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Redox Modulation: New Trends, Biological and Therapeutical Implication

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Biochemistry".

Deadline for manuscript submissions: closed (31 March 2023) | Viewed by 17289

Special Issue Editor

Special Issue Information

Dear Colleagues,

Redox reactions are involved in several biochemical pathways, playing a key role in both physiological and pathological events. Redox equilibria in living systems, as well as the modulation of the redox signaling, are even more frequently studied as targets for a novel class of therapeutic compounds, and to explain the mechanism of several pathologies.

This special issue is leading by Dr. Claudio Santi and assisting by our Topical Advisory Panel Member Dr. Francesca Mangiavacchi (University of Perugia). All contributions focused in the field will be welcome by this special issue, with particular interest on the development of new redox modulators, and drugs acting via redox mechanisms. We will also appreciate new insights into the molecular mechanisms of redox enzymes and proteins, and their mimetics.

Topics include, but are not limited to:

  1. Antioxidants agents
  2. Pro-oxidant agents 
  3. System Thinking approach in Redox investigation(s)

Prof. Dr. Claudio Santi
Guest Editor

Manuscript Submission Information

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Keywords

  • ROS
  • oxygen
  • peroxides
  • radical reactions
  • antioxidant
  • enzyme inhibition
  • oxidative damnage
  • complexity
  • system thinking

Published Papers (6 papers)

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Research

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13 pages, 2420 KiB  
Article
Unraveling the Antioxidant Activity of 2R,3R-dihydroquercetin
by Yaping Xu, Zhengwen Li, Yue Wang, Chujie Li, Ming Zhang, Haiming Chen, Wenxue Chen, Qiuping Zhong, Jianfei Pei, Weijun Chen, Guido R. M. M. Haenen and Mohamed Moalin
Int. J. Mol. Sci. 2023, 24(18), 14220; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms241814220 - 18 Sep 2023
Cited by 1 | Viewed by 797
Abstract
It has been reported that in an oxidative environment, the flavonoid 2R,3R-dihydroquercetin (2R,3R-DHQ) oxidizes into a product that rearranges to form quercetin. As quercetin is a very potent antioxidant, much better than 2R,3R-DHQ, [...] Read more.
It has been reported that in an oxidative environment, the flavonoid 2R,3R-dihydroquercetin (2R,3R-DHQ) oxidizes into a product that rearranges to form quercetin. As quercetin is a very potent antioxidant, much better than 2R,3R-DHQ, this would be an intriguing form of targeting the antioxidant quercetin. The aim of the present study is to further elaborate on this targeting. We can confirm the previous observation that 2R,3R-DHQ is oxidized by horseradish peroxidase (HRP), with H2O2 as the oxidant. However, HPLC analysis revealed that no quercetin was formed, but instead an unstable oxidation product. The inclusion of glutathione (GSH) during the oxidation process resulted in the formation of a 2R,3R-DHQ-GSH adduct, as was identified using HPLC with IT-TOF/MS detection. GSH adducts appeared on the B-ring of the 2R,3R-DHQ quinone, indicating that during oxidation, the B-ring is oxidized from a catechol to form a quinone group. Ascorbate could reduce the quinone back to 2R,3R-DHQ. No 2S,3R-DHQ was detected after the reduction by ascorbate, indicating that a possible epimerization of 2R,3R-DHQ quinone to 2S,3R-DHQ quinone does not occur. The fact that no epimerization of the oxidized product of 2R,3R-DHQ is observed, and that GSH adducts the oxidized product of 2R,3R-DHQ on the B-ring, led us to conclude that the redox-modulating activity of 2R,3R-DHQ quinone resides in its B-ring. This could be confirmed by chemical calculation. Apparently, the administration of 2R,3R-DHQ in an oxidative environment does not result in ‘biotargeting’ quercetin. Full article
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14 pages, 2377 KiB  
Article
The Key Role of Chalcogenurane Intermediates in the Reduction Mechanism of Sulfoxides and Selenoxides by Thiols Explored In Silico
by Andrea Madabeni and Laura Orian
Int. J. Mol. Sci. 2023, 24(9), 7754; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24097754 - 24 Apr 2023
Cited by 1 | Viewed by 974
Abstract
Sulfoxides and selenoxides oxidize thiols to disulfides while being reduced back to sulfides and selenides. While the reduction mechanism of sulfoxides to sulfides has been thoroughly explored experimentally as well as computationally, less attention has been devoted to the heavier selenoxides. In this [...] Read more.
Sulfoxides and selenoxides oxidize thiols to disulfides while being reduced back to sulfides and selenides. While the reduction mechanism of sulfoxides to sulfides has been thoroughly explored experimentally as well as computationally, less attention has been devoted to the heavier selenoxides. In this work, we explore the reductive mechanism of dimethyl selenoxide, as an archetypal selenoxide and, for the sake of comparison, the reductive mechanism of dimethyl sulfoxide to gain insight into the role of the chalcogen on the reaction substrate. Particular attention is devoted to the key role of sulfurane and selenurane intermediates. Moreover, the capacity of these system to oxidize selenols rather than thiols, leading to the formation of selenyl sulfide bridges, is explored in silico. Notably, this analysis provides molecular insight into the role of selenocysteine in methionine sulfoxide reductase selenoenzyme. The activation strain model of chemical reactivity is employed in the studied reactions as an intuitive tool to bridge the computationally predicted effect of the chalcogen on the chalcogenoxide as well as on the chalcogenol. Full article
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Review

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39 pages, 6716 KiB  
Review
Antioxidant Metabolism Pathways in Vitamins, Polyphenols, and Selenium: Parallels and Divergences
by Celia María Curieses Andrés, José Manuel Pérez de la Lastra, Celia Andrés Juan, Francisco J. Plou and Eduardo Pérez-Lebeña
Int. J. Mol. Sci. 2024, 25(5), 2600; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms25052600 - 23 Feb 2024
Cited by 1 | Viewed by 688
Abstract
Free radicals (FRs) are unstable molecules that cause reactive stress (RS), an imbalance between reactive oxygen and nitrogen species in the body and its ability to neutralize them. These species are generated by both internal and external factors and can damage cellular lipids, [...] Read more.
Free radicals (FRs) are unstable molecules that cause reactive stress (RS), an imbalance between reactive oxygen and nitrogen species in the body and its ability to neutralize them. These species are generated by both internal and external factors and can damage cellular lipids, proteins, and DNA. Antioxidants prevent or slow down the oxidation process by interrupting the transfer of electrons between substances and reactive agents. This is particularly important at the cellular level because oxidation reactions lead to the formation of FR and contribute to various diseases. As we age, RS accumulates and leads to organ dysfunction and age-related disorders. Polyphenols; vitamins A, C, and E; and selenoproteins possess antioxidant properties and may have a role in preventing and treating certain human diseases associated with RS. In this review, we explore the current evidence on the potential benefits of dietary supplementation and investigate the intricate connection between SIRT1, a crucial regulator of aging and longevity; the transcription factor NRF2; and polyphenols, vitamins, and selenium. Finally, we discuss the positive effects of antioxidant molecules, such as reducing RS, and their potential in slowing down several diseases. Full article
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44 pages, 12852 KiB  
Review
Superoxide Anion Chemistry—Its Role at the Core of the Innate Immunity
by Celia María Curieses Andrés, José Manuel Pérez de la Lastra, Celia Andrés Juan, Francisco J. Plou and Eduardo Pérez-Lebeña
Int. J. Mol. Sci. 2023, 24(3), 1841; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms24031841 - 17 Jan 2023
Cited by 40 | Viewed by 7433
Abstract
Classically, superoxide anion O2•− and reactive oxygen species ROS play a dual role. At the physiological balance level, they are a by-product of O2 reduction, necessary for cell signalling, and at the pathological level they are considered harmful, as they [...] Read more.
Classically, superoxide anion O2•− and reactive oxygen species ROS play a dual role. At the physiological balance level, they are a by-product of O2 reduction, necessary for cell signalling, and at the pathological level they are considered harmful, as they can induce disease and apoptosis, necrosis, ferroptosis, pyroptosis and autophagic cell death. This revision focuses on understanding the main characteristics of the superoxide O2•−, its generation pathways, the biomolecules it oxidizes and how it may contribute to their modification and toxicity. The role of superoxide dismutase, the enzyme responsible for the removal of most of the superoxide produced in living organisms, is studied. At the same time, the toxicity induced by superoxide and derived radicals is beneficial in the oxidative death of microbial pathogens, which are subsequently engulfed by specialized immune cells, such as neutrophils or macrophages, during the activation of innate immunity. Ultimately, this review describes in some depth the chemistry related to O2•− and how it is harnessed by the innate immune system to produce lysis of microbial agents. Full article
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26 pages, 5849 KiB  
Review
Insights into Manganese Superoxide Dismutase and Human Diseases
by Mengfan Liu, Xueyang Sun, Boya Chen, Rongchen Dai, Zhichao Xi and Hongxi Xu
Int. J. Mol. Sci. 2022, 23(24), 15893; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms232415893 - 14 Dec 2022
Cited by 25 | Viewed by 3377
Abstract
Redox equilibria and the modulation of redox signalling play crucial roles in physiological processes. Overproduction of reactive oxygen species (ROS) disrupts the body’s antioxidant defence, compromising redox homeostasis and increasing oxidative stress, leading to the development of several diseases. Manganese superoxide dismutase (MnSOD) [...] Read more.
Redox equilibria and the modulation of redox signalling play crucial roles in physiological processes. Overproduction of reactive oxygen species (ROS) disrupts the body’s antioxidant defence, compromising redox homeostasis and increasing oxidative stress, leading to the development of several diseases. Manganese superoxide dismutase (MnSOD) is a principal antioxidant enzyme that protects cells from oxidative damage by converting superoxide anion radicals to hydrogen peroxide and oxygen in mitochondria. Systematic studies have demonstrated that MnSOD plays an indispensable role in multiple diseases. This review focuses on preclinical evidence that describes the mechanisms of MnSOD in diseases accompanied with an imbalanced redox status, including fibrotic diseases, inflammation, diabetes, vascular diseases, neurodegenerative diseases, and cancer. The potential therapeutic effects of MnSOD activators and MnSOD mimetics are also discussed. Targeting this specific superoxide anion radical scavenger may be a clinically beneficial strategy, and understanding the therapeutic role of MnSOD may provide a positive insight into preventing and treating related diseases. Full article
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36 pages, 2172 KiB  
Review
Aryl Hydrocarbon Receptor in Oxidative Stress as a Double Agent and Its Biological and Therapeutic Significance
by Alevtina Y. Grishanova and Maria L. Perepechaeva
Int. J. Mol. Sci. 2022, 23(12), 6719; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23126719 - 16 Jun 2022
Cited by 26 | Viewed by 3375
Abstract
The aryl hydrocarbon receptor (AhR) has long been implicated in the induction of a battery of genes involved in the metabolism of xenobiotics and endogenous compounds. AhR is a ligand-activated transcription factor necessary for the launch of transcriptional responses important in health and [...] Read more.
The aryl hydrocarbon receptor (AhR) has long been implicated in the induction of a battery of genes involved in the metabolism of xenobiotics and endogenous compounds. AhR is a ligand-activated transcription factor necessary for the launch of transcriptional responses important in health and disease. In past decades, evidence has accumulated that AhR is associated with the cellular response to oxidative stress, and this property of AhR must be taken into account during investigations into a mechanism of action of xenobiotics that is able to activate AhR or that is susceptible to metabolic activation by enzymes encoded by the genes that are under the control of AhR. In this review, we examine various mechanisms by which AhR takes part in the oxidative-stress response, including antioxidant and prooxidant enzymes and cytochrome P450. We also show that AhR, as a participant in the redox balance and as a modulator of redox signals, is being increasingly studied as a target for a new class of therapeutic compounds and as an explanation for the pathogenesis of some disorders. Full article
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