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Antioxidants
Special Issues
Oxidative Stress in Hemoglobin and Red Blood Cells
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Oxidative Stress in Hemoglobin and Red Blood Cells

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 (31 March 2025) | Viewed by 2311

Special Issue Editor

Dr. David Baron

E-Mail Website
Guest Editor
Department of Anesthesia, General Intensive Care, and Pain Management, Medical University of Vienna, 1090 Vienna, Austria
Interests: oxidative stress; transfusion; anemia; red blood cells/erythrocytes; hemoglobin; intensive care medicine/critical care medicine; trauma; hematology

Special Issue Information

Dear Colleagues,

Oxidative stress has a multitude of effects on the physiology of hemoglobin and red blood cells, with profound consequences for both health and disease. Hemoglobin, the protein responsible for oxygen transport in the blood, is highly susceptible to oxidative damage due to its constant exposure to oxygen and reactive oxygen species. Exposure to oxidative stress can induce various molecular and structural alterations in red blood cells, thereby compromising their function. This oxidative damage not only impairs the oxygen-carrying capacity of red blood cells, but also triggers a cascade of cellular responses, including inflammation and cell death. Furthermore, oxidative stress in red blood cells can exacerbate conditions such as anemia, cardiovascular disease, and even accelerate the ageing process in vivo and during storage. Understanding the mechanisms underlying oxidative stress in hemoglobin and red blood cells is crucial for developing targeted interventions that mitigate its harmful effects and improve overall health outcomes. This Special Issue is focused on the effects of oxidative stress on red blood cells and hemoglobin. We will consider in vitro, translational and clinical studies from all (bio)medical fields. Through this collection of studies, our aim is to promote a deeper understanding of the complex mechanisms underlying oxidative stress in hemoglobin and red blood cells, providing insights that may pave the way for future therapeutic interventions and medical advances.

Dr. David Baron
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

  • oxidative stress
  • transfusion
  • red blood cells/erythrocytes
  • hemoglobin
  • hematology

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Published Papers (3 papers)

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Research

17 pages, 2932 KiB  
Article
Time Course of Plasma Proteomic and Oxylipin Changes Induced by LPS Challenge and Modulated by Antioxidant Supplementation in a Randomized Controlled Trial
by Gerhard Hagn, Andrea Bileck, Thomas Mohr, Doreen Schmidl, David M. Baron, Bernd Jilma, Leopold Schmetterer, Gerhard Garhöfer and Christopher Gerner
Antioxidants 2025, 14(5), 536; https://doi.org/10.3390/antiox14050536 - 29 Apr 2025
Viewed by 60
Abstract
Systemic molecular responses to pathogen-associated molecular patterns and their modulation by antioxidants are poorly understood in humans. Here, we present a two-stage clinical interventional study in healthy humans challenged with lipopolysaccharide. In the first step, the kinetics of inflammatory modulators within 8 h [...] Read more.
Systemic molecular responses to pathogen-associated molecular patterns and their modulation by antioxidants are poorly understood in humans. Here, we present a two-stage clinical interventional study in healthy humans challenged with lipopolysaccharide. In the first step, the kinetics of inflammatory modulators within 8 h were investigated by plasma proteomics and lipidomics. In a second step, the effects of a placebo-controlled antioxidant intervention on the individual responses prior to another lipopolysaccharide challenge were determined. Plasma proteomics revealed an early involvement of the endothelium and platelets, followed by the induction of liver-derived acute phase proteins and an innate immune cell response. Untargeted lipidomics revealed an early release of fatty acids and taurocholic acid, followed by complex regulatory events exerted by oxylipins. The consistent lipopolysaccharide-induced downregulation of lysophospholipids suggested the involvement of the Lands cycle, and the downregulation of deoxycholic acid reinforced emerging links between the inflammasome and bile acids. Groups of molecules with similar kinetics to lipopolysaccharide challenge were observed to share precursors, synthesizing enzymes or cellular origin. Dietary antioxidant supplementation prior to lipopolysaccharide challenge had no detectable effect on protein kinetics but significantly downregulated pro-inflammatory sphingosine-1-phosphate and increased levels of oxylipins, 20-HEPE, and 22-HDoHE, which have been described to facilitate the resolution of inflammation. The present study identified a complex network of lipid mediators deregulated in plasma upon lipopolysaccharide challenge and highlighted the role of platelets, endothelial cells, and erythrocytes as potential inflammatory modulators. While dietary antioxidant supplementation hardly affected the initiation of inflammation, it may exert its effects supporting the resolution of inflammation. Full article
(This article belongs to the Special Issue Oxidative Stress in Hemoglobin and Red Blood Cells)
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22 pages, 25466 KiB  
Article
Oxidative Stress and Cytoskeletal Reorganization in Hypertensive Erythrocytes
by Ivette Martínez-Vieyra, Isaac Hernández-Rojo, Víctor Hugo Rosales-García, Aracely Evangelina Chávez-Piña and Doris Cerecedo
Antioxidants 2025, 14(1), 5; https://doi.org/10.3390/antiox14010005 - 24 Dec 2024
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Abstract
Oxidative stress is widely recognized as a key mechanism in the development of hypertension. Under pathological conditions, such as in hypertension, oxidative stress leads to irreversible posttranslational modifications of proteins, which result in loss of protein function and cellular damage. We have previously [...] Read more.
Oxidative stress is widely recognized as a key mechanism in the development of hypertension. Under pathological conditions, such as in hypertension, oxidative stress leads to irreversible posttranslational modifications of proteins, which result in loss of protein function and cellular damage. We have previously documented physiological and morphological changes across various blood and bone marrow cell lineages, all of which exhibit elevated oxidative stress. While cytoskeletal changes in erythrocytes have been well characterized in hereditary diseases, this is the first study, to our knowledge, to investigate cytoskeletal reorganization in erythrocytes from hypertensive patients. To this end, we compared the expression patterns and subcellular distribution of key cytoskeletal proteins in erythrocytes from hypertensive individuals with those from normotensive subjects using Western blot, flow cytometry, and confocal microscopy. Our results revealed the presence of three erythrocyte subpopulations with differential expression of glycophorin A. The persistent oxidative environment in hypertensive patients causes dysregulation in the expression of glycophorin A, Band 3 protein, protein 4.1, and ankyrin, as well as the reorganization of spectrin. These alterations in protein expression and distribution suggest that oxidative stress in hypertensive individuals may induce structural modifications, ultimately impairing erythrocyte membrane elasticity and function. Full article
(This article belongs to the Special Issue Oxidative Stress in Hemoglobin and Red Blood Cells)
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13 pages, 1576 KiB  
Article
Increased Adhesiveness of Blood Cells Induced by Mercury Chloride: Protective Effect of Hydroxytyrosol
by Pasquale Perrone, Raquel Ortega-Luna, Caterina Manna, Ángeles Álvarez-Ribelles and Victor Collado-Diaz
Antioxidants 2024, 13(12), 1576; https://doi.org/10.3390/antiox13121576 - 20 Dec 2024
Cited by 1 | Viewed by 803
Abstract
Mercury (Hg) is a highly toxic environmental contaminant that can harm human health, ultimately leading to endothelial dysfunction. Hg toxicity is partially mediated by the exposure of the cell membrane’s surface of erythrocytes (RBCs) to phosphatidylserine (PS). In the context of these challenges, [...] Read more.
Mercury (Hg) is a highly toxic environmental contaminant that can harm human health, ultimately leading to endothelial dysfunction. Hg toxicity is partially mediated by the exposure of the cell membrane’s surface of erythrocytes (RBCs) to phosphatidylserine (PS). In the context of these challenges, hydroxytyrosol, a phenolic compound of olive oil, has the ability to mitigate the toxic effects of Hg. This study aims to analyze the effect of Hg on the adhesion of RBCs and polymorphonuclear cells (PMNs) to the vascular endothelium and the potential protective effect of hydroxytyrosol, as these interactions are crucial in the development of cardiovascular diseases (CVDs). RBCs, PMNs, and human vein endothelial cells (HUVECs) were treated with increasing concentrations of HgCl2 and, in some cases, with hydroxytyrosol, and their adhesion to HUVECs and the expression of adhesion molecules were subsequently analyzed. Our results demonstrate that HgCl2 significantly increases the adhesion of both RBCs (2.72 ± 0.48 S.E.M., p-value < 0.02) and PMNs (11.19 ± 1.96 S.E.M., p-value < 0.05) to HUVECs and that their adhesiveness is significantly reduced following treatment with hydroxytyrosol (RBCs, 1.2 ± 1.18 S.E.M., p-value < 0.02 and PMNs, 4.04 ± 1.35 S.E.M., p-value < 0.06). Interestingly, HgCl2 does not alter the expression of adhesion molecules on either HUVECs or RBCs, suggesting that reduced exposure to PS is a key factor in hydroxytyrosol protection against HgCl2-induced RBC adhesion to the endothelium. On the other hand, HgCl2 induces increased expression of several PMN adhesion molecules (CD11b 215.4 ± 30.83 S.E.M. p-value < 0.01), while hydroxytyrosol inhibits their expression (e.g., CD11b 149 ± 14.35 S.E.M., p-value < 0.03), which would seem to be the mechanism by which hydroxytyrosol restricts PMN–endothelium interactions. These results provide new insights into the molecular mechanisms through which hydroxytyrosol mitigates the harmful effects of Hg on cardiovascular health, highlighting its potential as a therapeutic agent that can reduce the cardiovascular risk related to heavy metal exposure. Full article
(This article belongs to the Special Issue Oxidative Stress in Hemoglobin and Red Blood Cells)
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