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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam
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A mechanism for slow release of biomagnified cyanobacterial neurotoxins and neurodegenerative disease in Guam

机译：关岛生物放大的蓝细菌神经毒素和神经退行性疾病的缓慢释放机制

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摘要

As root symbionts of cycad trees, cyanobacteria of the genus Nostoc produce beta-methylamino-L-alanine (BMAA), a neurotoxic nonprotein amino acid. The bionnagnification of BMAA through the Guam ecosystem fits a classic triangle of increasing concentrations of toxic compounds up the food chain. However, because BMAA is polar and nonlipophilic, a mechanism for its bionnagnification through increasing trophic levels has been unclear. We report that BMAA occurs not only as a free amino acid in the Guam ecosystem but also can be released from a bound form by acid hydrolysis, After first removing free amino acids from tissue samples of various trophic levels (cyanobacteria, root symbioses, cycad seeds, cycad flour, flying foxes eaten by the Chamorro people, and brain tissues of Chamorros who died from amyotrophic lateral sclerosis/ Parkinsonism dementia complex), we then hydrolyzed the remaining fraction and found BMAA concentrations increased 10- to 240-fold. This bound form of BMAA may function as an endogenous neurotoxic reservoir, accumulating and being transported between trophic levels and subsequently being released during digestion and protein metabolism. Within brain tissues, the endogenous neurotoxic reservoir can slowly release free BMAA, thereby causing incipient and recurrent neurological damage over years or even decades, which may explain the observed long latency period for neurological disease onset among the Chamorro people. The presence of BMAA in brain tissues from Canadian patients who died of Alzheimer's disease suggests that exposure to cyanobacterial neurotoxins occurs outside of Guam.
机译：作为苏铁树的根共生体，Nostoc属的蓝细菌产生β-甲基氨基-L-丙氨酸（BMAA），一种神经毒性的非蛋白质氨基酸。通过关岛生态系统对BMAA的生物放大倍数符合食物链中有毒化合物浓度不断增加的经典三角形。但是，由于BMAA是极性且非亲脂性的，因此通过增加营养水平使其生物学特性的机制尚不清楚。我们报道BMAA不仅在关岛生态系统中以游离氨基酸的形式出现，而且还可以通过酸水解从结合形式中释放出来。首先从各种营养水平（蓝细菌，根共生体，苏铁种子）的组织样品中去除游离氨基酸后， ，苏铁粉，查莫罗人吃掉的果蝠，以及因肌萎缩性侧索硬化/帕金森病痴呆症而死亡的查莫罗斯的脑组织），然后我们将其余部分水解，发现BMAA浓度增加了10到240倍。这种结合形式的BMAA可以充当内源性神经毒性储库，在营养级之间积累和运输，然后在消化和蛋白质代谢过程中释放。在脑组织内，内源性神经毒性储库可以缓慢释放游离的BMAA，从而在数年甚至数十年内引起初期和反复的神经系统损害，这可能解释了在查莫罗人中出现的神经系统疾病发作的潜伏期长。在死于阿尔茨海默氏病的加拿大患者的脑组织中存在BMAA，这表明暴露于蓝细菌神经毒素的发生在关岛以外。

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