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厌氧 RSH 依赖型碲酸盐还原有助于大肠杆菌耐受碲酸盐。

Anaerobic RSH-dependent tellurite reduction contributes to Escherichia coli tolerance against tellurite.

机构信息

Laboratorio Microbiología Molecular, Departamento de Biología, Facultad de Química Y Biología, Universidad de Santiago de Chile, Santiago, Chile.

Laboratorio de Genómica Microbiana, Centro de Genómica Y Bioinformática, Universidad Mayor, Santiago, Chile.

出版信息

Biol Res. 2022 Mar 21;55(1):13. doi: 10.1186/s40659-022-00383-5.

DOI:10.1186/s40659-022-00383-5
PMID:35313991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8935827/
Abstract

BACKGROUND

Tellurium is a rare metalloid that exerts high toxicity on cells, especially on bacteria, partly due to reactive oxygen species (ROS) generation. Moreover, it has also been observed that tellurite can target free cell thiols groups (RSH) (i.e. reduced glutathione (GSH)), enhancing the cellular redox imbalance. Additionally, in vitro experiments have suggested that several enzymes can reduce tellurite (IV) to its elemental form (0); where RSH present on their active sites may be responsible for the process. Nevertheless, the mechanisms implemented by bacteria for tellurite reduction and its role in resistance have not been evaluated in vivo.

RESULTS

This work shows that tellurite reduction to elemental tellurium is increased under anaerobic conditions in E. coli cells. The in vivo tellurite reduction is related to the intracellular concentration of total RSH, in the presence and absence of oxygen. This metabolization of tellurite directly contributes to the resistance of the bacteria to the oxyanion.

CONCLUSIONS

We demonstrated that in vivo tellurite reduction is related to the intracellular thiol concentration, i.e. large availability of cellular RSH groups, results in a more significant reduction of tellurite. Furthermore, we observed that, when the bacterium exhibits less resistance to the oxyanion, a decreased tellurite reduction was seen, affecting the growth fitness. Together, these results let us propose that tellurite reduction and the intracellular RSH content are related to the oxyanion bacterial resistance, this tripartite mechanism in an oxygen-independent anaerobic process.

摘要

背景

碲是一种稀有类金属,对细胞具有高毒性,部分原因是它会产生活性氧物种(ROS)。此外,还观察到亚碲酸盐可以靶向游离细胞硫醇基团(RSH)(即还原型谷胱甘肽(GSH)),从而增强细胞氧化还原失衡。此外,体外实验表明,几种酶可以将亚碲酸盐(IV)还原为其元素形式(0);其活性部位存在的 RSH 可能负责该过程。然而,细菌对亚碲酸盐还原的机制及其在耐药性中的作用尚未在体内进行评估。

结果

本工作表明,在大肠杆菌细胞中,缺氧条件下亚碲酸盐还原为元素碲的能力增强。体内亚碲酸盐还原与总 RSH 的细胞内浓度有关,无论是否存在氧气。这种亚碲酸盐的代谢直接有助于细菌对含氧阴离子的抗性。

结论

我们证明了体内亚碲酸盐还原与细胞内硫醇浓度有关,即细胞内 RSH 基团的大量存在导致亚碲酸盐的还原更为显著。此外,我们观察到,当细菌对含氧阴离子的抗性较低时,亚碲酸盐的还原减少,影响生长适应性。综上所述,这些结果使我们提出亚碲酸盐还原和细胞内 RSH 含量与细菌对含氧阴离子的抗性有关,这是一种在无氧过程中与氧气无关的三方机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/bc48402e6790/40659_2022_383_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/88977eeb7404/40659_2022_383_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/4f438aa717ba/40659_2022_383_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/51f25f6db51f/40659_2022_383_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/ddef6de6ce29/40659_2022_383_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/8440701baede/40659_2022_383_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/7fc4c72d8ca3/40659_2022_383_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/bf95ac8c579b/40659_2022_383_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/bc48402e6790/40659_2022_383_Fig8_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/88977eeb7404/40659_2022_383_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/4f438aa717ba/40659_2022_383_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/51f25f6db51f/40659_2022_383_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/ddef6de6ce29/40659_2022_383_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/8440701baede/40659_2022_383_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/7fc4c72d8ca3/40659_2022_383_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/bf95ac8c579b/40659_2022_383_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e40a/8935827/bc48402e6790/40659_2022_383_Fig8_HTML.jpg

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