The School of Biotechnology and Biomolecular Sciences, The University of New South Wales, Sydney, NSW 2052, Australia.
Int J Environ Res Public Health. 2011 Sep;8(9):3728-46. doi: 10.3390/ijerph8093728. Epub 2011 Sep 16.
The association of α-amino-β-methylaminopropionic acid (BMAA) with elevated incidence of amyotrophic lateral sclerosis/Parkinson's disease complex (ALS/PDC) was first identified on the island of Guam. BMAA has been shown to be produced across the cyanobacterial order and its detection has been reported in a variety of aquatic and terrestrial environments worldwide, suggesting that it is ubiquitous. Various in vivo studies on rats, mice, chicks and monkeys have shown that it can cause neurodegenerative symptoms such as ataxia and convulsions. Zebrafish research has also shown disruption to neural development after BMAA exposure. In vitro studies on mice, rats and leeches have shown that BMAA acts predominantly on motor neurons. Observed increases in the generation of reactive oxygen species (ROS) and Ca(2+) influx, coupled with disruption to mitochondrial activity and general neuronal death, indicate that the main mode of activity is via excitotoxic mechanisms. The current review pertaining to the neurotoxicity of BMAA clearly demonstrates its ability to adversely affect neural tissues, and implicates it as a potentially significant compound in the aetiology of neurodegenerative disease. When considering the potential adverse health effects upon exposure to this compound, further research to better understand the modes of toxicity of BMAA and the environmental exposure limits is essential.
α-氨基-β-亚甲基丙氨酸（BMAA）与肌萎缩侧索硬化症/帕金森病复合征（ALS/PDC）发病率升高的关联最初在关岛被发现。已经证明，蓝细菌目中的各种细菌都能产生 BMAA，并且已经在全球范围内的各种水生和陆地环境中检测到它的存在，这表明它无处不在。对大鼠、小鼠、小鸡和猴子的各种体内研究表明，它会导致共济失调和抽搐等神经退行性症状。斑马鱼研究还表明，BMAA 暴露后会破坏神经发育。对小鼠、大鼠和水蛭的体外研究表明，BMAA 主要作用于运动神经元。观察到活性氧（ROS）生成增加和 Ca(2+)内流，加上线粒体活性和一般神经元死亡的破坏，表明其主要作用模式是通过兴奋毒性机制。关于 BMAA 的神经毒性的这篇综述清楚地表明，它有能力对神经组织产生不利影响，并暗示它可能是神经退行性疾病病因学中的一个重要化合物。当考虑到接触这种化合物可能产生的潜在健康影响时，需要进一步研究以更好地了解 BMAA 的毒性模式和环境暴露限值。
