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13.3
Journals
Oxygen
Special Issues
Feature Papers in Oxygen Volume III
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Feature Papers in Oxygen Volume III

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

Deadline for manuscript submissions: closed (31 March 2026) | Viewed by 7647

Special Issue Editor

Prof. Dr. John T. Hancock

E-Mail Website
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
Special Issues, Collections and Topics in MDPI journals

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 250 words) can be sent to the Editorial Office for assessment.

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 1200 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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Further information on MDPI's Special Issue policies can be found here.

Published Papers (4 papers)

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Research

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15 pages, 1452 KB  
Article
Mitophagy-Inducing Nanocarriers Restore Mitochondrial Quality and Cell Functions in Senescent Retinal Pigment Epithelial Cells
by Rinko Aso, Kohei Shibusawa, Sogo Aoki, Kiyoshi Sato and Hiroyoshi Kawakami
Oxygen 2026, 6(1), 1; https://doi.org/10.3390/oxygen6010001 - 25 Dec 2025
Viewed by 851
Abstract
Age-related macular degeneration (AMD) is an age-associated disease characterized by damage to the central retina and represents a leading cause of acquired blindness, with increasing prevalence in aging populations. However, effective therapeutic options remain limited. The accumulation of dysfunctional mitochondria in retinal pigment [...] Read more.
Age-related macular degeneration (AMD) is an age-associated disease characterized by damage to the central retina and represents a leading cause of acquired blindness, with increasing prevalence in aging populations. However, effective therapeutic options remain limited. The accumulation of dysfunctional mitochondria in retinal pigment epithelial (RPE) cells leads to excessive production of reactive oxygen species (ROS), triggering cellular senescence and cell death that contribute to the pathogenesis of AMD. Therefore, removal of accumulated dysfunctional mitochondria in senescent RPE cells is expected to treat AMD. Herein, we investigated transferrin (Trf)-modified mitophagy-inducing dual-drug nanocarriers (Trf-M-NCs) for the treatment of a senescent RPE cell. To evaluate efficacy, we used sodium iodate-treated ARPE-19 cells. The Trf-M-NCs exhibited significantly higher uptake by ARPE-19 cells than the unmodified M-NCs. Importantly, Trf-M-NC treatment alleviated cellular senescence by restoring the mitochondrial functions. Furthermore, Trf-M-NC treatment not only restored the production of α-ketoglutarate, an essential energy source for photoreceptor cells, but also reduced the secretion of IL-6, a key inflammatory cytokine. These findings suggest that improving mitochondrial quality in RPE cells is a novel and promising therapeutic approach for AMD. Full article
(This article belongs to the Special Issue Feature Papers in Oxygen Volume III)
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10 pages, 709 KB  
Article
Sex- and Age-Specific Trajectories of Hemoglobin and Aerobic Power in Competitive Youth Athletes
by Jonas Haferanke, Lisa Baumgartner, Maximilian Dettenhofer, Stefanie Huber, Frauke Mühlbauer, Tobias Engl, Renate Oberhoffer, Thorsten Schulz and Sebastian Freilinger
Oxygen 2025, 5(4), 25; https://doi.org/10.3390/oxygen5040025 - 22 Nov 2025
Cited by 1 | Viewed by 1597
Abstract
Maximal aerobic power (V̇O2peak) in youth depends on hemoglobin (Hb)—mediated oxygen transport. While sex- and age-specific patterns are established in untrained cohorts, further research is needed in competitive adolescent athletes. We studied 124 young athletes matched by age and sex (62 [...] Read more.
Maximal aerobic power (V̇O2peak) in youth depends on hemoglobin (Hb)—mediated oxygen transport. While sex- and age-specific patterns are established in untrained cohorts, further research is needed in competitive adolescent athletes. We studied 124 young athletes matched by age and sex (62 boys, 62 girls; 10–16 years). Hb was measured from fasting blood samples, and V̇O2peak was determined via cardiopulmonary exercise testing (CPET). Boys showed higher Hb than girls (14.43 ± 0.85 g/dL vs. 13.6 ± 0.74 g/dL; p < 0.001) and a significant age-related increase (B = 0.29, p < 0.001), whereas girls remained stable. V̇O2peak was also higher in boys (50.03 ± 6.18 mL/min/kg, p < 0.001). Regression analysis identified Hb as a strong predictor of V̇O2peak (β = 0.40, p < 0.001). These findings demonstrate that classical developmental Hb trajectories persist in highly trained youth and confirm Hb as a key determinant of aerobic power. Monitoring hematological status, particularly in female athletes, is essential for optimizing performance and development. Full article
(This article belongs to the Special Issue Feature Papers in Oxygen Volume III)
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Review

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115 pages, 4102 KB  
Review
Redox-Based Mechanisms of O2 Sensing in Hypoxic Pulmonary Vasoconstriction: Where Are We Now?
by Philip I. Aaronson, Jeremy P. T. Ward, Asuncion Rocher and Jesus Prieto-Lloret
Oxygen 2026, 6(1), 4; https://doi.org/10.3390/oxygen6010004 - 22 Feb 2026
Viewed by 1335
Abstract
Hypoxic pulmonary vasoconstriction (HPV) is a rapid and reversible constrictor response of the pulmonary vasculature, and especially its small muscular precapillary arteries, which is initiated by episodes of local alveolar hypoxia. Acting as a protective homeostatic vasomotor mechanism, HPV enables maximal gas exchange [...] Read more.
Hypoxic pulmonary vasoconstriction (HPV) is a rapid and reversible constrictor response of the pulmonary vasculature, and especially its small muscular precapillary arteries, which is initiated by episodes of local alveolar hypoxia. Acting as a protective homeostatic vasomotor mechanism, HPV enables maximal gas exchange by diverting blood from poorly ventilated alveoli into those rich in oxygen, thereby optimizing oxygen uptake and the ventilation–perfusion (V/Q) ratio so as to maintain the arterial oxygen partial pressure (PaO2) within the physiological range. HPV is an intrinsic mechanism of pulmonary artery smooth muscle cells (PASMCs), and requires an O2 sensor which acts through mediator(s) to trigger effector mechanisms within these cells to evoke constriction. Whereas HPV effector mechanisms are reasonably well defined, the nature of the O2 sensor and mediators remains in dispute, and a number of proposals have been developed to account for these. Some (but not all) of these share a focus on the concept that hypoxia activates effector mechanisms by inducing a change in the PASMC cytoplasmic redox state. Of these, the Redox Theory, first proposed by Kenneth Weir and Stephen Archer in 1995, proposes that hypoxia inhibits mitochondrial production of reactive oxygen species (ROS), thereby causing the cytoplasm to become more reduced. This inhibits ongoing vasorelaxation maintained by the opening of voltage-gated K+ channels. In contrast, according to the Mitochondrial ROS hypothesis, introduced by Paul Schumacker and Naveen Chandel in 2001, hypoxia increases mitochondrial ROS production, causing an oxidizing shift in the cytoplasmic redox state that activates several vasoconstricting pathways. In a third redox-based scenario, developed by Michael Wolin and Sachin Gupte, hypoxia evokes contraction by causing a fall in H2O2 production by NADPH oxidase and by activating the pentose phosphate pathway. These effects inhibit basal vasorelaxation maintained by the guanylate cyclase and protein kinase G and also stimulate vasoconstricting mechanisms. In this comprehensive review, we first provide a detailed summary of the key studies contributing to the development of these proposals and then subject the evidence supporting them to a critical appraisal, based in part on how well they accord with the wider literature and recent developments in our understanding of how cells shape and deploy redox mechanisms in order to regulate cell function. Full article
(This article belongs to the Special Issue Feature Papers in Oxygen Volume III)
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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
Cited by 7 | Viewed by 2982
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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