Homeostatic response of calcium and potassium ions in Microcystis spp. and Chlorella to MC-LR

IF 6.1 2区 环境科学与生态学 Q1 ENVIRONMENTAL SCIENCES
Chen Cheng , Alan D. Steinman , Qingju Xue , Yilin Shu , Shuyu He , Yongjiu Cai , Yanjie Cai , Liqiang Xie
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Abstract

Cyanobacteria and green microalgae often co-exist during toxic algal blooms, but the influence of microcystins (MCs) on ionic homeostasis of these algae is not well-studied. This study used non-invasive micro-test technology to examine effects of MC-LR (0, 1, 10 and 100 μg/L) on calcium (Ca2+) and potassium ion (K+) fluxes, physiological parameters related to ATP synthesis and oxidative stress, and growth, in toxic Microcystis aeruginosa, non-toxic Microcystis wesenbergii, and Chlorella vulgaris during a 44-day mono-culture experiment. Gd3+ treatments also were set to analyze the relationships between ion homeostasis and growth based on pharmacology experiment results. The growth of tested strains also was explored in a 28-day co-culture experiment. Results revealed that MC-LR caused the greatest percent decrease in cell density in C. vulgaris, with decreases ranging from −14.1 % to −31.9 % at 100 μg/L compared to the control group in the short term. In addition, there was a greater percent decrease in cell density (-2.9 % to −9.6 %) and a 10.8–24.3 % lower percent increase in cell density (depending on MC-LR concentration) in the subsequent incubation phase in M. aeruginosa than in M. wesenbergii in mono-culture experiments. In co-culture experiments, MC-LR significantly decreased the temporal stability of C. vulgaris, which resulted in variable population dynamics, and also caused a greater percent decrease in cell density in M. aeruginosa than in M. wesenbergii on some sampling dates. We propose that the inhibition of C. vulgaris stemmed from the extreme oxidative stress induced by MC-LR, whereas we attribute the inhibition of M. aeruginosa to a decrease in ATP content, originating from MC-LR-induced oxidative stress and decreases in ferredoxin (FDX) content and α-amylase activity. Acute and 8 days MC-LR exposure of between 1 and 100 μg/L caused a decrease in K+ flux in the two Microcystis spp. and Ca2+ flux in C. vulgaris, with a stronger decrease in K+ flux for M. aeruginosa than for M. wesenbergii. Pharmacology experiment results reflected the possible regulatory role of Ca2+ or K+ in MC-affected physiological indicators. These results revealed that the microbial taxa used in this study respond differently to MC-LR; the stronger self-poisoning observed in toxic Microcystis compared to the non-toxic strain confers a competitive advantage to the latter over other co-existing algae, thereby enhancing our understanding of the ecotoxicity and ecological function of MC-LR.
微囊藻和小球藻钙、钾离子对MC-LR的稳态响应。
在有毒藻华期间,蓝藻与绿色微藻经常共存,但微囊藻毒素对这些藻类离子稳态的影响尚未得到很好的研究。在44天的单培养实验中,采用无创微检测技术研究了MC-LR(0、1、10和100 μg/L)对有毒铜绿微囊藻、无毒wesenbergii微囊藻和寻常小球藻钙(Ca2+)和钾离子(K+)通量、ATP合成和氧化应激相关生理参数以及生长的影响。同时设置Gd3+处理,根据药理学实验结果分析离子稳态与生长的关系。在28天的共培养实验中,对所测菌株的生长情况进行了探讨。结果表明,在100 μg/L浓度下,MC-LR对黄颡鱼细胞密度的影响最大,与对照组相比,短期内细胞密度下降幅度为-14.1 % ~ -31.9 %。此外,在单培养实验中,铜绿假单胞菌的细胞密度下降幅度更大(-2.9 %至-9.6 %),细胞密度增加幅度(取决于MC-LR浓度)比韦森伯格假单胞菌低10.8-24.3 %。在共培养实验中,MC-LR显著降低了C. vulgaris的时间稳定性,导致种群动态变化,并且在某些采样数据上导致M. aeruginosa细胞密度比M. wesenbergii下降的百分比更大。我们认为,对C. vulgaris的抑制源于MC-LR诱导的极端氧化应激,而对M. aeruginosa的抑制则源于MC-LR诱导的氧化应激引起的ATP含量的降低,以及铁氧化还蛋白(FDX)含量和α-淀粉酶活性的降低。1 ~ 100 μg/L的MC-LR急性暴露和8 d暴露均导致两种微囊藻的K+通量和C. vulgaris的Ca2+通量下降,其中铜绿假单胞菌的K+通量下降幅度大于wesenbergii。药理学实验结果反映Ca2+或K+对mc影响生理指标的可能调控作用。这些结果表明,本研究中使用的微生物类群对MC-LR的响应不同;与无毒菌株相比,有毒微囊藻的自毒作用更强,这使得后者比其他共存的藻类具有竞争优势,从而增强了我们对MC-LR的生态毒性和生态功能的理解。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
12.10
自引率
5.90%
发文量
1234
审稿时长
88 days
期刊介绍: Ecotoxicology and Environmental Safety is a multi-disciplinary journal that focuses on understanding the exposure and effects of environmental contamination on organisms including human health. The scope of the journal covers three main themes. The topics within these themes, indicated below, include (but are not limited to) the following: Ecotoxicology、Environmental Chemistry、Environmental Safety etc.
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