首页 > 最新文献

Redox Biochemistry and Chemistry最新文献

英文 中文
Nitro-fatty acid signaling: Therapeutic potential in inflammatory diseases 硝基脂肪酸信号传导:炎症性疾病的治疗潜力
Pub Date : 2024-05-14 DOI: 10.1016/j.rbc.2024.100027
Homero Rubbo, Andrés Trostchansky

This review explores the interaction between nitric oxide-derived reactive species and unsaturated fatty acids, leading to the formation of electrophilic nitroalkenes, named nitro-fatty acids (NO2-FA). These species serve as endogenously produced anti-inflammatory signaling mediators, demonstrating protective effects in pre-clinical animal disease models. The discussion herein focuses on the cell signaling actions of NO2-FA, drawing insights from both existing knowledge and recent in vivo data. Additionally, this review addresses the potential pharmacological utility of NO2-FA and ongoing trials, highlighting their promising prospects based on the gathered information.

这篇综述探讨了一氧化氮衍生的活性物种与不饱和脂肪酸之间的相互作用,从而形成亲电的硝基烯烃,即硝基脂肪酸(NO2-FA)。这些物质可作为内源性抗炎信号介质,在临床前动物疾病模型中显示出保护作用。本文将重点讨论 NO2-FA 的细胞信号传导作用,从现有知识和最新体内数据中汲取启示。此外,这篇综述还探讨了 NO2-FA 的潜在药理作用和正在进行的试验,并根据收集到的信息强调了它们的广阔前景。
{"title":"Nitro-fatty acid signaling: Therapeutic potential in inflammatory diseases","authors":"Homero Rubbo,&nbsp;Andrés Trostchansky","doi":"10.1016/j.rbc.2024.100027","DOIUrl":"https://doi.org/10.1016/j.rbc.2024.100027","url":null,"abstract":"<div><p>This review explores the interaction between nitric oxide-derived reactive species and unsaturated fatty acids, leading to the formation of electrophilic nitroalkenes, named nitro-fatty acids (NO<sub>2</sub>-FA). These species serve as endogenously produced anti-inflammatory signaling mediators, demonstrating protective effects in pre-clinical animal disease models. The discussion herein focuses on the cell signaling actions of NO<sub>2</sub>-FA, drawing insights from both existing knowledge and recent <em>in vivo</em> data. Additionally, this review addresses the potential pharmacological utility of NO<sub>2</sub>-FA and ongoing trials, highlighting their promising prospects based on the gathered information.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100027"},"PeriodicalIF":0.0,"publicationDate":"2024-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000087/pdfft?md5=851897c0771f768914061f5f1797696a&pid=1-s2.0-S2773176624000087-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140950376","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The chemical biology of dinitrogen trioxide 三氧化二氮的化学生物学
Pub Date : 2024-05-09 DOI: 10.1016/j.rbc.2024.100026
Matías N. Möller , Darío A. Vitturi

Dinitrogen trioxide (N2O3) mediates low-molecular weight and protein S- and N-nitrosation, with recent reports suggesting a role in the formation of nitrating intermediates as well as in nitrite-dependent hypoxic vasodilatation. However, the reactivity of N2O3 in biological systems results in an extremely short half-life that renders this molecule essentially undetectable by currently available technologies. As a result, evidence for in vivo N2O3 formation derives from the detection of nitrosated products as well as from in vitro kinetic determinations, isotopic labeling studies, and spectroscopic analyses. This review will discuss mechanisms of N2O3 formation, reactivity and decomposition, as well as address the role of sub-cellular localization as a key determinant of its actions. Finally, evidence will be discussed supporting different roles for N2O3 as a biologically relevant signaling molecule.

三氧化二氮(N2O3)可介导低分子量、蛋白质 S-和 N-亚硝基化,最近的报告表明,它在硝化中间产物的形成以及亚硝酸盐依赖性缺氧性血管扩张中发挥了作用。然而,由于 N2O3 在生物系统中的反应性,其半衰期极短,目前可用的技术基本上检测不到这种分子。因此,体内 N2O3 形成的证据来自亚硝酸盐化产物的检测以及体外动力学测定、同位素标记研究和光谱分析。本综述将讨论 N2O3 的形成、反应和分解机制,并探讨亚细胞定位作为其作用的关键决定因素的作用。最后,还将讨论支持 N2O3 作为生物相关信号分子发挥不同作用的证据。
{"title":"The chemical biology of dinitrogen trioxide","authors":"Matías N. Möller ,&nbsp;Darío A. Vitturi","doi":"10.1016/j.rbc.2024.100026","DOIUrl":"https://doi.org/10.1016/j.rbc.2024.100026","url":null,"abstract":"<div><p>Dinitrogen trioxide (N<sub>2</sub>O<sub>3</sub>) mediates low-molecular weight and protein S- and N-nitrosation, with recent reports suggesting a role in the formation of nitrating intermediates as well as in nitrite-dependent hypoxic vasodilatation. However, the reactivity of N<sub>2</sub>O<sub>3</sub> in biological systems results in an extremely short half-life that renders this molecule essentially undetectable by currently available technologies. As a result, evidence for <em>in vivo</em> N<sub>2</sub>O<sub>3</sub> formation derives from the detection of nitrosated products as well as from <em>in vitro</em> kinetic determinations, isotopic labeling studies, and spectroscopic analyses. This review will discuss mechanisms of N<sub>2</sub>O<sub>3</sub> formation, reactivity and decomposition, as well as address the role of sub-cellular localization as a key determinant of its actions. Finally, evidence will be discussed supporting different roles for N<sub>2</sub>O<sub>3</sub> as a biologically relevant signaling molecule.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100026"},"PeriodicalIF":0.0,"publicationDate":"2024-05-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000075/pdfft?md5=a6dcbb5b09dfa3f7a85e72ede30c0872&pid=1-s2.0-S2773176624000075-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140950371","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Direct fitting improves the accuracy of the horse radish peroxidase competition assay for peroxidase activity 直接拟合提高了萝卜过氧化物酶竞争测定法测定过氧化物酶活性的准确性
Pub Date : 2024-04-26 DOI: 10.1016/j.rbc.2024.100025
Christopher J. Barry , Ché S. Pillay , Johann M. Rohwer

The peroxiredoxins are an important antioxidant protein family and their ability to neutralise oxidants is regularly investigated using horse radish peroxidase in a competition assay system. In this method, the rate constant of a peroxiredoxin is calculated from the fractional inhibition of horse radish peroxidase activity caused by competition with the peroxiredoxin for an oxidant substrate. We developed a model capable of simulating this assay and, using this model, demonstrate that the fractional inhibition calculation significantly and systematically mis-estimates the rate constant under fairly common conditions. We go on to develop a method for fitting simulated assay time-courses to experimental data directly, which significantly outperforms the fractional inhibition method yielding more accurate results. Based on our findings, we recommend using the direct fitting approach to determine peroxidase rate constants from horseradish peroxidase experiments.

过氧化还原酶是一个重要的抗氧化蛋白家族,人们经常使用竞争分析系统中的萝卜过氧化物酶来研究它们中和氧化剂的能力。在这种方法中,过氧化还原酶的速率常数是通过与过氧化还原酶竞争氧化剂底物而导致的萝卜过氧化物酶活性抑制分数计算出来的。我们开发了一个能够模拟这种检测方法的模型,并利用该模型证明,在相当常见的条件下,分数抑制率计算会明显地、系统地误估速率常数。我们进而开发了一种方法,可将模拟测定的时间历程与实验数据直接拟合,其效果明显优于分数抑制法,得出的结果也更准确。根据我们的研究结果,我们建议使用直接拟合法来确定辣根过氧化物酶实验中的过氧化物酶速率常数。
{"title":"Direct fitting improves the accuracy of the horse radish peroxidase competition assay for peroxidase activity","authors":"Christopher J. Barry ,&nbsp;Ché S. Pillay ,&nbsp;Johann M. Rohwer","doi":"10.1016/j.rbc.2024.100025","DOIUrl":"https://doi.org/10.1016/j.rbc.2024.100025","url":null,"abstract":"<div><p>The peroxiredoxins are an important antioxidant protein family and their ability to neutralise oxidants is regularly investigated using horse radish peroxidase in a competition assay system. In this method, the rate constant of a peroxiredoxin is calculated from the fractional inhibition of horse radish peroxidase activity caused by competition with the peroxiredoxin for an oxidant substrate. We developed a model capable of simulating this assay and, using this model, demonstrate that the fractional inhibition calculation significantly and systematically mis-estimates the rate constant under fairly common conditions. We go on to develop a method for fitting simulated assay time-courses to experimental data directly, which significantly outperforms the fractional inhibition method yielding more accurate results. Based on our findings, we recommend using the direct fitting approach to determine peroxidase rate constants from horseradish peroxidase experiments.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100025"},"PeriodicalIF":0.0,"publicationDate":"2024-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000063/pdfft?md5=d1ae63fed576a6bb22d227fdefdd47ca&pid=1-s2.0-S2773176624000063-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140823817","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Decoding the enigmatic last gasotransmitter. The intriguing journey of HNO: From hidden origins to clues on reactivity and detection 解密神秘的最后一种气体递质。令人好奇的 HNO 之旅:从隐秘的起源到反应性和检测的线索。
Pub Date : 2024-04-22 DOI: 10.1016/j.rbc.2024.100024
Sebastian A. Suarez

This review focuses on HNO, a molecule of immense chemical and biological importance that has intrigued scientists for decades. Despite its elusive and transient nature, HNO may play an important role in various physiological processes, particularly in cardiovascular regulation. This review thoroughly examines the formation, chemical properties, and biological significance of HNO and highlights ongoing research efforts to unravel its mysteries. Challenges in studying HNO arise from its high reactivity, short half-life, and complex interactions with other nitrogen oxides, particularly nitric oxide. Detection and quantification of HNO in biological systems pose difficulties, prompting the development of advanced techniques. Active research into endogenous HNO formation is revealing intricate pathways within biological systems, the elucidation of which is crucial for exploiting its therapeutic potential. The multifaceted role of HNO in cardiovascular regulation, influencing vasorelaxation, blood pressure reduction, and enhanced cardiac contractility, underscores its profound impact on the circulatory system. Ongoing research holds promise for treating conditions such as hypertension and heart failure. As clinical applications expand, HNO research may unlock treatments for cardiovascular disease, inflammatory disorders, and cancer. The recent discovery of endogenous HNO production in plants adds a new dimension. While numerous clues have emerged, the scientific saga underscores that mysteries persist, evolve, and beckon to perpetual exploration in the realm of science.

HNO 是一种具有重要化学和生物学意义的分子,几十年来一直吸引着科学家的目光。尽管 HNO 具有难以捉摸和瞬时的特性,但它可能在各种生理过程,尤其是心血管调节过程中发挥着重要作用。本综述深入探讨了 HNO 的形成、化学性质和生物学意义,并重点介绍了为揭开其神秘面纱而正在进行的研究工作。研究 HNO 所面临的挑战来自于它的高反应性、短半衰期以及与其他氮氧化物(尤其是一氧化氮)之间复杂的相互作用。检测和定量生物系统中的 HNO 带来了困难,因此需要开发先进的技术。对内源性 HNO 形成的积极研究正在揭示生物系统中错综复杂的途径,而阐明这些途径对于开发其治疗潜力至关重要。HNO 在心血管调节中发挥着多方面的作用,影响着血管舒张、血压降低和心脏收缩力的增强,凸显了它对循环系统的深远影响。正在进行的研究为治疗高血压和心力衰竭等疾病带来了希望。随着临床应用的扩大,HNO 研究可能会开启心血管疾病、炎症性疾病和癌症的治疗方法。最近在植物中发现的内源性 HNO 的产生又增加了一个新的层面。虽然已经出现了许多线索,但这一科学传奇强调了科学领域的奥秘始终存在、不断发展,并召唤着人们不断探索。
{"title":"Decoding the enigmatic last gasotransmitter. The intriguing journey of HNO: From hidden origins to clues on reactivity and detection","authors":"Sebastian A. Suarez","doi":"10.1016/j.rbc.2024.100024","DOIUrl":"10.1016/j.rbc.2024.100024","url":null,"abstract":"<div><p>This review focuses on HNO, a molecule of immense chemical and biological importance that has intrigued scientists for decades. Despite its elusive and transient nature, HNO may play an important role in various physiological processes, particularly in cardiovascular regulation. This review thoroughly examines the formation, chemical properties, and biological significance of HNO and highlights ongoing research efforts to unravel its mysteries. Challenges in studying HNO arise from its high reactivity, short half-life, and complex interactions with other nitrogen oxides, particularly nitric oxide. Detection and quantification of HNO in biological systems pose difficulties, prompting the development of advanced techniques. Active research into endogenous HNO formation is revealing intricate pathways within biological systems, the elucidation of which is crucial for exploiting its therapeutic potential. The multifaceted role of HNO in cardiovascular regulation, influencing vasorelaxation, blood pressure reduction, and enhanced cardiac contractility, underscores its profound impact on the circulatory system. Ongoing research holds promise for treating conditions such as hypertension and heart failure. As clinical applications expand, HNO research may unlock treatments for cardiovascular disease, inflammatory disorders, and cancer. The recent discovery of endogenous HNO production in plants adds a new dimension. While numerous clues have emerged, the scientific saga underscores that mysteries persist, evolve, and beckon to perpetual exploration in the realm of science.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100024"},"PeriodicalIF":0.0,"publicationDate":"2024-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000051/pdfft?md5=072377c74312656eca6afa81588537c0&pid=1-s2.0-S2773176624000051-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140763633","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Oxidized guanosines induce mitochondrial dysfunction and loss of viability in β-cells 氧化鸟苷诱导β细胞线粒体功能障碍并丧失活力
Pub Date : 2024-04-04 DOI: 10.1016/j.rbc.2024.100022
Inga Sileikaite-Morvaközi , Ksenia Morozova , Nadezda A. Brazhe , Olga Sosnovtseva , Claus Desler , Thomas Mandrup-Poulsen , Michael J. Davies , Clare L. Hawkins

The production of reactive oxygen species and oxidative stress promote β-cell dysfunction and impair insulin secretion, thereby contributing to the pathogenesis of type 2 diabetes mellitus (T2DM). The nucleobase guanine is highly sensitive to oxidation, which results in the formation of 8-oxoguanosine (8oxoG) and 8-oxodeoxyguanosine (8oxodG). The urinary excretion of 8oxoG is associated with the risk of mortality in people with T2DM, including from diabetic complications such as cardiovascular disease. However, the cellular mechanisms responsible for this association are poorly defined. Therefore, in this study, we examined the effect of 8oxoG, 8oxodG and other oxidized guanosine derivatives, on the INS-1E β-cell line. Exposure of INS-1E cells to 8oxoG and 8oxodG decreased metabolic activity and promoted cell death by apoptosis. The change in cell viability was similar to that induced by treatment of INS-1E cells with the inflammatory cytokines interleukin 1β (Il-1β) and tumour necrosis factor α (TNFα). Changes in mitochondrial membrane permeability and superoxide radical formation were also observed with 8oxoG, but there was no significant change in the oxidation state of mitochondrial cytochromes or hydrogen peroxide levels in the INS-1E cells. Interestingly, exposure to 8oxoG and 8-oxodG also increased the mRNA expression of stress response genes, including NADPH dehydrogenase quinone 1 (NQO1), and thioredoxin-interacting protein (TXNIP). Together, these results support a potential role of oxidized guanosine derivatives in the induction of β-cell dysfunction, which could be relevant to the pathogenesis of T2DM.

活性氧的产生和氧化应激会促进β细胞功能障碍,影响胰岛素分泌,从而导致2型糖尿病(T2DM)的发病。核碱基鸟嘌呤对氧化高度敏感,会形成 8-氧代鸟苷(8oxoG)和 8-氧代脱氧鸟苷(8oxodG)。尿液中排出的 8oxoG 与 T2DM 患者的死亡风险有关,包括心血管疾病等糖尿病并发症。然而,造成这种关联的细胞机制尚不明确。因此,在本研究中,我们研究了 8oxoG、8oxodG 和其他氧化鸟苷衍生物对 INS-1E β 细胞系的影响。将 INS-1E 细胞暴露于 8oxoG 和 8oxodG 会降低代谢活性,促进细胞凋亡。细胞活力的变化类似于用白细胞介素 1β (Il-1β)和肿瘤坏死因子 α (TNFα)处理 INS-1E 细胞所引起的变化。8oxoG 还可观察到线粒体膜通透性和超氧自由基形成的变化,但 INS-1E 细胞中线粒体细胞色素的氧化状态或过氧化氢水平没有显著变化。有趣的是,暴露于 8oxoG 和 8-oxodG 还增加了应激反应基因的 mRNA 表达,包括 NADPH 脱氢酶醌 1(NQO1)和硫氧还蛋白相互作用蛋白(TXNIP)。这些结果共同支持了氧化鸟苷衍生物在诱导β细胞功能障碍中的潜在作用,这可能与T2DM的发病机制有关。
{"title":"Oxidized guanosines induce mitochondrial dysfunction and loss of viability in β-cells","authors":"Inga Sileikaite-Morvaközi ,&nbsp;Ksenia Morozova ,&nbsp;Nadezda A. Brazhe ,&nbsp;Olga Sosnovtseva ,&nbsp;Claus Desler ,&nbsp;Thomas Mandrup-Poulsen ,&nbsp;Michael J. Davies ,&nbsp;Clare L. Hawkins","doi":"10.1016/j.rbc.2024.100022","DOIUrl":"https://doi.org/10.1016/j.rbc.2024.100022","url":null,"abstract":"<div><p>The production of reactive oxygen species and oxidative stress promote β-cell dysfunction and impair insulin secretion, thereby contributing to the pathogenesis of type 2 diabetes mellitus (T2DM). The nucleobase guanine is highly sensitive to oxidation, which results in the formation of 8-oxoguanosine (8oxoG) and 8-oxodeoxyguanosine (8oxodG). The urinary excretion of 8oxoG is associated with the risk of mortality in people with T2DM, including from diabetic complications such as cardiovascular disease. However, the cellular mechanisms responsible for this association are poorly defined. Therefore, in this study, we examined the effect of 8oxoG, 8oxodG and other oxidized guanosine derivatives, on the INS-1E β-cell line. Exposure of INS-1E cells to 8oxoG and 8oxodG decreased metabolic activity and promoted cell death by apoptosis. The change in cell viability was similar to that induced by treatment of INS-1E cells with the inflammatory cytokines interleukin 1β (Il-1β) and tumour necrosis factor α (TNFα). Changes in mitochondrial membrane permeability and superoxide radical formation were also observed with 8oxoG, but there was no significant change in the oxidation state of mitochondrial cytochromes or hydrogen peroxide levels in the INS-1E cells. Interestingly, exposure to 8oxoG and 8-oxodG also increased the mRNA expression of stress response genes, including NADPH dehydrogenase quinone 1 (NQO1), and thioredoxin-interacting protein (TXNIP). Together, these results support a potential role of oxidized guanosine derivatives in the induction of β-cell dysfunction, which could be relevant to the pathogenesis of T2DM.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100022"},"PeriodicalIF":0.0,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000038/pdfft?md5=bdee5885ca4a34f13fa105f9aac9f767&pid=1-s2.0-S2773176624000038-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140539119","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Lactoperoxidase catalytically oxidize hydrogen sulfide via intermediate formation of sulfheme derivatives 乳过氧化物酶通过中间形成硫heme 衍生物催化氧化硫化氢
Pub Date : 2024-04-04 DOI: 10.1016/j.rbc.2024.100021
Bessie B. Ríos-González , Andrea Domán , Tamás Ditrói , Dorottya Garai , Leishka D. Crespo , Gary J. Gerfen , Paul G. Furtmüller , Péter Nagy , Juan López-Garriga

The biological chemistry of hydrogen sulfide (H2S) with physiologically important heme proteins is in the focus of redox biology research. In this study, we investigated the interactions of lactoperoxidase (LPO) with H2S in the presence and absence of molecular dioxygen (O2) or hydrogen peroxide (H2O2). Under anaerobic conditions, native LPO forms no heme-H2S complex upon sulfide exposure. However, under aerobic conditions or in the presence of H2O2 the formation of both ferrous and ferric sulfheme (sulfLPO) derivatives was observed based on the appearances of their characteristic optical absorptions at 638 nm and 727 nm, respectively. Interestingly, we demonstrate that LPO can catalytically oxidize H2S by H2O2 via intermediate formation of relatively short-lived ferrous and ferric sulfLPO derivatives. Pilot product analyses suggested that the turnover process generates oxidized sulfide species, which include sulfate (SO42−) and inorganic polysulfides (HSx; x = 2–5). These results indicated that H2S can serve as a non-classical LPO substrate by inducing a reversible sulfheme-like modification of the heme porphyrin ring during turnover. Furthermore, electron paramagnetic resonance data suggest that H2S can act as a scavenger of H2O2 in the presence of LPO without detectable formation of any carbon-centered protein radical species, suggesting that H2S might be capable of protecting the enzyme from radical-mediated damage. We propose possible mechanisms, which explain our results as well as contrasting observations with other heme proteins, where either no sulfheme formation was observed or the generation of sulfheme derivatives provided a dead end for enzyme functions.

硫化氢(H2S)与生理上重要的血红素蛋白的生物化学作用是氧化还原生物学研究的重点。在本研究中,我们研究了乳过氧化物酶(LPO)在分子二氧(O2)或过氧化氢(H2O2)存在和不存在的情况下与 H2S 的相互作用。在厌氧条件下,原生 LPO 暴露于硫化物时不会形成血红素-H2S 复合物。然而,在有氧条件下或有 H2O2 存在时,根据亚铁和铁硫heme(sulfLPO)衍生物分别在 638 纳米和 727 纳米出现的特征性光学吸收,可以观察到它们的形成。有趣的是,我们证明了 LPO 可以催化 H2O2 氧化 H2S,中间形成相对短效的亚铁和铁硫LPO 衍生物。先导产物分析表明,翻转过程会产生氧化的硫化物,其中包括硫酸盐(SO42-)和无机多硫化物(HSx-;x = 2-5)。这些结果表明,H2S 可作为非典型 LPO 底物,在翻转过程中诱导血红素卟啉环发生类似硫heme 的可逆修饰。此外,电子顺磁共振数据表明,在存在 LPO 的情况下,H2S 可作为 H2O2 的清除剂,而不会形成任何可检测到的碳中心蛋白自由基物种,这表明 H2S 可能能够保护酶免受自由基介导的损伤。我们提出了可能的机制,以解释我们的研究结果以及与其他血红素蛋白的对比观察结果,在其他血红素蛋白中,要么没有观察到亚硫酰血红素的形成,要么亚硫酰血红素衍生物的生成为酶的功能提供了一个死胡同。
{"title":"Lactoperoxidase catalytically oxidize hydrogen sulfide via intermediate formation of sulfheme derivatives","authors":"Bessie B. Ríos-González ,&nbsp;Andrea Domán ,&nbsp;Tamás Ditrói ,&nbsp;Dorottya Garai ,&nbsp;Leishka D. Crespo ,&nbsp;Gary J. Gerfen ,&nbsp;Paul G. Furtmüller ,&nbsp;Péter Nagy ,&nbsp;Juan López-Garriga","doi":"10.1016/j.rbc.2024.100021","DOIUrl":"https://doi.org/10.1016/j.rbc.2024.100021","url":null,"abstract":"<div><p>The biological chemistry of hydrogen sulfide (H<sub>2</sub>S) with physiologically important heme proteins is in the focus of redox biology research. In this study, we investigated the interactions of lactoperoxidase (LPO) with H<sub>2</sub>S in the presence and absence of molecular dioxygen (O<sub>2</sub>) or hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>). Under anaerobic conditions, native LPO forms no heme-H<sub>2</sub>S complex upon sulfide exposure. However, under aerobic conditions or in the presence of H<sub>2</sub>O<sub>2</sub> the formation of both ferrous and ferric sulfheme (sulfLPO) derivatives was observed based on the appearances of their characteristic optical absorptions at 638 nm and 727 nm, respectively. Interestingly, we demonstrate that LPO can catalytically oxidize H<sub>2</sub>S by H<sub>2</sub>O<sub>2</sub> via intermediate formation of relatively short-lived ferrous and ferric sulfLPO derivatives. Pilot product analyses suggested that the turnover process generates oxidized sulfide species, which include sulfate (SO<sub>4</sub><sup>2−</sup>) and inorganic polysulfides (HS<sub>x</sub><sup>−</sup>; x = 2–5). These results indicated that H<sub>2</sub>S can serve as a non-classical LPO substrate by inducing a reversible sulfheme-like modification of the heme porphyrin ring during turnover. Furthermore, electron paramagnetic resonance data suggest that H<sub>2</sub>S can act as a scavenger of H<sub>2</sub>O<sub>2</sub> in the presence of LPO without detectable formation of any carbon-centered protein radical species, suggesting that H<sub>2</sub>S might be capable of protecting the enzyme from radical-mediated damage. We propose possible mechanisms, which explain our results as well as contrasting observations with other heme proteins, where either no sulfheme formation was observed or the generation of sulfheme derivatives provided a dead end for enzyme functions.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"8 ","pages":"Article 100021"},"PeriodicalIF":0.0,"publicationDate":"2024-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000026/pdfft?md5=c98d3efbf75f1105ec44b5dd1c758983&pid=1-s2.0-S2773176624000026-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140549042","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Chemistry of nitrogen dioxide and its biological implicatios 二氧化氮的化学性质及其生物学意义
Pub Date : 2024-03-22 DOI: 10.1016/j.rbc.2024.100020
Sara Goldstein , Amram Samuni

Nitrogen dioxide (NO2) is a radical gas that forms part of air pollution and is produced chemically, photochemically and by ionizing radiation in aqueous and non-aqueous solutions as well as by various endogenous pathways in biological systems. This review describes the: (i) sources of NO2; (ii) kinetics and mechanism of NO2 reactions; (iii) NO2 as a key player in cellular oxidative and nitrosative stress leading to pathological conditions, and (iv) use of diverse antioxidants to reduce NO2 toxic effects.

二氧化氮(-NO2)是一种自由基气体,是空气污染的一部分,可通过化学、光化学、水溶液和非水溶液中的电离辐射以及生物系统中的各种内源途径产生。本综述介绍了(i) -NO2 的来源;(ii) -NO2 反应的动力学和机理;(iii) -NO2 是导致病理状况的细胞氧化和亚硝酸应激的关键因素,以及 (iv) 使用多种抗氧化剂来减少 -NO2 的毒性效应。
{"title":"Chemistry of nitrogen dioxide and its biological implicatios","authors":"Sara Goldstein ,&nbsp;Amram Samuni","doi":"10.1016/j.rbc.2024.100020","DOIUrl":"10.1016/j.rbc.2024.100020","url":null,"abstract":"<div><p>Nitrogen dioxide (<sup>•</sup>NO<sub>2</sub>) is a radical gas that forms part of air pollution and is produced chemically, photochemically and by ionizing radiation in aqueous and non-aqueous solutions as well as by various endogenous pathways in biological systems. This review describes the: (<em>i</em>) sources of <sup>•</sup>NO<sub>2</sub>; (<em>ii</em>) kinetics and mechanism of <sup>•</sup>NO<sub>2</sub> reactions; (<em>iii</em>) <sup>•</sup>NO<sub>2</sub> as a key player in cellular oxidative and nitrosative stress leading to pathological conditions, and <em>(iv)</em> use of diverse antioxidants to reduce <sup>•</sup>NO<sub>2</sub> toxic effects.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"7 ","pages":"Article 100020"},"PeriodicalIF":0.0,"publicationDate":"2024-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176624000014/pdfft?md5=1281d8224d83c88cf2e2284ffe34567c&pid=1-s2.0-S2773176624000014-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140268890","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Activation of cellular signalling pathways and apoptosis by the aldehyde acrolein – A major environmental hazard 醛类丙烯醛激活细胞信号通路和细胞凋亡--对环境的一大危害
Pub Date : 2023-12-12 DOI: 10.1016/j.rbc.2023.100019
Diana A. Averill-Bates, André Tanel

Interest in the molecular actions of acrolein has increased in light of growing knowledge that implicates this reactive aldehyde in a wide range of pathophysiologies including neurodegenerative diseases, various lung disorders including chronic obstructive pulmonary disease, atherosclerosis, and certain cancers. This is rendered complex because acrolein exists in mixtures of environmental pollutants. Reactive α,β-unsaturated aldehydes like acrolein are major components of common environmental pollutants like cigarettes, automobile exhaust, and smoke from wood, coal, forest and house fires. It is a natural constituent of several foods and is generated in the human body during inflammation or oxidation of unsaturated lipids. Acrolein is also a toxic metabolic product of the widely used anticancer drug cyclophosphamide and is generated from the enzymatic oxidation of polyamines. It is a toxic by-product of lipid peroxidation and has been implicated as a mediator of oxidative damage in cells and tissues. The purpose of this review is to assess the literature about the activation of cell signalling pathways and transcription factors, and cell survival and cell death pathways by acrolein. Several reports show that anti-apoptosis processes dominate at lower dose exposures to acrolein, whereas pro-apoptotic processes and necrosis dominate at higher dose exposures. There has been improved understanding about the deleterious molecular and cellular mechanisms that are triggered in cells in response to acrolein injury. However, more progress is required to define the contributions of acrolein to human diseases and to design efficient therapeutic strategies based on the biochemical modulation of acrolein activity.

越来越多的知识表明,丙烯醛与神经退行性疾病、各种肺部疾病(包括慢性阻塞性肺病)、动脉粥样硬化和某些癌症等多种病理生理现象有关,因此,人们对丙烯醛分子作用的兴趣与日俱增。由于丙烯醛存在于环境污染物的混合物中,因此情况变得更加复杂。像丙烯醛这样的反应性 α、β-不饱和醛类是香烟、汽车尾气以及木材、煤炭、森林和房屋火灾产生的烟雾等常见环境污染物的主要成分。它是几种食物的天然成分,在炎症或不饱和脂质氧化过程中会在人体内产生。丙烯醛也是广泛使用的抗癌药物环磷酰胺的一种有毒代谢产物,由多胺的酶促氧化生成。它是脂质过氧化反应的一种有毒副产品,被认为是细胞和组织氧化损伤的介质。本综述旨在评估有关丙烯醛激活细胞信号通路和转录因子以及细胞存活和细胞死亡通路的文献。一些报告显示,在接触较低剂量的丙烯醛时,抗细胞凋亡过程占主导地位,而在接触较高剂量的丙烯醛时,促细胞凋亡过程和细胞坏死占主导地位。人们对细胞在受到丙烯醛伤害时引发的有害分子和细胞机制有了更深入的了解。然而,要确定丙烯醛对人类疾病的影响,并根据丙烯醛活性的生化调节来设计有效的治疗策略,还需要取得更多进展。
{"title":"Activation of cellular signalling pathways and apoptosis by the aldehyde acrolein – A major environmental hazard","authors":"Diana A. Averill-Bates,&nbsp;André Tanel","doi":"10.1016/j.rbc.2023.100019","DOIUrl":"10.1016/j.rbc.2023.100019","url":null,"abstract":"<div><p>Interest in the molecular actions of acrolein has increased in light of growing knowledge that implicates this reactive aldehyde in a wide range of pathophysiologies including neurodegenerative diseases, various lung disorders including chronic obstructive pulmonary disease, atherosclerosis, and certain cancers. This is rendered complex because acrolein exists in mixtures of environmental pollutants. Reactive α,β-unsaturated aldehydes like acrolein are major components of common environmental pollutants like cigarettes, automobile exhaust, and smoke from wood, coal, forest and house fires. It is a natural constituent of several foods and is generated in the human body during inflammation or oxidation of unsaturated lipids. Acrolein is also a toxic metabolic product of the widely used anticancer drug cyclophosphamide and is generated from the enzymatic oxidation of polyamines. It is a toxic by-product of lipid peroxidation and has been implicated as a mediator of oxidative damage in cells and tissues. The purpose of this review is to assess the literature about the activation of cell signalling pathways and transcription factors, and cell survival and cell death pathways by acrolein. Several reports show that anti-apoptosis processes dominate at lower dose exposures to acrolein, whereas pro-apoptotic processes and necrosis dominate at higher dose exposures. There has been improved understanding about the deleterious molecular and cellular mechanisms that are triggered in cells in response to acrolein injury. However, more progress is required to define the contributions of acrolein to human diseases and to design efficient therapeutic strategies based on the biochemical modulation of acrolein activity.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"7 ","pages":"Article 100019"},"PeriodicalIF":0.0,"publicationDate":"2023-12-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176623000184/pdfft?md5=9c33fed1db3a45958274b57c9b23009a&pid=1-s2.0-S2773176623000184-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138988898","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Selenocyanate (SeCN−) acts as an efficient competitive substrate for myeloperoxidase and decreases biological damage induced by hypochlorous acid 硒氰酸酯(SeCN-)是髓过氧化物酶的高效竞争性底物,可减少次氯酸对生物的损伤
Pub Date : 2023-11-28 DOI: 10.1016/j.rbc.2023.100018
Xing Zhang , Shuqi Xu , Christine Y. Chuang , Brian J. Day , Clare L. Hawkins , Michael J. Davies

The leukocyte-derived enzyme myeloperoxidase (MPO) is a key component of the innate immune response and mediates the killing of pathogens via the generation of the powerful oxidant hypochlorous acid (HOCl). Unintended or excessive formation of this species can however result in damage to host tissues, and this is linked with multiple pathologies associated with acute or chronic inflammation. The active (Compound I) form of MPO is promiscuous and can oxidize multiple alternative anions, in addition to the Cl used to generate HOCl. These alternative substrates may therefore modulate MPO-mediated HOCl damage. In the current study we examined the hypothesis that selenocyanate (SeCN), the selenium analogue of thiocyanate (SCN, a well-established competitive MPO substrate) would inhibit HOCl-mediated damage to human plasma fibronectin (hpFN) or the extracellular matrix laid down by human coronary artery smooth muscle cells. SeCN modulated HOCl and MPO-mediated damage, in a dose-dependent manner. These data are consistent with SeCN acting as both a competitive substrate for Compound I of MPO (with IC50 ∼23 μM), and as a direct scavenger of HOCl. Inhibition of protein damage by SeCN was also detected in the presence of the physiological anions Br, I and SCN at the concentrations typically present in human plasma, consistent with a high affinity of SeCN for MPO Compound I. In addition, the protective effects of SeCN and SCN, as competitive MPO substrates, were additive. Together these data indicate that modest concentrations of SeCN can, like its sulfur analogue SCN, act as an effective modulator of inflammation-induced damage.

白细胞衍生的髓过氧化物酶(MPO)是先天性免疫反应的关键组成部分,通过产生强氧化剂次氯酸(HOCl)来杀死病原体。然而,这种物质的意外或过量形成会导致宿主组织受损,这与急性或慢性炎症相关的多种病症有关。MPO 的活性(化合物 I)形式具有杂合性,除了用于生成 HOCl 的 Cl- 外,还能氧化多种替代阴离子。因此,这些替代底物可能会调节 MPO 介导的 HOCl 损伤。在本研究中,我们研究了硫氰酸硒类似物(SCN-,一种公认的 MPO 竞争性底物)硒氰酸酯(SeCN-)会抑制 HOCl 介导的对人血浆纤连蛋白(hpFN)或人冠状动脉平滑肌细胞铺设的细胞外基质的损伤这一假设。SeCN- 对 HOCl 和 MPO 介导的损伤有调节作用,且呈剂量依赖性。这些数据表明,SeCN- 既是 MPO 化合物 I 的竞争性底物(IC50 ∼ 23 μM),也是 HOCl 的直接清除剂。此外,SeCN- 和 SCN-作为 MPO 竞争性底物,其保护作用是相加的。这些数据共同表明,适度浓度的 SeCN- 可像其硫类似物 SCN- 一样,成为炎症诱导的损伤的有效调节剂。
{"title":"Selenocyanate (SeCN−) acts as an efficient competitive substrate for myeloperoxidase and decreases biological damage induced by hypochlorous acid","authors":"Xing Zhang ,&nbsp;Shuqi Xu ,&nbsp;Christine Y. Chuang ,&nbsp;Brian J. Day ,&nbsp;Clare L. Hawkins ,&nbsp;Michael J. Davies","doi":"10.1016/j.rbc.2023.100018","DOIUrl":"https://doi.org/10.1016/j.rbc.2023.100018","url":null,"abstract":"<div><p>The leukocyte-derived enzyme myeloperoxidase (MPO) is a key component of the innate immune response and mediates the killing of pathogens via the generation of the powerful oxidant hypochlorous acid (HOCl). Unintended or excessive formation of this species can however result in damage to host tissues, and this is linked with multiple pathologies associated with acute or chronic inflammation. The active (Compound I) form of MPO is promiscuous and can oxidize multiple alternative anions, in addition to the Cl<sup>−</sup> used to generate HOCl. These alternative substrates may therefore modulate MPO-mediated HOCl damage. In the current study we examined the hypothesis that selenocyanate (SeCN<sup>−</sup>), the selenium analogue of thiocyanate (SCN<sup>−</sup>, a well-established competitive MPO substrate) would inhibit HOCl-mediated damage to human plasma fibronectin (hpFN) or the extracellular matrix laid down by human coronary artery smooth muscle cells. SeCN<sup>−</sup> modulated HOCl and MPO-mediated damage, in a dose-dependent manner. These data are consistent with SeCN<sup>−</sup> acting as both a competitive substrate for Compound I of MPO (with IC<sub>50</sub> ∼23 μM), and as a direct scavenger of HOCl. Inhibition of protein damage by SeCN<sup>−</sup> was also detected in the presence of the physiological anions Br<sup>−</sup>, I<sup>−</sup> and SCN<sup>−</sup> at the concentrations typically present in human plasma, consistent with a high affinity of SeCN<sup>−</sup> for MPO Compound I. In addition, the protective effects of SeCN<sup>−</sup> and SCN<sup>−</sup>, as competitive MPO substrates, were additive. Together these data indicate that modest concentrations of SeCN<sup>−</sup> can, like its sulfur analogue SCN<sup>−</sup>, act as an effective modulator of inflammation-induced damage.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"7 ","pages":"Article 100018"},"PeriodicalIF":0.0,"publicationDate":"2023-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2773176623000172/pdfft?md5=4ce4a3466ab4e55a3ca75be7e8b6ea2f&pid=1-s2.0-S2773176623000172-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138549547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Arsenic exposure and increased C-reactive protein are independently associated with lower erythrocyte glutathione peroxidase activity in Bangladeshi children 砷暴露和c反应蛋白升高与孟加拉国儿童红细胞谷胱甘肽过氧化物酶活性降低独立相关
Pub Date : 2023-09-27 DOI: 10.1016/j.rbc.2023.100015
Dorian M. Cheff , Helena Skröder , Evana Akhtar , Qing Cheng , Matthew D. Hall , Rubhana Raqib , Maria Kippler , Marie Vahter , Elias S.J. Arnér

Toxic metal contaminants present in food and water have widespread effects on health and disease. Chalcophiles, such as arsenic, cadmium, and mercury, show a high affinity to selenium and exposure to these metals could have a modulating effect on enzymes dependent on selenocysteine in their active sites. The aim of this study was to assess the influence of these metals on the activity of the selenoprotein glutathione peroxidase 1 (GPX1) in erythrocytes of 100 children residing in rural Bangladesh, where drinking water often contains arsenic. GPX1 expression, as measured using high-throughput immunoblotting, showed little correlation with GPX activity (rs = 0.02, p = 0.87) in blood samples. Toxic metals and selenium measured in erythrocytes using inductively coupled plasma mass spectrometry (ICP-MS) and C-reactive protein (CRP) measured in plasma, were all considered as effectors of this divergence in GPX enzymatic activity. Arsenic concentrations in erythrocytes were most influential for GPX1 activity (rs = −0.395, p < 0.0001), and CRP levels also negatively impacted GPX1 activity (rs = −0.443, p < 0.0001). These effects appear independent of each other as arsenic concentrations and CRP showed no correlation (rs = 0.124, p = 0.2204). Erythrocyte selenium, cadmium, and mercury did not show any correlation with GPX1 activity, nor with CRP or arsenic. Our findings suggest that childhood exposure to inorganic arsenic, as well as inflammation triggering the release of CRP, may negatively affect GPX1 activity in erythrocytes.

食物和水中存在的有毒金属污染物对健康和疾病有着广泛的影响。亲查尔类物质,如砷、镉和汞,对硒具有很高的亲和力,接触这些金属可能会对活性位点依赖硒半胱氨酸的酶产生调节作用。本研究的目的是评估这些金属对居住在孟加拉国农村的100名儿童红细胞中硒蛋白谷胱甘肽过氧化物酶1(GPX1)活性的影响,孟加拉国农村的饮用水通常含有砷。使用高通量免疫印迹法测量的GPX1表达与血液样本中的GPX活性几乎没有相关性(rs=0.02,p=0.87)。使用电感耦合等离子体质谱法(ICP-MS)测量红细胞中的有毒金属和硒,以及在血浆中测量C反应蛋白(CRP),都被认为是GPX酶活性差异的影响因素。红细胞中的砷浓度对GPX1活性的影响最大(rs=-0.395,p<;0.0001),CRP水平也对GPX1活动产生负面影响(rs=−0.443,p&lgt;0.0001,汞与GPX1活性、CRP或砷均无相关性。我们的研究结果表明,儿童时期接触无机砷,以及引发CRP释放的炎症,可能会对红细胞中GPX1的活性产生负面影响。
{"title":"Arsenic exposure and increased C-reactive protein are independently associated with lower erythrocyte glutathione peroxidase activity in Bangladeshi children","authors":"Dorian M. Cheff ,&nbsp;Helena Skröder ,&nbsp;Evana Akhtar ,&nbsp;Qing Cheng ,&nbsp;Matthew D. Hall ,&nbsp;Rubhana Raqib ,&nbsp;Maria Kippler ,&nbsp;Marie Vahter ,&nbsp;Elias S.J. Arnér","doi":"10.1016/j.rbc.2023.100015","DOIUrl":"https://doi.org/10.1016/j.rbc.2023.100015","url":null,"abstract":"<div><p>Toxic metal contaminants present in food and water have widespread effects on health and disease. Chalcophiles, such as arsenic, cadmium, and mercury, show a high affinity to selenium and exposure to these metals could have a modulating effect on enzymes dependent on selenocysteine in their active sites. The aim of this study was to assess the influence of these metals on the activity of the selenoprotein glutathione peroxidase 1 (GPX1) in erythrocytes of 100 children residing in rural Bangladesh, where drinking water often contains arsenic. GPX1 expression, as measured using high-throughput immunoblotting, showed little correlation with GPX activity (<em>r</em><sub><em>s</em></sub> = 0.02, p = 0.87) in blood samples. Toxic metals and selenium measured in erythrocytes using inductively coupled plasma mass spectrometry (ICP-MS) and <em>C</em>-reactive protein (CRP) measured in plasma, were all considered as effectors of this divergence in GPX enzymatic activity. Arsenic concentrations in erythrocytes were most influential for GPX1 activity (<em>r</em><sub><em>s</em></sub> = −0.395, p &lt; 0.0001), and CRP levels also negatively impacted GPX1 activity (<em>r</em><sub><em>s</em></sub> = −0.443, p &lt; 0.0001). These effects appear independent of each other as arsenic concentrations and CRP showed no correlation (<em>r</em><sub><em>s</em></sub> = 0.124, p = 0.2204). Erythrocyte selenium, cadmium, and mercury did not show any correlation with GPX1 activity, nor with CRP or arsenic. Our findings suggest that childhood exposure to inorganic arsenic, as well as inflammation triggering the release of CRP, may negatively affect GPX1 activity in erythrocytes.</p></div>","PeriodicalId":101065,"journal":{"name":"Redox Biochemistry and Chemistry","volume":"5 ","pages":"Article 100015"},"PeriodicalIF":0.0,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49726672","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
期刊
Redox Biochemistry and Chemistry
全部 Acc. Chem. Res. ACS Applied Bio Materials ACS Appl. Electron. Mater. ACS Appl. Energy Mater. ACS Appl. Mater. Interfaces ACS Appl. Nano Mater. ACS Appl. Polym. Mater. ACS BIOMATER-SCI ENG ACS Catal. ACS Cent. Sci. ACS Chem. Biol. ACS Chemical Health & Safety ACS Chem. Neurosci. ACS Comb. Sci. ACS Earth Space Chem. ACS Energy Lett. ACS Infect. Dis. ACS Macro Lett. ACS Mater. Lett. ACS Med. Chem. Lett. ACS Nano ACS Omega ACS Photonics ACS Sens. ACS Sustainable Chem. Eng. ACS Synth. Biol. Anal. Chem. BIOCHEMISTRY-US Bioconjugate Chem. BIOMACROMOLECULES Chem. Res. Toxicol. Chem. Rev. Chem. Mater. CRYST GROWTH DES ENERG FUEL Environ. Sci. Technol. Environ. Sci. Technol. Lett. Eur. J. Inorg. Chem. IND ENG CHEM RES Inorg. Chem. J. Agric. Food. Chem. J. Chem. Eng. Data J. Chem. Educ. J. Chem. Inf. Model. J. Chem. Theory Comput. J. Med. Chem. J. Nat. Prod. J PROTEOME RES J. Am. Chem. Soc. LANGMUIR MACROMOLECULES Mol. Pharmaceutics Nano Lett. Org. Lett. ORG PROCESS RES DEV ORGANOMETALLICS J. Org. Chem. J. Phys. Chem. J. Phys. Chem. A J. Phys. Chem. B J. Phys. Chem. C J. Phys. Chem. Lett. Analyst Anal. Methods Biomater. Sci. Catal. Sci. Technol. Chem. Commun. Chem. Soc. Rev. CHEM EDUC RES PRACT CRYSTENGCOMM Dalton Trans. Energy Environ. Sci. ENVIRON SCI-NANO ENVIRON SCI-PROC IMP ENVIRON SCI-WAT RES Faraday Discuss. Food Funct. Green Chem. Inorg. Chem. Front. Integr. Biol. J. Anal. At. Spectrom. J. Mater. Chem. A J. Mater. Chem. B J. Mater. Chem. C Lab Chip Mater. Chem. Front. Mater. Horiz. MEDCHEMCOMM Metallomics Mol. Biosyst. Mol. Syst. Des. Eng. Nanoscale Nanoscale Horiz. Nat. Prod. Rep. New J. Chem. Org. Biomol. Chem. Org. Chem. Front. PHOTOCH PHOTOBIO SCI PCCP Polym. Chem.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
0
微信
客服QQ
Book学术公众号 扫码关注我们
反馈
×
意见反馈
请填写您的意见或建议
请填写您的手机或邮箱
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
现在去查看 取消
×
提示
确定
Book学术官方微信
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术
文献互助 智能选刊 最新文献 互助须知 联系我们:info@booksci.cn
Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。
Copyright © 2023 Book学术 All rights reserved.
ghs 京公网安备 11010802042870号 京ICP备2023020795号-1