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关于蓝藻次生代谢物的溞类和微囊藻的生理相互作用。

Physiological interaction of Daphnia and Microcystis with regard to cyanobacterial secondary metabolites.

机构信息

University of Cologne, Cologne Biocenter, Zülpicher Straße 47b, 50674 Cologne, Germany.

University of Cologne, Cologne Biocenter, Zülpicher Straße 47b, 50674 Cologne, Germany.

出版信息

Aquat Toxicol. 2014 Nov;156:96-105. doi: 10.1016/j.aquatox.2014.08.003. Epub 2014 Aug 17.

Abstract

Cyanobacterial blooms in freshwater ecosystems are a matter of high concern with respect to human health and ecosystem services. Investigations on the role of cyanobacterial secondary metabolites have largely been confined to microcystins, although cyanobacteria produce a huge variety of toxic or inhibitory secondary metabolites. Mass occurrences of toxic cyanobacteria strongly impact freshwater zooplankton communities; especially the unselective filter feeder Daphnia. Daphnids have been shown to successfully suppress bloom formation. However, the opposite situation, i.e. the suppression of Daphnia populations by cyanobacteria can be observed as well. To understand these contradictory findings the elucidation of the underlying physiological mechanisms that help daphnids to cope with cyanotoxins is crucial. We fed Daphnia magna with the cyanobacterium Microcystis aeruginosa PCC7806 for 24h and used high-resolution LCMS analytics to analyze the Microcystis cells, the Daphnia tissue and the surrounding medium in order to investigate the fate of seven investigated cyanobacterial compounds (cyanopeptolins A-C, microcyclamide 7806A and aerucyclamides B-D). For none of these bioactive compounds evidence for biotransformation or biodegradation by Daphnia were found. Instead feeding and subsequent release experiments point at the importance of transport mechanisms in Daphnia with regard to the cyanopeptolins A and C and microcyclamide 7806A. In addition we found hints for new inducible defense mechanism in Microcystis against predation by Daphnia. These putative defense mechanisms include the elevated production of toxic compounds other than microcystins, as could be demonstrated here for aerucyclamide B and D, cyanopoeptolin B and microcyclamide 7806A. Moreover, our data demonstrate the elevated active export of at least one cyanobacterial compound (microcyclamide 7806A) into the surrounding medium as a response to grazer presence, which might constitute an entirely new not yet described cyanobacterial defense mechanism.

摘要

淡水生态系统中的蓝藻水华是一个与人类健康和生态系统服务密切相关的问题。尽管蓝藻产生了大量的有毒或抑制性的次生代谢产物,但对蓝藻次生代谢产物的作用的研究主要局限于微囊藻毒素。有毒蓝藻的大量出现强烈影响淡水浮游动物群落;特别是非选择性滤食者水蚤。已经证明水蚤能够成功抑制水华的形成。然而,也可以观察到相反的情况,即蓝藻对水蚤种群的抑制。为了理解这些矛盾的发现,阐明有助于水蚤应对蓝藻毒素的潜在生理机制是至关重要的。我们用蓝藻铜绿微囊藻 PCC7806 喂养大型溞 24 小时,并使用高分辨率 LCMS 分析技术来分析微囊藻细胞、水蚤组织和周围介质,以研究 7 种被调查的蓝藻化合物(蓝藻肽 A-C、微环酰胺 7806A 和苍环酰胺 B-D)的命运。对于这些生物活性化合物,都没有发现被水蚤生物转化或生物降解的证据。相反,喂养和随后的释放实验表明,在蓝藻肽 A 和 C 以及微环酰胺 7806A 方面,运输机制在水蚤中非常重要。此外,我们还发现了微囊藻中针对水蚤捕食的新的诱导防御机制的迹象。这些推测的防御机制包括产生除微囊藻毒素以外的有毒化合物,如这里可以证明的苍环酰胺 B 和 D、蓝藻肽 B 和微环酰胺 7806A。此外,我们的数据表明,至少有一种蓝藻化合物(微环酰胺 7806A)作为对食草动物存在的反应,被主动分泌到周围介质中,这可能构成一种全新的、尚未描述的蓝藻防御机制。

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