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Active transport, substrate specificity, and methylation of Hg(ll) in anaerobic bacteria

机译:厌氧细菌中Hg(II)的主动转运,底物特异性和甲基化

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The formation of methylmercury (MeHg), which is biomagnified in aquatic food chains and poses a risk to human health, is effected by some iron- and sulfate-reducing bacteria (FeRB and SRB) in anaerobic environments. However, very little is known regarding the mechanism of uptake of inorganic Hg by these organisms, in part because of the inherent difficulty in measuring the intracellular Hg concentration. By using the FeRB Geobacter sulfurreducens and the SRB Desulfovibrio desulfuricans ND132 as model organisms, we demonstrate that Hg(ll) uptake occurs by active transport. We also establish that Hg(ll) uptake by 6. sulfurreducens is highly dependent on the characteristics of the thiols that bind Hg(ll) in the external medium, with some thiols promoting uptake and methylation and others inhibiting both. The Hg(ll) uptake system of D. desulfuricans has a higher affinity than that of 6. sulfurreducens and promotes Hg methylation in the presence of stronger complexing thiols. We observed a tight coupling between Hg methylation and MeHg export from the cell, suggesting that these two processes may serve to avoid the build up and toxicity of cellular Hg. Our results bring up the question of whether cellular Hg uptake is specific for Hg(ll) or accidental, occurring via some essential metal importer. Our data also point at Hg(ll) complexation by thiols as an important factor controlling Hg methylation in anaerobic environments.
机译:甲基汞(MeHg)的形成在水生食物链中被生物放大,对人体健康构成威胁,这是由厌氧环境中的某些铁和硫酸盐还原细菌(FeRB和SRB)引起的。然而,关于这些生物体吸收无机汞的机理知之甚少,部分是由于测量细胞内汞浓度固有的困难。通过使用FeRB还原杆菌和SRB Desulfovibrio desulfuricans ND132作为模型生物,我们证明了Hg(II)的吸收是通过主动运输发生的。我们还确定了6.硫还原剂对Hg(II)的吸收高度依赖于与外部介质中Hg(II)结合的硫醇的特征,其中一些硫醇促进摄取和甲基化,而另一些硫醇则抑制两者。 D. desulfuricans的Hg(II)吸收系统比6.硫还原剂具有更高的亲和力,并在更强的络合硫醇存在下促进Hg甲基化。我们观察到汞甲基化与MeHg从细胞输出之间的紧密耦合,表明这两个过程可能有助于避免细胞汞的积累和毒性。我们的结果提出了一个问题,即是否通过某些必需的金属进口商发生的细胞摄取汞是针对汞(II)还是偶然的问题。我们的数据还指出,巯基的Hg(II)络合是控制厌氧环境中Hg甲基化的重要因素。

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