绍了蓝藻毒素的分析检测方法 ,最后还从加强监测控制、完善检测手段、制定相应水质标准等方面提出了建议 ,相信对更好地认识及控制蓝藻及其毒素会有一定的帮助     

硝酸盐浓度对南极亚历山大藻毒素含量和组成的影响

研究了不同硝酸盐浓度(50～250 μmol/L)对南极塔玛亚历山大藻Alexandrium tamarense Polar(ATP)麻痹性毒素含量和组成的影响.结果表明,ATP所产毒素主要为N-磺酰氨甲酰基类毒素(C2毒素),占细胞毒素总量的90%,此外还含有少量的膝沟藻毒素(GTXs),如GTX5和GTX3,但未检出到其它麻痹性毒素.硝酸盐浓度的变化对ATP的细胞密度和生长率影响不大,但对GTXs和C毒素的单细胞毒素含量(fmol/cell)和毒素产量(μmol/L)均有显著影响.在培养期后期(第5天起),高硝氮浓度组(150 μmol/L及以上)单细胞毒素含量比低硝氮浓度组(100 μmol/L及以下)单细胞毒素含量增加了2～3倍,毒素产量提高20%～60%.但在整个生长过程中ATP的毒素组成保持相对稳定,均以C2为主要毒素组成.本研究结果表明,在海洋环境中硝酸盐浓度的增加可能会提高南极塔玛亚历山大藻细胞毒素的含量,从而提高了其潜在毒性.     

五脏排毒最简单有效的方法

我们每个人体内都有毒素吗?很多身体问题就是毒素引发的吗?面对排毒的风潮和疑问,中医是如何作为的?中医认为五脏之内都可能留存毒素,堆积了毒素的     

松针褐斑病菌毒素的专化性研究

用松针褐斑病菌毒素粗提液处理湿地松、火炬松、黑松和马尾松的切根苗,发现湿地松和火炬松对毒素最为敏感,其次为马尾松,黑松最不敏感。毒素生测的结果与松树在田间自然感染的情况有一定的相似性,但不完全一致。不同湿地松抗病无性系对毒素的反应存在着差别,其中３３ 号所受伤害较轻,１０ 号及３６ 号较重。结合毒素薄层层析半定量试验,利用寄主愈伤组织对毒素的反应,发现毒素对寄主愈伤组织的最低作用浓度应在１００ μｇ／ｍ Ｌ 以下。试验了５ 种杂草对毒素的反应,其中空心莲子草和稞草对毒素敏感。进一步研究利用毒素作为除草剂不失为毒素利用的一个新思路。上述研究表明该毒素为非寄主专化性毒素。     

酵母菌对饲料中黄曲霉毒素B_1的降解和脱除作用研究

研究了含有活性酵母菌、酵母菌细胞壁及水合铝硅酸盐等酵母霉菌毒素降解剂对霉变饲料中黄曲霉毒素B_1的降解和脱除效果.结果表明:随着酵母霉菌毒素降解剂添加量的增加,对黄曲霉毒素B_1的体外吸附率逐渐升高,而且试验用鸡粪便中黄曲霉毒素B_1排出率也逐渐升高,当加入的毒素降解剂质量浓度为0.25 mg/m L时,对黄曲霉毒素B_1的体外吸附率效果最好,达到98.21%,黄曲霉毒素B_1的排出率达到86.07%.试验结果表明该毒素降解剂对霉变饲料中的黄曲霉毒素B_1脱除和降解效果显著,可有效预防动物食用霉变饲料中毒.     

植物病原真菌毒素研究进展

综述了近年来有关植物病原真菌毒素的研究进展 ,对产毒真菌的种类和毒素的化学类别 ,病原真菌的产毒培养条件、毒素的提取纯化以及结构鉴定方法 ,毒素的 3种检测途径与致病机理 ,以及毒素的分子遗传学和毒素的应用研究作了简要概括     

玉米中的黄曲霉毒素及检测方法研究

玉米中含有一些黄曲霉毒素,而这些毒素如果进入到人与动物的身体中会产生肝癌等疾病问题。如果长期的服用低浓度的黄曲霉毒素饲料也会导致动物胚胎中毒,还会降低奶牛的产量,也会导致牛奶中含有转型的黄曲霉毒素,如果黄曲霉毒素进入到人体内,会诱发肝癌等严重的后果。基于此,该文主要对玉米黄曲霉毒素进行了分析,探究了黄曲霉毒素的检测方式与手段,仅供参考。     

Botulinum C2 toxin ADP-ribosylates actin

ADP-ribosylation of regulatory proteins is an important pathological mechanism by which various bacterial toxins affect eukaryotic cell functions. While diphtheria toxin catalyses the ADP-ribosylation of elongation factor 2, which results in inhibition of protein synthesis, cholera toxin and pertussis toxin ADP-ribosylate Ns and Ni, respectively, the GTP-binding regulatory components of the adenylate cyclase system, thereby modulating the bidirectional hormonal regulation of the adenylate cyclase. Botulinum C2 toxin is another toxin which has been reported to possess ADP-ribosyltransferase activity. This extremely toxic agent is produced by certain strains of Clostridium botulinum and induces hypotension, an increase in intestinal secretion, vascular permeability and haemorrhaging in the lungs. In contrast to botulinum neurotoxins, the botulinum C2 toxin apparently lacks any neurotoxic effects. Here we report that botulinum C2 toxin ADP-ribosylates a protein of relative molecular mass 43,000 (43K) in intact cells and in cell-free preparations. We present evidence that the 43K protein substrate is actin, which is apparently mono-ADP-ribosylated by the toxin. Botulinum C2 toxin also ADP-ribosylated purified liver G-actin, whereas liver F-actin was only poorly ADP-ribosylated and skeletal muscle actin was not ADP-ribosylated in either its G form or its F form. ADP-ribosylation of liver G-actin by botulinum C2 toxin resulted in a drastic reduction in viscosity of actin polymerized in vitro.     

松针褐斑病菌毒素的确定及其基本性质研究

以ＭＳ液体培养基培养２０ｄ左右至菌丝大量生长并紧密交织成团时病菌即可大量产生毒素,病菌是否产孢对产毒量大小无显著影响。毒素原液中仅非蛋白质部分具致病活性,经高温高压灭菌１５ｍｉｎ后活性仍不丧失,且有所加强。该毒素在冷冻条件或灭菌后于室温下可保存两个月以上而不失活。毒素粗提液中活性成分为一类极性较大的物质,易溶于水、甲醇、乙醇,可溶于正丁醇,微溶于乙酸乙酯,不溶于苯,可被活性炭吸附并为甲醇所洗脱。毒素粗提液的ｐＨ值为６０,渗透势为－１２２ｋＰａ,经试验确定毒素粗提液的毒性非溶液的酸度或渗透势所致,从而进一步确定了病菌人工培养滤液中存在具致病活性的毒素物质。     

Kluyveromyces lactis killer toxin inhibits adenylate cyclase of sensitive yeast cells

K1 killer toxin secreted by the K1 strain of Saccharomyces cerevisiae, has been well characterized. It is a simple protein of molecular weight (MW) 11,470 (ref. 3), encoded by a double-stranded, linear RNA plasmid, called M RNA, of MW 1.1-1.7 x 10(6) (refs 4-6). It is lethal to sensitive Saccharomyces cerevisiae which does not carry M RNA. Leakage of K+ and ATP is the first distinct response in sensitive cells, and the toxic action is thought to be due to its action as a protonophore or K+ ionophore. Recently, a further killer toxin has been found in Kluyveromyces lactis IFO 1267, and it is associated with the presence of the double-stranded linear DNA plasmids, pGK1-1 (MW 5.4 x 10(6)) and pGK1-2 (MW 8.4 x 10(6)). It has been shown, by curing pGK1-1 or deletion mapping, that the structural gene for the killer toxin and immunity-determining gene reside on the smaller plasmid. Moreover, the plasmids could be transferred from K. lactis to S. cerevisiae by protoplast fusion and protoplast transformation. As the K. lactis toxin is encoded by a DNA plasmid and has a relatively wider action spectrum than K1 killer toxin, the mode of action of the toxin is highly interesting. Here we report that K. lactis toxin inhibits adenylate cyclase in sensitive yeast cells and brings about arrest of the cells at the G1 stage.     

Retrograde transport of endocytosed Shiga toxin to the endoplasmic reticulum.

Shiga toxin and some other protein toxins that act on targets in the cytosol have previously been shown to enter the trans-Golgi network. Transport by this route may be necessary for translocation of the toxin to the cytosol and for intoxication, but it is not known whether the enzymatically active part of the toxins actually enters the cytosol from the trans-Golgi network. It has been suggested that such toxins are transported in a retrograde manner to the endoplasmic reticulum and that translocation occurs in this organelle, but retrograde transport of endocytosed material beyond the trans-Golgi network has never been demonstrated. Here we show that in butyric acid-treated A431 cells endocytosed Shiga toxin is not only transported to the trans-Golgi network, but also to all Golgi stacks, to the endoplasmic reticulum and to the nuclear envelope. Furthermore, butyric acid sensitizes the cells to Shiga toxin, which is consistent with the possibility that retrograde transport is required for translocation of the toxin to the cytosol.     

Voltage-sensor activation with a tarantula toxin as cargo

The opening and closing of voltage-activated Na+, Ca2+ and K+ (Kv) channels underlies electrical and chemical signalling throughout biology, yet the structural basis of voltage sensing is unknown. Hanatoxin is a tarantula toxin that inhibits Kv channels by binding to voltage-sensor paddles, crucial helix-turn-helix motifs within the voltage-sensing domains that are composed of S3b and S4 helices. The active surface of the toxin is amphipathic, and related toxins have been shown to partition into membranes, raising the possibility that the toxin is concentrated in the membrane and interacts only weakly and transiently with the voltage sensors. Here we examine the kinetics and state dependence of the toxin-channel interaction and the physical location of the toxin in the membrane. We find that hanatoxin forms a strong and stable complex with the voltage sensors, far outlasting fluctuations of the voltage sensors between resting (closed) conformations at negative voltages and activated (open) conformations at positive voltages. Toxin affinity is reduced by voltage-sensor activation, explaining why the toxin stabilizes the resting conformation. We also find that when hanatoxin partitions into membranes it is localized to an interfacial region, with Trp 30 positioned about 8.5 A from the centre of the bilayer. These results demonstrate that voltage-sensor paddles activate with a toxin as cargo, and suggest that the paddles traverse no more than the outer half of the bilayer during activation.     

Intracellularly injected tetanus toxin inhibits exocytosis in bovine adrenal chromaffin cells

The clostridial neurotoxins tetanus and botulinum toxin type A are known to block transmitter release from nerve terminals, probably by interfering with some essential process controlling exocytosis after the entry of Ca2+ ions. Although exocytosis occurs in many secretory cells, these toxins show a high specificity for neurones and the secretory response of cultured bovine adrenal medullary cells is not inhibited by exposure to medium containing tetanus or botulinum toxin type A (although it is by botulinum toxin type D). Here we report that when tetanus toxin and botulinum neurotoxin type A are injected intracellularly into chromaffin cells they strongly inhibit secretion, as revealed by the measurement of cell capacitance. These results indicate that these toxins are normally ineffective in chromaffin cells because they are not bound and internalized, so do not reach their site of action. Furthermore, we have localized the secretion-blocking effects of the toxin to a fragment comprising the light chain covalently linked to part of the heavy chain, suggesting that this part of the molecule contains the active site.     

Autocatalytic cleavage of Clostridium difficile toxin B

Clostridium difficile, the causative agent of nosocomial antibiotic-associated diarrhoea and pseudomembranous colitis, possesses two main virulence factors: the large clostridial cytotoxins A and B. It has been proposed that toxin B is cleaved by a cytosolic factor of the eukaryotic target cell during its cellular uptake. Here we report that cleavage of not only toxin B, but also all other large clostridial cytotoxins, is an autocatalytic process dependent on host cytosolic inositolphosphate cofactors. A covalent inhibitor of aspartate proteases, 1,2-epoxy-3-(p-nitrophenoxy)propane, completely blocked toxin B function on cultured cells and was used to identify its catalytically active protease site. To our knowledge this is the first report on a bacterial toxin that uses eukaryotic signals for induced autoproteolysis to deliver its toxic domain into the cytosol of target cells. On the basis of our data, we present an integrated model for the uptake and inositolphosphate-induced activation of toxin B.     

链格孢菌毒素对紫茎泽兰致病性及生物测定方法的研究

以紫茎泽兰（Eupatorium adenophorum Spreng.）为生物测定材料,对链格孢菌毒素的生物测定方法进行了比较研究,筛同离体叶片针刺法可作为该毒素的生物测定方法,为进一步研究该毒素提供了可靠的生物检测手段。     

饮用水中藻类及藻毒素去除技术进展

水体富营养化日趋严重,藻类及藻毒素给饮用水处理带来很多不利影响,对饮用水中藻类与藻毒素去除技术从物理、化学、生物及其他方法进行具体论述,系统分析了各种技术的去除效果和局限性,并对饮用水中藻类及藻毒素去除技术进行了展望。     

赤星菌毒素对烟草幼苗致病特性的研究

文章首先测验了3种培养液对烟苗生长的影响和赤星病菌在培养液中产生毒素的能力,据此选出查彼培养液用于产生毒素的培养。病菌在查彼培养液中生长28天后,表现出最高的毒素活性,毒素活性临界值(TWE50)为32。然后用毒素粗提液处理幼苗,以幼苗悬滴接种法为对比。烟苗在12小时内可见对毒素发生明显反应,表现为根部变褐和须根脱落,对悬滴接种的反应要到72小时后才可鉴别。毒素处理后36小时内烟苗进而萎蔫,21个品种的萎蔫程度与12小时内的根部反应趋势一致,根部反应和萎蔫的程度又同时与品种对悬滴接种的反应趋势相一致,3种反应间的吻合度平均近80％。