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Metal Ions in Health and Disease

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

Deadline for manuscript submissions: closed (30 November 2023) | Viewed by 3907

Special Issue Editor


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Guest Editor
School of Chemical Engineering, Faculty of Engineering, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece
Interests: bioinorganic chemistry; molecular engineering; hybrid materials; metallodrugs; cell (patho)physiologies; neurodegeneration; neoplastic process
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Special Issue Information

Dear Colleagues,

A plethora of metal ions exists in abiotic and biological systems, with prevalent cases involving essential inorganic cofactors in well-defined complex forms that are present in proteins and enzymes in humans. Such relevant human systems exhibit specificity with respect to the function and sustainability of physiology in cellular tissues and sensitive loci of the human body (e.g., the brain liver, pancreas, and other organs). Environmental pressure, originating from the exposure of humans to high concentrations of exogenous metal ions (including known environmental metallotoxins), formulates internal fluid and organ conditions that (a) promote aberrant interactions with (sub)cellular molecular targets and (b) lead to symptomatic pathologies (such as neurodegeneration and neoplasias). The impact of such metal ions on phenotypic changes is intimately associated with interactions involving low- and high-molecular-mass substrates, as well as targets at the protein and genomic levels. These types of interactions constitute the crux of the present effort to organize, evaluate, and collectively configure scientific knowledge geared toward providing insight into neurodegenerative and neoplastic molecular processes. Based on the premise that a select concentration of scientific advancements in this interdisciplinary field is anticipated to trigger further discussion, addressing metal ion biotoxicity and involvement in pathogenic pathways, diagnostics, and therapeutics, the herein announced Special Issue solicits aspiring contributions in chemistry, biology, medicine, and the interface of these fields, focusing on metal ions in neurodegenerative and/or neoplastic processes.

Prof. Dr. Athanasios Salifoglou
Guest Editor

Manuscript Submission Information

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Keywords

  • metallotoxins
  • metal-induced neurodegeneration
  • cancer
  • metal-induced reactivity
  • metal-gene interactions
  • metal-dependent oxidative stress
  • biotoxic metal ions and genomics
  • biotoxic metal ion proteomics

Published Papers (2 papers)

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28 pages, 3671 KiB  
Article
Iron(III) Complexes with Non-Steroidal Anti-Inflammatory Drugs: Structure, Antioxidant and Anticholinergic Activity, and Interaction with Biomolecules
by Filitsa Dimiza, Amalia Barmpa, Antonios Chronakis, Antonios G. Hatzidimitriou, Yiannis Sanakis, Athanasios N. Papadopoulos and George Psomas
Int. J. Mol. Sci. 2023, 24(7), 6391; https://doi.org/10.3390/ijms24076391 - 28 Mar 2023
Cited by 2 | Viewed by 1367
Abstract
One the main research goals of bioinorganic chemists is the synthesis of novel coordination compounds possessing biological potency. Within this context, three novel iron(III) complexes with the non-steroidal anti-inflammatory drugs diflunisal and diclofenac in the presence or absence of the nitrogen donors 1,10-phenanthroline [...] Read more.
One the main research goals of bioinorganic chemists is the synthesis of novel coordination compounds possessing biological potency. Within this context, three novel iron(III) complexes with the non-steroidal anti-inflammatory drugs diflunisal and diclofenac in the presence or absence of the nitrogen donors 1,10-phenanthroline or pyridine were isolated and characterized by diverse techniques. The complexes were evaluated for their ability to scavenge in vitro free radicals such as hydroxyl, 1,1-diphenyl-2-picrylhydrazyl and 2,2′-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid) radicals, revealing their selective potency towards hydroxyl radicals. The in vitro inhibitory activity of the complexes towards the enzymes acetylcholinesterase and butyrylcholinesterase was evaluated, and their potential to achieve neuroprotection appeared promising. The interaction of the complexes with calf-thymus DNA was examined in vitro, revealing their ability to intercalate in-between DNA nucleobases. The affinity of the complexes for serum albumins was evaluated in vitro and revealed their tight and reversible binding. Full article
(This article belongs to the Special Issue Metal Ions in Health and Disease)
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Review

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23 pages, 2037 KiB  
Review
Mechanisms of Cadmium Neurotoxicity
by Madelyn A. Arruebarrena, Calvin T. Hawe, Young Min Lee and Rachel C. Branco
Int. J. Mol. Sci. 2023, 24(23), 16558; https://doi.org/10.3390/ijms242316558 - 21 Nov 2023
Cited by 4 | Viewed by 2077
Abstract
Cadmium is a heavy metal that increasingly contaminates food and drink products. Once ingested, cadmium exerts toxic effects that pose a significant threat to human health. The nervous system is particularly vulnerable to prolonged, low-dose cadmium exposure. This review article provides an overview [...] Read more.
Cadmium is a heavy metal that increasingly contaminates food and drink products. Once ingested, cadmium exerts toxic effects that pose a significant threat to human health. The nervous system is particularly vulnerable to prolonged, low-dose cadmium exposure. This review article provides an overview of cadmium’s primary mechanisms of neurotoxicity. Cadmium gains entry into the nervous system via zinc and calcium transporters, altering the homeostasis for these metal ions. Once within the nervous system, cadmium disrupts mitochondrial respiration by decreasing ATP synthesis and increasing the production of reactive oxygen species. Cadmium also impairs normal neurotransmission by increasing neurotransmitter release asynchronicity and disrupting neurotransmitter signaling proteins. Cadmium furthermore impairs the blood–brain barrier and alters the regulation of glycogen metabolism. Together, these mechanisms represent multiple sites of biochemical perturbation that result in cumulative nervous system damage which can increase the risk for neurological and neurodegenerative disorders. Understanding the way by which cadmium exerts its effects is critical for developing effective treatment and prevention strategies against cadmium-induced neurotoxic insult. Full article
(This article belongs to the Special Issue Metal Ions in Health and Disease)
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