首页> 美国卫生研究院文献>Applied and Environmental Microbiology >Evidence for paralytic shellfish poisons in the freshwater cyanobacterium Lyngbya wollei (Farlow ex Gomont) comb. nov.
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Evidence for paralytic shellfish poisons in the freshwater cyanobacterium Lyngbya wollei (Farlow ex Gomont) comb. nov.

机译:淡水蓝藻Lyngbya wollei(Farlow ex Gomont)梳中有麻痹性贝类毒素的证据。十一月

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摘要

Lyngbya wollei (Farlow ex Gomont) comb. nov., a perennial mat-forming filamentous cyanobacterium prevalent in lakes and reservoirs of the southeastern United States, was found to produce a potent, acutely lethal neurotoxin when tested in the mouse bioassay. Signs of poisoning were similar to those of paralytic shellfish poisoning. As part of the Tennessee Valley Authority master plan for Guntersville Reservoir, the mat-forming filamentous cyanobacterium L. wollei, a species that had recently invaded from other areas of the southern United States, was studied to determine if it could produce any of the known cyanotoxins. Of the 91 field samples collected at 10 locations at Guntersville Reservoir, Ala., on the Tennessee River, over a 3-year period, 72.5% were toxic. The minimum 100% lethal doses of the toxic samples ranged from 150 to 1,500 mg kg of lyophilized L. wollei cells-1, with the majority of samples being toxic at 500 mg kg-1. Samples bioassayed for paralytic shellfish toxins by the Association of Official Analytical Chemists method exhibited saxitoxin equivalents ranging from 0 to 58 micrograms g (dry weight)-1. Characteristics of the neurotoxic compound(s), such as the lack of adsorption by C18 solid-phase extraction columns, the short retention times on C18 high-performance liquid chromatography (HPLC) columns, the interaction of the neurotoxins with saxiphilin (a soluble saxitoxin-binding protein), and external blockage of voltage-sensitive sodium channels, led to our discovery that this neurotoxin(s) is related to the saxitoxins, the compounds responsible for paralytic shellfish poisonings. The major saxitoxin compounds thus far identified by comparison of HPLC fluorescence retention times are decarbamoyl gonyautoxins 2 and 3. There was no evidence of paralytic shellfish poison C toxins being produced by L. wollei. Fifty field samples were placed in unialgal culture and grown under defined culture conditions. Toxicity and signs of poisoning for these laboratory-grown strains of L. wollei were similar to those of the field collection samples.
机译:Lyngbya wollei(法罗·戈蒙的远亲)梳子。 nov。,一种在美国东南部的湖泊和水库中普遍存在的多年生形成垫的丝状蓝细菌,在小鼠生物测定法中进行测试后发现会产生强效的急性致死神经毒素。中毒迹象与麻痹性贝类中毒相似。作为田纳西河谷管理局Guntersville水库总体规划的一部分,对形成垫状丝状蓝藻L. wollei(最近从美国南部其他地区入侵)进行了研究,以确定它是否可以产生已知的氰毒素。在3年的时间里,在田纳西州河州阿拉巴马州Guntersville水库的10个地点收集的91个野外样品中,有72.5%是有毒的。毒性样品的最低100%致死剂量范围是150至1,500 mg kg冻干的沃尔氏乳杆菌细胞-1,大多数样品在500 mg kg-1时具有毒性。通过官方分析化学家协会方法对麻痹性贝类毒素进行生物分析的样品显示的毒毒素当量范围为0至58微克g(干重)-1。神经毒性化合物的特征,例如缺乏C18固相萃取柱的吸附,在C18高效液相色谱(HPLC)柱上的保留时间短,神经毒素与Saxiphilin(可溶性Saxitoxin)的相互作用-结合蛋白)和电压敏感钠通道的外部阻滞,导致我们发现这种神经毒素与沙门毒素有关,沙门毒素是造成麻痹性贝类中毒的化合物。迄今为止,通过HPLC荧光保留时间的比较鉴定出的主要毒素毒素化合物是氨基甲酰淋菌毒素2和3。没有证据表明沃尔氏乳杆菌会产生麻痹性贝类毒素C毒素。将五十个田间样品置于单藻培养物中,并在规定的培养条件下生长。这些实验室生长的沃氏乳杆菌菌株的毒性和中毒迹象与现场采集的样本相似。

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