Production of the neurotoxin BMAA by a marine cyanobacterium.
Production of the neurotoxin BMAA by a marine cyanobacterium.
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DOI：
10.3390/md504180
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发表时间：
2007-12-06
期刊：
影响因子：
5.4
通讯作者：
Cox PA
中科院分区：
文献类型：
--
作者：
Banack SA;Johnson HE;Cheng R;Cox PA
最近发现多种蓝藻产生神经毒性非蛋白质氨基酸β-甲氨基-L-丙氨酸（BMAA）。在关岛，研究表明，BMAA可能是查莫罗土著人饮食中的一种环境毒素，已知这些人患有高度肌萎缩性侧索硬化症/帕金森氏痴呆综合症。BMAA已被发现在北美进行性神经退行性疾病患者的脑组织中积累。在关岛，发现BMAA是由生活在特殊苏铁根中的念珠藻属内共生蓝细菌产生的。我们在这里报告检测BMAA在实验室培养的自由生活的海洋物种念珠藻。我们成功地检测到BMAA在这一海洋物种的念珠藻与五种不同的方法：HPLC-FD，UPLC-UV，氨基酸分析仪，LC/MS，和三重四极杆LC/MS/MS。这五种不同的分析方法的共识明确地证明了BMAA在这种海洋蓝藻的存在。由于与蛋白质相关的BMAA可以在食物链中积累越来越多的水平，因此BMAA的生物放大可能发生在海洋生态系统中，类似于BMAA在陆地生态系统中的生物放大。海洋蓝细菌产生BMAA可能是人类暴露于BMAA的另一种途径。由于低浓度的BMAA会导致运动神经元死亡，因此低水平的BMAA暴露可能会引发遗传易感个体的运动神经元疾病。
Diverse species of cyanobacteria have recently been discovered to produce the neurotoxic non-protein amino acid β-methylamino-L-alanine (BMAA). In Guam, BMAA has been studied as a possible environmental toxin in the diets of indigenous Chamorro people known to have high levels of Amyotrophic Lateral Sclerosis/ Parkinsonism Dementia Complex (ALS/PDC). BMAA has been found to accumulate in brain tissues of patients with progressive neurodegenerative illness in North America. In Guam, BMAA was found to be produced by endosymbiotic cyanobacteria of the genus Nostoc which live in specialized cycad roots. We here report detection of BMAA in laboratory cultures of a free-living marine species of Nostoc. We successfully detected BMAA in this marine species of Nostoc with five different methods: HPLC-FD, UPLC-UV, Amino Acid Analyzer, LC/MS, and Triple Quadrupole LC/MS/MS. This consensus of five different analytical methods unequivocally demonstrates the presence of BMAA in this marine cyanobacterium. Since protein-associated BMAA can accumulate in increasing levels within food chains, it is possible that biomagnification of BMAA could occur in marine ecosystems similar to the biomagnification of BMAA in terrestrial ecosystems. Production of BMAA by marine cyanobacteria may represent another route of human exposure to BMAA. Since BMAA at low concentrations causes the death of motor neurons, low levels of BMAA exposure may trigger motor neuron disease in genetically vulnerable individuals.