Responses of enzymatic antioxidants and non-enzymatic antioxidants in the cyanobacterium Microcystis aeruginosa to the allelochemical ethyl 2-methyl acetoacetate (EMA) isolated from reed (Phragmites communis)
Responses of enzymatic antioxidants and non-enzymatic antioxidants in the cyanobacterium Microcystis aeruginosa to the allelochemical ethyl 2-methyl acetoacetate (EMA) isolated from reed (Phragmites communis)
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DOI：
10.1016/j.jplph.2007.10.007
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发表时间：
2008-01-01
影响因子：
4.3
通讯作者：
Li, Feng-Min
中科院分区：
文献类型：
--
作者：
Hong, Yu;Hu, Hong-Ying;Li, Feng-Min
大型植物化感物质被认为是控制藻类的一种环境友好型和有前途的替代品。布鲁姆。然而，研究化感物质对藻类的潜在抑制机制的研究很少。从芦苇中分离得到的化感物质2-甲基乙酰乙酸乙酯(EMA)对铜绿微囊藻的生长有很强的化感抑制作用。为了了解EMA抑制藻类生长的机制，研究了EMA对铜绿微囊藻的抗氧化反应。成长。分析了不同浓度的EMA对铜绿假单胞菌细胞内酶类抗氧化剂超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性以及非酶类抗氧化剂还原型谷胱甘肽(GSH)和抗坏血酸(AsA)含量的影响。铜绿假单胞菌暴露于EMA后，酶活性和非酶类抗氧化剂含量发生了不同程度的变化。EMA作用4h后，SOD活性开始下降，40h后下降更为明显，CAT活性在EMA作用4h后无明显变化，40h后明显升高。EMA处理4h后，AsA和GSH含量显著增加，60h后，两种浓度的EMA仍能提高CAT活性和AsA、GSH含量，但高浓度的EMA对CAT活性和AsA、GSH含量有明显的抑制作用。在所有暴露时间内，EMA均使脱氢抗坏血酸(DHAsA)和氧化谷胱甘肽(GSSG)含量增加。60h后，高浓度的EMA降低了AsA和GSH的再生率(分别用AsA/DHAsA和GSH/GSSG表示)。这些结果表明，CAT的激活以及AsA和GSH在早期暴露对对抗EMA诱导的氧化应激具有重要作用，而SOD的失活可能是EMA抑制铜绿假单胞菌生长的关键。(C)2007年爱思唯尔股份有限公司。版权所有。
Macrophytic allelochemicals are considered an environment-friendly and promising alternative to control algal. bloom. However, studies examining the potential mechanisms of inhibitory allelochemicals on algae are few. The allelochemical ethyl 2-methyl acetoacetate (EMA), isolated from reed (Phragmites communis), was a strong allelopathic inhibitor on the growth of Microcystis aeruginosa. EMA-induced antioxidant responses were investigated in the cyanobacterium M. aeruginosa to understand the mechanism of EMA inhibition on algal. growth. The activities of enzymatic antioxidants superoxide dismutase (SOD) and catalase (CAT), and the contents of non-enzymatic antioxidants reduced glutathione (GSH) and ascorbic acid (AsA) of M. aeruginosa cells were analyzed after treatments with different concentrations of EMA. Exposure of M. aeruginosa to EMA caused changes in enzyme activities and contents of non-enzymatic antioxidants in different manners. The decrease in SOD activity occurred first after 4 h of EMA exposure, and more markedly after 40 h. CAT activity did not change after 4 h of EMA exposure, but increased obviously after 40h. The contents of AsA and GSH were increased greatly by EMA after 4 h. After 60 h, tow EMA concentrations still increased the CAT activity and the contents of AsA and GSH, but high EMA concentrations started to impose a marked suppression on them. EMA increased dehydroascorbate (DHAsA) and oxidized glutathione (GSSG) contents during all exposure times. After 60 h, the regeneration rates of AsA and GSH (represented by the AsA/DHAsA ratio and GSH/GSSG ratio, respectively) were reduced by high EMA concentrations. These results suggest that the activation of CAT and the availability of AsA and GSH at early exposure are important to counteract the oxidative stress induced by EMA, and the inactivation of SOD may be crucial to the growth inhibition of M. aeruginosa by EMA. (c) 2007 Elsevier GmbH. All rights reserved.