Pantoja Munoz L, Purchase D, Jones H, Raab A, Urgast D, Feldmann J, Garelick H
Department of Natural Sciences, School of Science and Technology, Middlesex University, The Burroughs, London NW4 4BT, United Kingdom.
College of Physical Sciences - Chemistry, Trace Element Speciation Laboratory (TESLA), University of Aberdeen, Meston Walk, Aberdeen AB24 3UE, United Kingdom.
Aquat Toxicol. 2016 Jun;175:56-72. doi: 10.1016/j.aquatox.2016.02.020. Epub 2016 Mar 3.
The response of Chlorella vulgaris when challenged by As(III), As(V) and dimethylarsinic acid (DMA) was assessed through experiments on adsorption, efflux and speciation of arsenic (reduction, oxidation, methylation and chelation with glutathione/phytochelatin [GSH/PC]). Our study indicates that at high concentrations of phosphate (1.62mM of HPO4(2-)), upon exposure to As(V), cells are able to shift towards methylation of As(V) rather than PC formation. Treatment with As(V) caused a moderate decrease in intracellular pH and a strong increase in the concentration of free thiols (GSH). Passive surface adsorption was found to be negligible for living cells exposed to DMA and As(V). However, adsorption of As(III) was observed to be an active process in C. vulgaris, because it did not show saturation at any of the exposure periods. Chelation of As(III) with GS/PC and to a lesser extent hGS/hPC is a major detoxification mechanism employed by C. vulgaris cells when exposed to As(III). The increase of bound As-GS/PC complexes was found to be strongly related to an increase in concentration of As(III) in media. C. vulgaris cells did not produce any As-GS/PC complex when exposed to As(V). This may indicate that a reduction step is needed for As(V) complexation with GSH/PC. C. vulgaris cells formed DMAS(V)-GS upon exposure to DMA independent of the exposure period. As(III) triggers the formation of arsenic complexes with PC and homophytochelatins (hPC) and their compartmentalisation to vacuoles. A conceptual model was devised to explain the mechanisms involving ABCC1/2 transport. The potential of C. vulgaris to bio-remediate arsenic from water appeared to be highly selective and effective without the potential hazard of reducing As(V) to As(III), which is more toxic to humans.
通过对砷的吸附、外排和形态变化(还原、氧化、甲基化以及与谷胱甘肽/植物螯合肽[GSH/PC]的螯合作用)进行实验,评估了普通小球藻在受到三价砷(As(III))、五价砷(As(V))和二甲基砷酸(DMA)挑战时的反应。我们的研究表明,在高浓度磷酸盐(1.62mM的HPO4(2-))存在的情况下,当暴露于As(V)时,细胞能够转向As(V)的甲基化而非PC的形成。用As(V)处理导致细胞内pH适度下降,游离巯基(GSH)浓度大幅增加。对于暴露于DMA和As(V)的活细胞,被动表面吸附可忽略不计。然而,观察到As(III)的吸附在普通小球藻中是一个活跃过程,因为在任何暴露时间段它都未显示出饱和现象。As(III)与GS/PC以及程度较轻的hGS/hPC的螯合是普通小球藻细胞在暴露于As(III)时采用的主要解毒机制。发现结合的As-GS/PC复合物的增加与培养基中As(III)浓度的增加密切相关。普通小球藻细胞在暴露于As(V)时不产生任何As-GS/PC复合物。这可能表明As(V)与GSH/PC的络合需要一个还原步骤。普通小球藻细胞在暴露于DMA时,无论暴露时间段如何,都会形成DMAS(V)-GS。As(III)触发了与PC和同型植物螯合肽(hPC)的砷复合物的形成及其向液泡的区室化。设计了一个概念模型来解释涉及ABCC1/2转运的机制。普通小球藻从水中生物修复砷的潜力似乎具有高度选择性和有效性,且不存在将毒性对人类更大的As(V)还原为As(III)的潜在危害。