Feature Papers in Oxygen Volume III

A special issue of Oxygen (ISSN 2673-9801).

Deadline for manuscript submissions: 31 March 2026 | Viewed by 1115

Special Issue Editor


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Guest Editor
School of Applied Sciences, University of the West of England, Bristol, UK
Interests: redox signaling; reactive oxygen species; hydrogen sulfide; hydrogen gas; nitric oxide
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Special Issue Information

Dear Colleagues,

We are delighted to organize Volume III of this Special Issue, entitled “Feature Papers in Oxygen Volume III”, especially given the success of Volume Ⅰ and Volume Ⅱ, which you can read here, along with other publications, free of charge:

https://www.mdpi.com/journal/oxygen/special_issues/Feature_Papers_Oxygen

https://www.mdpi.com/journal/oxygen/special_issues/D63219B609.

This Special Issue aims to emphasize the importance of this molecule in both chemistry and biology. Written by members of the Editorial Board and leading researchers in the field, articles will cover the recent research of some of these groups, whilst other manuscripts will take the form of reviews and opinion pieces. It is hoped that the ideas and thoughts raised here will inspire young researchers who are interested in the biology and chemistry of oxygen. Therefore, this SI should cover areas such as oxidative stress and redox in cells, the uses of oxygen in biological reactions, the role of oxygen-based molecules in cell signaling, the structure and reactivity of oxygen-based molecules, atmospheric and dissolved oxygen, and the ways in which oxygen can be used in industries and for medical therapies.

Prof. Dr. John T. Hancock
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. Oxygen is an international peer-reviewed open access quarterly 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 1000 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

  • chemical properties of oxygen
  • oxides
  • oxygen reduction reaction
  • reactive oxygen species and oxygen free radicals
  • antioxidants
  • chemical properties of oxides
  • redox reactions
  • uses of oxygen
  • diatomic oxygen

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Published Papers (1 paper)

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Review

23 pages, 1339 KB  
Review
Current State of Knowledge on Amiodarone (AMD)-Induced Reactive Oxygen Species (ROS) Production in In Vitro and In Vivo Models
by Konrad A. Szychowski
Oxygen 2025, 5(3), 16; https://doi.org/10.3390/oxygen5030016 - 26 Aug 2025
Viewed by 722
Abstract
Amiodarone (AMD) is an effective antiarrhythmic drug whose long-term use is limited by multi-organ toxicities linked to oxidative stress. This review synthesizes current evidence on how AMD induces reactive oxygen species (ROS) generation in vitro and in vivo, and the mechanistic pathways involved. [...] Read more.
Amiodarone (AMD) is an effective antiarrhythmic drug whose long-term use is limited by multi-organ toxicities linked to oxidative stress. This review synthesizes current evidence on how AMD induces reactive oxygen species (ROS) generation in vitro and in vivo, and the mechanistic pathways involved. AMD promotes ROS production through both direct and indirect mechanisms. Directly, AMD accumulates in mitochondria and impairs the electron transport chain, leading to electron leakage and superoxide formation. It also undergoes redox cycling, forming radical intermediates that trigger lipid peroxidation and deplete cellular antioxidants. AMD and its metabolites inhibit antioxidant enzymes (SOD, CAT, GPx) expression and/or activities and reduce glutathione level, compounding oxidative injury. Indirectly, AMD activates signaling pathways that exacerbate ROS generation. This compound can induce pro-inflammatory mediators such as TNF-α and modulate nuclear receptors such as AhR, PXR, CAR, and PPARs, altering the expression of metabolic enzymes and endogenous antioxidants. These processes are time- and dose-dependent: short exposures at low concentrations may transiently scavenge radicals, whereas chronic or higher-dose exposures consistently lead to net ROS accumulation. The oxidative effects of AMD vary by tissue and experimental models. In chronic models, organs such as the lung and liver show pronounced ROS-mediated injury, whereas acute or cell-based systems typically exhibit subtler changes. AMD-induced toxicity arises from multifactorial oxidative stress involving mitochondrial dysfunction, increased radical formation, depletion of antioxidant defenses, and activation of pro-oxidant signaling pathways. Recognizing these pathways suggests that antioxidant and mitochondria-targeted co-therapies could ameliorate the side effects of AMD. Full article
(This article belongs to the Special Issue Feature Papers in Oxygen Volume III)
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