Exposure of the cyanobacterium Nostoc muscorum from Portuguese rice fields to Molinate (Ordram®): Effects on the antioxidant system and fatty acid profile

Exposure of the cyanobacterium Nostoc muscorum from Portuguese rice fields to Molinate (Ordram®): Effects on the antioxidant system and fatty acid profile
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DOI:
10.1016/j.aquatox.2010.11.011
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发表时间:
2011-01-25
期刊:
影响因子:
4.5
通讯作者:
Peixoto, Francisco
Peixoto, Francisco
中科院分区:
环境科学与生态学2区
文献类型:
--
作者:
Galhano, Victor;Gomes-Laranjo, Jose;Peixoto, Francisco

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除草剂对水生生态系统的污染是一个严重的全球性环境问题。几种除草剂增强细胞内活性氧的形成,并可导致大分子的损伤,并降低包括蓝藻在内的多种非目标微生物的氧化防御能力。研究了molinate(一种硫代氨基甲酸酯除草剂,用于控制稻田杂草)对葡萄牙稻田中广泛分布的淡水蓝藻Nostoc muscorum中超氧化物歧化酶、过氧化氢酶、抗坏血酸过氧化物酶、谷胱甘肽还原酶和谷胱甘肽s -转移酶等抗氧化酶活性的影响。这些是在暴露于浓度为0.75至2 mM的molinate的情况下急性(72 h)的N. musum培养物中测定的。本研究还分析了molinate对:(1)非酶抗氧化剂含量(还原和氧化谷胱甘肽,类胡萝卜素和脯氨酸),(2)氧化细胞损伤(脂质过氧化(MDA水平)和电解质泄漏(质膜完整性)),以及(3)总脂肪酸谱的影响。结果表明,处理72 h后,各抗氧化酶活性均随molinate浓度的升高而显著降低,MDA呈时间依赖性和浓度依赖性增加,细胞膜渗漏增加,提示脂质过氧化、自由基形成和氧化损伤。与对照相比,施用0.75、1.5和2 mM molinate处理72 h后,脂质过氧化作用分别增加5.4%、19%和28%。同样,除草剂胁迫导致电解质泄漏增加(分别比对照增加5.8%、29.5%和30.2%,分别为0.75、1.5和2 mM molinate)。当molinate浓度升高(0.75、1.5和2 mM)时,脯氨酸的产量分别比对照提高45%、95%和156%,表明这种渗透保护剂参与了自由基清除机制。此外,还观察到谷胱甘肽库、类胡萝卜素和饱和脂肪酸的急剧下降。本研究结果表明:(1)molinate对白僵菌酶促和非酶促抗氧化防御系统均有显著影响;(2)molinate诱导过氧化反应;(3)molinate导致细胞膜脂肪酸不饱和水平升高。在除草剂生物转化和生物标志物响应研究以及环境监测规划中,应充分考虑这些证据。皇冠版权所有(C) 2010由Elsevier B.V.出版。
Herbicide contamination of aquatic ecosystems is a serious global environmental concern. Several herbicides enhance the intracellular formation of reactive oxygen species, and can lead to the damage of macromolecules and to a decrease of oxidant defenses in a wide range of non-target microorganisms including cyanobacteria. The effects of molinate (a thiocarbamate herbicide used for controlling grassy weeds in rice fields) on the activities of antioxidant enzymes such as superoxide dismutase, catalase, ascorbate peroxidase, glutathione reductase, and glutathione S-transferase were evaluated in Nostoc muscorum, a freshwater cyanobacterium with a significant spread in Portuguese rice fields. These were determined in N. muscorum cultures acutely (72 h) exposed to concentrations ranging from 0.75 to 2 mM of molinate. This study also analyzed the effects of molinate on: (1) the nonenzymatic antioxidant contents (reduced and oxidized glutathione, carotenoids, and proline), (2) the oxidative cell damage measured in terms of lipid peroxidation (MDA level) and electrolyte leakage (intactness of plasma membrane), and (3) the total fatty acid profile. The results showed that the activities of all antioxidant enzymes decreased dramatically with the rising concentration of molinate after 72 h. Time-dependent and concentration-dependent increase in MDA and enhanced cell membrane leakage were indicative of lipid peroxidation, formation of free radicals and oxidative damage. Compared to control, 72-h herbicide exposure increased lipid peroxidation by 5.4%, 19% and 28% with 0.75, 1.5 and 2 mM of molinate, respectively. Similarly, herbicide stress induced an increase in electrolyte leakage (5.8%, 29.5% and 30.2% above control, with 0.75, 1.5 and 2 mM of molinate, respectively). The increased production of proline at higher molinate concentrations (the values rose above control by 45%, 95% and 156% with 0.75, 1.5 and 2 mM, respectively) indicated the involvement of this osmoprotectant in a free radical scavenging mechanism. Moreover, a radical decline in both glutathione pool, carotenoids and saturated fatty acids were also observed. The results of the present study lead us to conclude that: (1) both enzymatic and nonenzymatic antioxidative defense system of N. muscorum are dramatically affected by molinate, (2) the herbicide induces peroxidation, (3) it contributes to an increase of the unsaturation level of cell membrane fatty acids. These evidences should be taken in account when using N. muscorum as an environmental indicator species in studies of herbicide biotransformation and biomarker response as well as in environmental monitoring programmes. Crown Copyright (C) 2010 Published by Elsevier B.V. All rights reserved.