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NRF2和硫氧还蛋白还原酶1作为锌与硒相互作用的调节因子

NRF2 and Thioredoxin Reductase 1 as Modulators of Interactions between Zinc and Selenium.

作者信息

Löser Alina, Schwarz Maria, Kipp Anna Patricia

机构信息

Department of Nutritional Physiology, Institute of Nutritional Sciences, Friedrich Schiller University Jena, 07743 Jena, Germany.

TraceAge-DFG Research Unit on Interactions of Essential Trace Elements in Healthy and Diseased Elderly, Potsdam-Berlin-Jena-Wuppertal, 14558 Nuthetal, Germany.

出版信息

Antioxidants (Basel). 2024 Oct 8;13(10):1211. doi: 10.3390/antiox13101211.

DOI:10.3390/antiox13101211
PMID:39456464
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11505002/
Abstract

BACKGROUND

Selenium and zinc are essential trace elements known to regulate cellular processes including redox homeostasis. During inflammation, circulating selenium and zinc concentrations are reduced in parallel, but underlying mechanisms are unknown. Accordingly, we modulated the zinc and selenium supply of HepG2 cells to study their relationship.

METHODS

HepG2 cells were supplied with selenite in combination with a short- or long-term zinc treatment to investigate intracellular concentrations of selenium and zinc together with biomarkers describing their status. In addition, the activation of the redox-sensitive transcription factor NRF2 was analyzed.

RESULTS

Zinc not only increased the nuclear translocation of NRF2 after 2 to 6 h but also enhanced the intracellular selenium content after 72 h, when the cells were exposed to both trace elements. In parallel, the activity and expression of the selenoprotein thioredoxin reductase 1 (TXNRD1) increased, while the gene expression of other selenoproteins remained unaffected or was even downregulated. The zinc effects on the selenium concentration and TXNRD activity were reduced in cells with stable NRF2 knockdown in comparison to control cells.

CONCLUSIONS

This indicates a functional role of NRF2 in mediating the zinc/selenium crosstalk and provides an explanation for the observed unidirectional behavior of selenium and zinc.

摘要

背景

硒和锌是已知可调节包括氧化还原稳态在内的细胞过程的必需微量元素。在炎症期间，循环中的硒和锌浓度会同时降低，但其潜在机制尚不清楚。因此，我们调节了HepG2细胞的锌和硒供应，以研究它们之间的关系。

方法

用亚硒酸盐联合短期或长期锌处理HepG2细胞，以研究细胞内硒和锌的浓度以及描述其状态的生物标志物。此外，还分析了氧化还原敏感转录因子NRF2的激活情况。

结果

当细胞同时暴露于这两种微量元素时，锌不仅在2至6小时后增加了NRF2的核转位，而且在72小时后提高了细胞内硒含量。同时，硒蛋白硫氧还蛋白还原酶1（TXNRD1）的活性和表达增加，而其他硒蛋白的基因表达未受影响或甚至下调。与对照细胞相比，在稳定敲低NRF2的细胞中，锌对硒浓度和TXNRD活性的影响降低。

结论

这表明NRF2在介导锌/硒相互作用中发挥功能作用，并为观察到的硒和锌的单向行为提供了解释。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/bde593b8b0c8/antioxidants-13-01211-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/19f848fa4cda/antioxidants-13-01211-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/0ba00f4742ae/antioxidants-13-01211-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/11fe1279cad6/antioxidants-13-01211-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/ef60f5a43e2d/antioxidants-13-01211-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/bde593b8b0c8/antioxidants-13-01211-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/19f848fa4cda/antioxidants-13-01211-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/0ba00f4742ae/antioxidants-13-01211-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/11fe1279cad6/antioxidants-13-01211-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/ef60f5a43e2d/antioxidants-13-01211-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/74cf/11505002/bde593b8b0c8/antioxidants-13-01211-g005.jpg

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3
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4
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