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金属硫蛋白系统是铁诱导性的。

The Metallothionein System in Is Iron-Inducible.

作者信息

Gualandris Davide, Rotondo Davide, Lorusso Candida, La Terza Antonietta, Calisi Antonio, Dondero Francesco

机构信息

Department of Science and Technological Innovation, Università degli Studi del Piemonte Orientale, Viale Michel 11, 15121 Alessandria, Italy.

School of Biosciences and Veterinary Medicine, University of Camerino, 62032 Camerino, Italy.

出版信息

Toxics. 2024 Oct 8;12(10):725. doi: 10.3390/toxics12100725.

DOI:10.3390/toxics12100725
PMID:39453145
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11511230/
Abstract

Metallothioneins are multifunctional proteins implicated in various cellular processes. They have been used as biomarkers of heavy metal exposure and contamination due to their intrinsic ability to bind heavy metals and their transcriptional response to both physiological and noxious metal ions such as cadmium (Cd) and mercury (Hg). In this study, we aimed to clarify the role of iron and reactive oxygen species (ROSs) in the induction of the metallothionein system (Mtt) in the ciliate protozoan . We investigated the relative mRNA abundances of the metallothionein genes Mtt1, Mtt2/4, and Mtt5, revealing for the first time their responsiveness to iron exposure. Furthermore, by using inhibitors of superoxide dismutase (SOD) and catalase (CAT), alone or in combination with iron, we highlighted the roles of superoxide ion and endogenous hydrogen peroxide, as well as the complex interplay between the metal and ROSs. These results enhance our understanding of the metallothionein system in ciliates and suggest that ROSs may be a primary evolutionary driver for the selection of these proteins in nature.

摘要

金属硫蛋白是参与多种细胞过程的多功能蛋白质。由于它们具有结合重金属的内在能力以及对生理和有害金属离子(如镉(Cd)和汞(Hg))的转录反应,它们已被用作重金属暴露和污染的生物标志物。在本研究中,我们旨在阐明铁和活性氧(ROS)在纤毛虫原生动物中金属硫蛋白系统(Mtt)诱导中的作用。我们研究了金属硫蛋白基因Mtt1、Mtt2/4和Mtt5的相对mRNA丰度,首次揭示了它们对铁暴露的反应性。此外,通过单独或与铁联合使用超氧化物歧化酶(SOD)和过氧化氢酶(CAT)抑制剂,我们突出了超氧离子和内源性过氧化氢的作用,以及金属与ROS之间的复杂相互作用。这些结果增进了我们对纤毛虫中金属硫蛋白系统的理解,并表明ROS可能是自然界中选择这些蛋白质的主要进化驱动力。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/352580e9173c/toxics-12-00725-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/034dcc71c6e4/toxics-12-00725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/4c17db69c66b/toxics-12-00725-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/352580e9173c/toxics-12-00725-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/034dcc71c6e4/toxics-12-00725-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/4c17db69c66b/toxics-12-00725-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3eef/11511230/352580e9173c/toxics-12-00725-g003.jpg

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Microbiol Res. 2024 Mar;280:127565. doi: 10.1016/j.micres.2023.127565. Epub 2023 Dec 13.
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Insights of antiparasitic activity of sodium diethyldithiocarbamate against different strains of Trypanosoma cruzi.二乙氨基二硫代甲酸钠抗不同株克氏锥虫的驱虫活性研究。
Sci Rep. 2021 May 27;11(1):11200. doi: 10.1038/s41598-021-90719-0.
3
Iron in parasitic protists - from uptake to storage and where we can interfere.
寄生原生动物中的铁——从摄取到储存,以及我们可以在何处进行干预。
Metallomics. 2020 Sep 23;12(9):1335-1347. doi: 10.1039/d0mt00125b.
4
Stress-induced upregulation of the ubiquitin-relative Hub1 modulates pre-mRNA splicing and facilitates cadmium tolerance in Saccharomyces cerevisiae.应激诱导的泛素相关 Hub1 的上调调节了酿酒酵母的前体 mRNA 剪接,并促进了其对镉的耐受性。
Biochim Biophys Acta Mol Cell Res. 2020 Feb;1867(2):118565. doi: 10.1016/j.bbamcr.2019.118565. Epub 2019 Oct 27.
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The role of catalases in the prevention/promotion of oxidative stress.过氧化氢酶在预防/促进氧化应激中的作用。
J Inorg Biochem. 2019 Aug;197:110699. doi: 10.1016/j.jinorgbio.2019.110699. Epub 2019 Apr 26.
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Sodium azide induces mitochondria‑mediated apoptosis in PC12 cells through Pgc‑1α‑associated signaling pathway.叠氮化钠通过 Pgc-1α 相关信号通路诱导 PC12 细胞线粒体介导的细胞凋亡。
Mol Med Rep. 2019 Mar;19(3):2211-2219. doi: 10.3892/mmr.2019.9853. Epub 2019 Jan 14.
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AP-1 (bZIP) Transcription Factors as Potential Regulators of Metallothionein Gene Expression in .AP-1(碱性亮氨酸拉链)转录因子作为……中金属硫蛋白基因表达的潜在调节因子
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PLoS One. 2017 Dec 5;12(12):e0189076. doi: 10.1371/journal.pone.0189076. eCollection 2017.