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密克罗尼西亚苏铁(苏铁目)植物体内缺乏内生蓝细菌时会增加β-甲基氨基-L-丙氨酸。

Cycas micronesica (Cycadales) plants devoid of endophytic cyanobacteria increase in beta-methylamino-L-alanine.

机构信息

Western Pacific Tropical Research Center, University of Guam, Mangilao, Guam 96923, USA.

出版信息

Toxicon. 2010 Sep 15;56(4):563-8. doi: 10.1016/j.toxicon.2010.05.015. Epub 2010 Jun 2.

DOI:10.1016/j.toxicon.2010.05.015
PMID:20570592
Abstract

Cycads are among the most ancient of extant Spermatophytes, and are known for their pharmacologically active compounds. beta-methylamino-l-alanine (BMAA) is one metabolite that been implicated as causal of human neurodegenerative diseases in Guam. We grew Cycas micronesica seedlings without endophytic cyanobacteria symbiosis, and quantified initial and ending BMAA in various plant tissues. BMAA increased 79% during nine months of seedling growth, and root tissue contained 75% of the ultimate BMAA pool. Endophytic cyanobacteria symbionts were not the source of BMAA increase in these seedlings, which contradicts previously reported claims that biosynthesis of this toxin by cyanobacteria initiates its accumulation in the Guam environment. The preferential loading of root tissue with BMAA does not support earlier reports that this toxin serves a defensive role against herbivory of leaf or seed tissues. The long history of conflicting results in Guam's cycad toxin research continues, and recent developments underscore the sense of urgency in continued research as this endangered cycad population approaches extirpation from the island.

摘要

苏铁是现存最古老的种子植物之一,以其具有药理活性的化合物而闻名。β-甲基氨基-L-丙氨酸(BMAA)是一种代谢物,被认为是关岛人类神经退行性疾病的病因。我们在没有内生蓝藻共生的情况下种植了密克罗尼西亚苏铁幼苗,并定量了各种植物组织中初始和最终的 BMAA。在九个月的幼苗生长过程中,BMAA 增加了 79%,根组织中含有最终 BMAA 池的 75%。内生蓝藻共生体不是这些幼苗中 BMAA 增加的来源,这与先前报道的蓝藻生物合成这种毒素会引发其在关岛环境中积累的说法相矛盾。根组织中 BMAA 的优先加载并不能支持早期关于这种毒素在抵御叶片或种子组织的食草性方面具有防御作用的报告。在关岛的苏铁毒素研究中,长期以来一直存在相互矛盾的结果,最近的事态发展突显了继续研究的紧迫性,因为这个濒危的苏铁种群正在从岛上灭绝。

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