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Antioxidants
Special Issues
Zinc and Oxidative Stress
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Zinc and Oxidative Stress

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 4778

Special Issue Editor

Prof. Dr. Irina G. Gazaryan

E-Mail Website
Guest Editor
Department of Chemistry and Physical Sciences, Dyson College of Art and Sciences, Pace University, 861 Bedford Road, Pleasantville, NY 10570, USA
Interests: enzyme mechanisms; hypoxia; oxidative stress; reporter assay; drug discovery

Special Issue Information

Dear Colleagues,

Zinc is an important mineral supplement and has been recently recommended for patiens infected with COVID-19 as a booster of the immune response. Zinc can be found in the active site of many enzymes and is also a major component of one class of transcription factors; however, zinc may target and inactivate the enzymes and proteins that contain redox active cysteine or selenocysteine residues. Such enzymes and proteins are involved in the antioxidant defense; hence, free zinc may exacerbate the oxidative damage to the cell. Excess zinc is known to be harmful for patients with neurodegeneration and to be beneficial for cancer patients. Whether zinc released from metallothioneines during oxidative stress can directly trigger the antioxidant program executed by Nrf2 - remains an open question. The molecular mechanisms behind the panoply of zinc effects still await their resolution.

For this Special Issue, we invite researchers to provide original research articles that report on the mechanism of zinc interaction with various cellular targets, such as individual proteins and organelles, and its potential for the treatment of conditions linked to oxidative stress. The interplay between calicum/zinc and iron/zinc in various
scenarios of oxidative damage is of particular interest. Review articles discussing the current state of the art in the field of novel targets and mechanisms of zinc effects at the cellular and organismal levels are also welcome.

Prof. Dr. Irina G. Gazaryan
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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

  • redox enzymes
  • thiols and selenothiols
  • Zn-enzymes
  • antioxidant program
  • ferroptosis
  • cancer
  • neurodegeneration

Published Papers (2 papers)

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Research

19 pages, 5909 KiB  
Article
The Inhibition of Zinc Excitotoxicity and AMPK Phosphorylation by a Novel Zinc Chelator, 2G11, Ameliorates Neuronal Death Induced by Global Cerebral Ischemia
by Dae Ki Hong, Jae-Won Eom, A Ra Kho, Song Hee Lee, Beom Seok Kang, Si Hyun Lee, Jae-Young Koh, Yang-Hee Kim, Bo Young Choi and Sang Won Suh
Antioxidants 2022, 11(11), 2192; https://doi.org/10.3390/antiox11112192 - 5 Nov 2022
Cited by 5 | Viewed by 1754
Abstract
AMP-activated protein kinase (AMPK) is necessary for maintaining a positive energy balance and essential cellular processes such as glycolysis, gene transcription, glucose uptake, and several other biological functions. However, brain injury-induced energy and metabolic stressors, such as cerebral ischemia, increase AMPK phosphorylation. Phosphorylated [...] Read more.
AMP-activated protein kinase (AMPK) is necessary for maintaining a positive energy balance and essential cellular processes such as glycolysis, gene transcription, glucose uptake, and several other biological functions. However, brain injury-induced energy and metabolic stressors, such as cerebral ischemia, increase AMPK phosphorylation. Phosphorylated AMPK contributes to excitotoxicity, oxidative, and metabolic problems. Furthermore, brain disease-induced release of zinc from synaptic vesicles contributes to neuronal damage via mechanisms including ROS production, apoptotic cell death, and DNA damage. For this reason, we hypothesized that regulating zinc accumulation and AMPK phosphorylation is critical for protection against global cerebral ischemia (GCI). Through virtual screening based on the structure of AMPK subunit alpha 2, we identified a novel compound, 2G11. In this study, we verified that 2G11 administration has neuroprotective effects via the blocking of zinc translocation and AMPK phosphorylation after GCI. As a result, we demonstrated that 2G11 protected hippocampal neurons against GCI and OGD/R-derived cellular damage. In conclusion, we propose that AMPK inhibition and zinc chelation by 2G11 may be a promising tool for preventing GCI-induced hippocampal neuronal death. Full article
(This article belongs to the Special Issue Zinc and Oxidative Stress)
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21 pages, 4587 KiB  
Article
Increased Mobile Zinc Regulates Retinal Ganglion Cell Survival via Activating Mitochondrial OMA1 and Integrated Stress Response
by Jiahui Tang, Zhe Liu, Jiaxu Han, Jingfei Xue, Liyan Liu, Jicheng Lin, Caiqing Wu, Qi Zhang, Siting Wu, Canying Liu, Haishun Huang, Yuanyuan Fu, Min Li, Yehong Zhuo and Yiqing Li
Antioxidants 2022, 11(10), 2001; https://doi.org/10.3390/antiox11102001 - 10 Oct 2022
Cited by 9 | Viewed by 2586
Abstract
Retinal ganglion cells (RGCs), the projection neurons of the eye, are irreversibly lost once the optic nerve is injured, which is a critical mechanism of glaucoma. Mobile zinc (Zn2+) levels rapidly increase in retinal interneuron amacrine cells and Zn2+ is [...] Read more.
Retinal ganglion cells (RGCs), the projection neurons of the eye, are irreversibly lost once the optic nerve is injured, which is a critical mechanism of glaucoma. Mobile zinc (Zn2+) levels rapidly increase in retinal interneuron amacrine cells and Zn2+ is then transferred to RGCs via the Zn2+ transporter protein ZnT-3, triggering RGC loss in optic nerve injury. Zn2+ chelation and ZnT-3 deletion promote long-term RGC survival. However, the downstream signaling pathways of Zn2+ in RGCs remains unknown. Here, we show that increased levels of Zn2+ upregulate the expression and activity of mitochondrial zinc metallopeptidase OMA1 in the retina, leading to the cleavage of DELE1 and activation of cytosolic eIF2α kinase PKR, triggering the integrated stress response (ISR) in RGCs. Our study identified OMA1 and ISR as the downstream molecular mechanisms of retinal Zn2+ and potential targets for preventing the progression of Zn2+-associated neuronal damage. Full article
(This article belongs to the Special Issue Zinc and Oxidative Stress)
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