Redox Active Metals and Metabolism

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (31 January 2022) | Viewed by 7634

Special Issue Editors


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Guest Editor
Department of Pediatrics, Neonatal-Perinatal Section, College of Medicine, University of Oklahoma Health Sciences Center, Oklahoma City, OK 73104, USA
Interests: metallomics; metabolomics; systems biology; oxidative stress; neurodevelopment; environmental exposures; mitochondria; maternal–fetal axis; developmental disorders

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Guest Editor
College of Pharmacy, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA
Interests: metal mixtures; immunology; autoimmunity; environmental health; community-engaged research and education

Special Issue Information

Dear Colleagues,

Redox active metals perform critical functions through regulatory, catalytic, and signaling roles. They are involved in many physiological processes such as defense against infectious agents; cellular signaling pathways, as cofactors for enzyme regulation; in redox signaling; and as structural components. Conversely, at high concentrations, redox active metals can be mediators of damage to biomolecules involving DNA, redox proteins, lipids, and metabolites.

Disturbed redox active metal homeostasis is implicated in the pathogenesis of multiple diseases that are not limited to amyotrophic lateral sclerosis (ALS), Alzheimer’s disease, Parkinson’s disease, ischemia heart disease, rheumatoid arthritis, cancer, diabetes, and inherited metabolic abnormalities. These diseases are governed by underlying metabolic and redox dysfunction that define the progression and or origin of disease. It is therefore critical to understand the molecular interface between redox active metals and metabolism in exposure, development, nutrition, health, immunity, aging, disease, and treatment strategies.

The aim of this Issue is to bring together cutting-edge research and new insights concerning the activity, control, and detection of redox active metals in the regulation of cell systems in physiological processes and pathological conditions. Experimental studies in humans and human relevant models, animal models, and in vitro studies are welcome. Review articles that describe new mechanisms; methodologies; modes of action; compartmental signaling events; systems biology; and omics approaches related to redox active metals, oxidative stress, and metabolism can also be submitted.

We look forward to your contributions!

Dr. Jolyn Fernandes
Dr. Esther O. Erdei
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Metals
  • Redox signaling
  • Metabolism
  • Antioxidants
  • Systems biology
  • Development
  • Nutrition
  • Toxicology
  • Immunology
  • Omics

Published Papers (2 papers)

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Research

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23 pages, 6136 KiB  
Article
In Vitro Enzymatic and Kinetic Studies, and In Silico Drug-Receptor Interactions, and Drug-Like Profiling of the 5-Styrylbenzamide Derivatives as Potential Cholinesterase and β-Secretase Inhibitors with Antioxidant Properties
by Malose J. Mphahlele, Emmanuel N. Agbo, Garland K. More and Samantha Gildenhuys
Antioxidants 2021, 10(5), 647; https://doi.org/10.3390/antiox10050647 - 22 Apr 2021
Cited by 6 | Viewed by 2106
Abstract
The 5-(styryl)anthranilamides were transformed into the corresponding 5-styryl-2-(p-tolylsulfonamido)benzamide derivatives. These 5-styrylbenzamide derivatives were evaluated through enzymatic assays in vitro for their capability to inhibit acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and β-secretase (BACE-1) activities as well as for antioxidant potential. An in vitro [...] Read more.
The 5-(styryl)anthranilamides were transformed into the corresponding 5-styryl-2-(p-tolylsulfonamido)benzamide derivatives. These 5-styrylbenzamide derivatives were evaluated through enzymatic assays in vitro for their capability to inhibit acetylcholinesterase (AChE), butyrylcholinesterase (BChE), and β-secretase (BACE-1) activities as well as for antioxidant potential. An in vitro cell-based antioxidant activity assay involving lipopolysaccharides (LPS)-induced reactive oxygen species (ROS) production revealed that compounds 2a and 3b have the capability of scavenging free radicals. The potential of the most active compound, 5-styrylbenzamide (2a), to bind copper (II) or zinc (II) ions has also been evaluated spectrophotometrically. Kinetic studies of the most active derivatives from each series against the AChE, BChE, and β-secretase activities have been performed. The experimental results are complemented with molecular docking studies into the active sites of these enzymes to predict the hypothetical protein–ligand binding modes. Their drug likeness properties have also been predicted. Full article
(This article belongs to the Special Issue Redox Active Metals and Metabolism)
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Review

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24 pages, 2470 KiB  
Review
Iron–Sulfur Cluster Biogenesis as a Critical Target in Cancer
by Michael S. Petronek, Douglas R. Spitz and Bryan G. Allen
Antioxidants 2021, 10(9), 1458; https://doi.org/10.3390/antiox10091458 - 14 Sep 2021
Cited by 16 | Viewed by 4672
Abstract
Cancer cells preferentially accumulate iron (Fe) relative to non-malignant cells; however, the underlying rationale remains elusive. Iron–sulfur (Fe–S) clusters are critical cofactors that aid in a wide variety of cellular functions (e.g., DNA metabolism and electron transport). In this article, we theorize that [...] Read more.
Cancer cells preferentially accumulate iron (Fe) relative to non-malignant cells; however, the underlying rationale remains elusive. Iron–sulfur (Fe–S) clusters are critical cofactors that aid in a wide variety of cellular functions (e.g., DNA metabolism and electron transport). In this article, we theorize that a differential need for Fe–S biogenesis in tumor versus non-malignant cells underlies the Fe-dependent cell growth demand of cancer cells to promote cell division and survival by promoting genomic stability via Fe–S containing DNA metabolic enzymes. In this review, we outline the complex Fe–S biogenesis process and its potential upregulation in cancer. We also discuss three therapeutic strategies to target Fe–S biogenesis: (i) redox manipulation, (ii) Fe chelation, and (iii) Fe mimicry. Full article
(This article belongs to the Special Issue Redox Active Metals and Metabolism)
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