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氟西汀通过增加氧化应激以及改变能量和脂质代谢来抑制模式硅藻的生长。

Fluoxetine Arrests Growth of the Model Diatom by Increasing Oxidative Stress and Altering Energetic and Lipid Metabolism.

作者信息

Feijão Eduardo, Cruz de Carvalho Ricardo, Duarte Irina A, Matos Ana Rita, Cabrita Maria Teresa, Novais Sara C, Lemos Marco F L, Caçador Isabel, Marques João Carlos, Reis-Santos Patrick, Fonseca Vanessa F, Duarte Bernardo

机构信息

MARE - Marine and Environmental Sciences Centre, Faculdade de Ciências da Universidade de Lisboa, Lisbon, Portugal.

cE3c - Centre for Ecology, Evolution and Environmental Changes, Faculdade de Ciências, Universidade de Lisboa, Lisbon, Portugal.

出版信息

Front Microbiol. 2020 Jul 31;11:1803. doi: 10.3389/fmicb.2020.01803. eCollection 2020.

Abstract

Pharmaceutical residues impose a new and emerging threat to aquatic environments and its biota. One of the most commonly prescribed pharmaceuticals is the antidepressant fluoxetine, a selective serotonin re-uptake inhibitor that has been frequently detected, in concentrations up to 40 μg L, in aquatic ecosystems. The present study aims to investigate the ecotoxicity of fluoxetine at environmentally relevant concentrations (0.3, 0.6, 20, 40, and 80 μg L) on cell energy and lipid metabolism, as well as oxidative stress biomarkers in the model diatom . Exposure to higher concentrations of fluoxetine negatively affected cell density and photosynthesis through a decrease in the active PSII reaction centers. Stress response mechanisms, like β-carotene (β-car) production and antioxidant enzymes [superoxide dismutase (SOD) and ascorbate peroxidase (APX)] up-regulation were triggered, likely as a positive feedback mechanism toward formation of fluoxetine-induced reactive oxygen species. Lipid peroxidation products increased greatly at the highest fluoxetine concentration whereas no variation in the relative amounts of long chain polyunsaturated fatty acids (LC-PUFAs) was observed. However, monogalactosyldiacylglycerol-characteristic fatty acids such as C16:2 and C16:3 increased, suggesting an interaction between light harvesting pigments, lipid environment, and photosynthesis stabilization. Using a canonical multivariate analysis, it was possible to evaluate the efficiency of the application of bio-optical and biochemical techniques as potential fluoxetine exposure biomarkers in . An overall classification efficiency to the different levels of fluoxetine exposure of 61.1 and 88.9% were obtained for bio-optical and fatty acids profiles, respectively, with different resolution degrees highlighting these parameters as potential efficient biomarkers. Additionally, the negative impact of this pharmaceutical molecule on the primary productivity is also evident alongside with an increase in respiratory oxygen consumption. From the ecological point of view, reduction in diatom biomass due to continued exposure to fluoxetine may severely impact estuarine and coastal trophic webs, by both a reduction in oxygen primary productivity and reduced availability of key fatty acids to the dependent heterotrophic upper levels.

摘要

药物残留对水生环境及其生物群构成了新的且不断出现的威胁。最常被处方的药物之一是抗抑郁药氟西汀,它是一种选择性5-羟色胺再摄取抑制剂,在水生生态系统中经常被检测到,浓度高达40微克/升。本研究旨在探究环境相关浓度(0.3、0.6、20、40和80微克/升)的氟西汀对模式硅藻细胞能量和脂质代谢以及氧化应激生物标志物的生态毒性。暴露于较高浓度的氟西汀会通过活性PSII反应中心的减少对细胞密度和光合作用产生负面影响。应激反应机制,如β-胡萝卜素(β-car)的产生和抗氧化酶[超氧化物歧化酶(SOD)和抗坏血酸过氧化物酶(APX)]的上调被触发,这可能是对氟西汀诱导的活性氧形成的一种正反馈机制。在最高氟西汀浓度下脂质过氧化产物大幅增加,而长链多不饱和脂肪酸(LC-PUFAs)的相对含量未观察到变化。然而,单半乳糖基二酰基甘油特征脂肪酸如C16:2和C16:3增加,表明光捕获色素、脂质环境和光合作用稳定之间存在相互作用。使用典型多变量分析,可以评估生物光学和生化技术作为潜在氟西汀暴露生物标志物在[此处原文缺失具体内容]中的应用效率。生物光学和脂肪酸谱对不同水平氟西汀暴露的总体分类效率分别为61.1%和88.9%,不同的分辨率程度突出了这些参数作为潜在有效生物标志物的特性。此外,这种药物分子对初级生产力的负面影响以及呼吸氧消耗的增加也很明显。从生态学角度来看,由于持续暴露于氟西汀导致硅藻生物量减少,可能会通过降低氧气初级生产力以及减少关键脂肪酸对依赖的异养上层的可用性,严重影响河口和沿海营养网。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/05bf/7411086/642a8c662c50/fmicb-11-01803-g001.jpg

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