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Antioxidants
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Blood Cells and Redox Homeostasis in Health and Disease, 2nd...
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Blood Cells and Redox Homeostasis in Health and Disease, 2nd Edition

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: 10 September 2025 | Viewed by 3281

Special Issue Editors

Prof. Dr. Angelo D'Alessandro

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Guest Editor
Department of Biochemistry and Molecular Genetics, University of Colorado Denver, Anschutz Medical Campus, Aurora, CO 80045, USA
Interests: blood cells; hypoxia; metabolism; cancer metabolism; trauma; ageing; hemoglobinopathies; transfusion medicine; omics markers
Special Issues, Collections and Topics in MDPI journals
Dr. Alkmini T. Anastasiadi

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Guest Editor Assistant
Department of Biochemistry, School of Medicine, University of Patras, 26504 Patras, Greece
Interests: red blood cells; redox biology; red blood cell metabolism; storage lesion; extracellular vesicles; donor variation effect; transfusion medicine; hemoglobinopathies

Special Issue Information

Dear Colleagues,

The interplay between blood cells and redox homeostasis is crucial in maintaining cellular health and preventing disease. Redox balance, which involves the regulation of reactive oxygen species (ROS) and antioxidant defenses, is essential to proper blood cell function and overall physiological stability. Disruptions to this balance can lead to a variety of health issues, including cardiovascular diseases, cancer, and neurodegenerative disorders.

This Special Issue, "Blood Cells and Redox Homeostasis in Health and Disease, 2nd Edition", builds on the insights provided by its predecessor, the 1st Edition, which set a strong foundation by addressing key aspects of how blood cells contribute to redox regulation and the consequences of dysregulation.

This second edition will continue this exploration with updated research and new perspectives. It will delve into the latest advancements in understanding the mechanisms by which blood cells manage oxidative stress and the resulting implications for various diseases. By expanding on the groundwork laid by the first edition, this Special Issue will enhance our comprehension of blood cells' roles in redox homeostasis and will advance diagnostic and therapeutic approaches.

Prof. Dr. Angelo D'Alessandro
Dr. Alkmini T. Anastasiadi
Guest Editors

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

  • blood
  • redox status
  • antioxidants
  • oxidative stress
  • redox therapy
  • oxidative stress biomarkers

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Published Papers (3 papers)

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Research

18 pages, 4846 KiB  
Article
The Nrf2 Activator CDDO-Imidazole Suppresses Inflammation-Induced Red Blood Cell Alloimmunization
by Che-Yu Chang, Rosario Hernández-Armengol, Kausik Paul, June Young Lee, Karina Nance, Tomohiro Shibata, Peibin Yue, Christian Stehlik and David R. Gibb
Antioxidants 2025, 14(6), 678; https://doi.org/10.3390/antiox14060678 - 3 Jun 2025
Viewed by 194
Abstract
Experimental Objective: During red blood cell (RBC) transfusion, inflammation promotes the production of anti-RBC alloantibodies that can cause significant hemolytic events. Avoiding RBC antigen exposure is the only strategy to prevent RBC alloimmunization in transfusion recipients. Identifying mechanisms that inhibit alloimmunization may lead [...] Read more.
Experimental Objective: During red blood cell (RBC) transfusion, inflammation promotes the production of anti-RBC alloantibodies that can cause significant hemolytic events. Avoiding RBC antigen exposure is the only strategy to prevent RBC alloimmunization in transfusion recipients. Identifying mechanisms that inhibit alloimmunization may lead to novel prophylactic interventions. One potential regulatory mechanism is the activation of the transcription factor nuclear factor erythroid-derived 2-like 2 (Nrf2), a master regulator of antioxidant pathways. Pharmacologic Nrf2 activators induce antioxidant production and improve the sequelae of inflammatory diseases. Thus, we tested the hypothesis that a Nrf2 activator, 1-[2-cyano-3-,12-dioxooleana-1,9(11)-dien-28-oyl]-imidazole (CDDO-Im), regulates inflammation-induced RBC alloimmunization. Methods: WT and Nrf2-deficient mice were treated with inflammatory stimuli and CDDO-Im prior to transfusion with RBCs expressing the KEL antigen (KEL+ RBCs). Anti-KEL IgM and IgG were measured in the serum of transfused mice. Nrf2-activated gene expression and interferon activity were measured in mice and human macrophages pre-treated with CDDO-Im and interferon stimuli. Results: Here, we report that CDDO-Im induces Nrf2-activated gene expression and inhibits type 1 interferon activity, which promotes RBC alloimmunization in transfusion models. In mice transfused with KEL+ RBCs, pre-treatment with CDDO-Im inhibited inflammation-induced anti-KEL antibody production and increased the post-transfusion recovery of KEL+ RBCs in a Nrf2-dependent manner. CDDO-Im also inhibited RBC alloimmunization in mice with pre-existing inflammation. Conclusions: These results indicate that the activation of the Nrf2 antioxidant pathway regulates RBC alloimmunization to the KEL antigen in a pre-clinical model. If these findings translate to other models and human studies, Nrf2 activators may represent a potential prophylactic intervention to inhibit alloimmunization. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease, 2nd Edition)
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13 pages, 2887 KiB  
Article
Role of Reactive Oxygen Species in Collagen-Induced Platelet Activation and the Protective Effects of Antioxidants
by Jin-Yi Han, Hideo Utsumi and Han-Young Chung
Antioxidants 2025, 14(4), 497; https://doi.org/10.3390/antiox14040497 - 20 Apr 2025
Viewed by 488
Abstract
Collagen plays a crucial role in platelet activation and thrombosis, yet the underlying mechanisms involving reactive oxygen species (ROS) remain incompletely understood. This study investigated how collagen modulates ROS generation and platelet aggregation both in vitro and in vivo, as well as evaluating [...] Read more.
Collagen plays a crucial role in platelet activation and thrombosis, yet the underlying mechanisms involving reactive oxygen species (ROS) remain incompletely understood. This study investigated how collagen modulates ROS generation and platelet aggregation both in vitro and in vivo, as well as evaluating the protective effects of antioxidants. In vitro, collagen induced dose-dependent platelet aggregation and increased ROS generation, evidenced by the enhanced EMPO adduct formation detected via electron spin resonance (ESR). In vivo experiments demonstrated that collagen administration significantly accelerated CAT-1 decay, indicating elevated oxidative stress with a transient peak around 1 minute post-treatment. Furthermore, escalating collagen doses correlated with increased ROS generation and reduced survival rates in mice, underscoring collagen’s impact on oxidative stress and thrombosis severity. Importantly, treatment with enzymatic antioxidants (superoxide dismutase, catalase) and non-enzymatic antioxidants (DMTU, Tiron, mannitol) significantly attenuated collagen-induced oxidative stress and improved animal survival. Collectively, these findings elucidate the pivotal role of ROS in collagen-induced platelet activation and thrombosis and highlight antioxidants as promising therapeutic candidates for preventing thrombotic disorders and managing cardiovascular risk. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease, 2nd Edition)
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17 pages, 1714 KiB  
Article
Modulation of Antioxidant Enzyme Expression of In Vitro Culture-Derived Reticulocytes
by Hannah D. Langlands, Deborah K. Shoemark and Ashley M. Toye
Antioxidants 2024, 13(9), 1070; https://doi.org/10.3390/antiox13091070 - 2 Sep 2024
Cited by 2 | Viewed by 1970
Abstract
The regulation of reactive oxygen species (ROS) in red blood cells (RBCs) is crucial for maintaining functionality and lifespan. Indeed, dysregulated ROS occurs in haematological diseases such as sickle cell disease and β-thalassaemia. In order to combat this, RBCs possess high levels of [...] Read more.
The regulation of reactive oxygen species (ROS) in red blood cells (RBCs) is crucial for maintaining functionality and lifespan. Indeed, dysregulated ROS occurs in haematological diseases such as sickle cell disease and β-thalassaemia. In order to combat this, RBCs possess high levels of protective antioxidant enzymes. We aimed to further boost RBC antioxidant capacity by overexpressing peroxiredoxin (Prxs) and glutathione peroxidase (GPxs) enzymes. Multiple antioxidant enzyme cDNAs were individually overexpressed in expanding immortalised erythroblasts using lentivirus, including Prx isoforms 1, 2, and 6 and GPx isoforms 1 and 4. Enhancing Prx protein expression proved straightforward, but GPx overexpression required modifications. For GPx4, these modifications included adding a SECIS element in the 3’UTR, the removal of a mitochondrial-targeting sequence, and removing putative ubiquitination sites. Culture-derived reticulocytes exhibiting enhanced levels of Prx and GPx antioxidant proteins were successfully engineered, demonstrating a novel approach to improve RBC resilience to oxidative stress. Further work is needed to explore the activity of these proteins and their impact on RBC metabolism, but this strategy shows promise for improving RBC function in physiological and pathological contexts and during storage for transfusion. Enhancing the antioxidant capacity of reticulocytes has exciting promise for developing culture-derived RBCs with enhanced resistance to oxidative damage and offers new therapeutic interventions in diseases with elevated oxidative stress. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease, 2nd Edition)
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