Mercury Uptake by Desulfovibrio desulfuricans ND132: Passive or Active?

Mercury Uptake by Desulfovibrio desulfuricans ND132: Passive or Active?
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DOI:
10.1021/acs.est.9b00047
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发表时间:
2019-06-04
影响因子:
11.4
通讯作者:
Gu, Baohua
Gu, Baohua
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
An, Jing;Zhang, Lijie;Gu, Baohua

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最近的研究已经确定HgcAB蛋白是负责汞[汞(II)]甲基化某些厌氧微生物。然而,微生物是被动还是主动吸收Hg(II)仍存在争议。在这里,我们研究的动态并发Hg(II)的吸附,吸收,和甲基化的可行的和灭活的细胞(热杀死或饥饿)或原生质球的硫酸盐还原菌脱硫脱硫弧菌ND 132在实验室培养。我们表明,在没有添加硫醇,>60%的添加汞(II)(25 nM)被采取被动在48小时内由活的和灭活的细胞,也与质子梯度解偶联剂,羰基氰-3-氯苯腙(CCCP)处理的细胞。灭活消除汞(II)甲基化,但细胞继续采取汞(II),可能通过竞争性结合或配体交换汞(II)的细胞内蛋白质或含巯基的细胞成分。同样,治疗CCCP损害的能力,原生质球甲基化汞(II),但没有停止汞(II)的吸收。球体表现出更大的能力,吸附汞(II)比整个细胞,和细胞质膜结合汞(II)的水平相关以及与甲基汞生产,汞(II)甲基化与细胞质HgcAB。我们的研究结果表明,活跃的代谢是不需要细胞汞(II)的吸收,从而提供了一个更好的理解汞(II)的生物利用度甲基化。
Recent studies have identified HgcAB proteins as being responsible for mercury [Hg(II)] methylation by certain anaerobic microorganisms. However, it remains controversial whether microbes take up Hg(II) passively or actively. Here, we examine the dynamics of concurrent Hg(II) adsorption, uptake, and methylation by both viable and inactivated cells (heat-killed or starved) or spheroplasts of the sulfate-reducing bacterium Desulfovibrio desulfuricans ND132 in laboratory incubations. We show that, without addition of thiols, >60% of the added Hg(II) (25 nM) was taken up passively in 48 h by live and inactivated cells and also by cells treated with the proton gradient uncoupler, carbonylcyanide-3-chlorophenylhydrazone (CCCP). Inactivation abolished Hg(II) methylation, but the cells continued taking up Hg(II), likely through competitive binding or ligand exchange of Hg(II) by intracellular proteins or thiol-containing cellular components. Similarly, treatment with CCCP impaired the ability of spheroplasts to methylate Hg(II) but did not stop Hg(II) uptake. Spheroplasts showed a greater capacity to adsorb Hg(II) than whole cells, and the level of cytoplasmic membrane-bound Hg(II) correlated well with MeHg production, as Hg(II) methylation is associated with cytoplasmic HgcAB. Our results indicate that active metabolism is not required for cellular Hg(II) uptake, thereby providing an improved understanding of Hg(II) bioavailability for methylation.