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Antioxidants
Special Issues
Blood Cells and Redox Homeostasis in Health and Disease
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Blood Cells and Redox Homeostasis in Health and Disease

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 July 2024 | Viewed by 8666

Special Issue Editors

Prof. Dr. Angelo D'Alessandro

E-Mail Website
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

E-Mail Website
Guest Editor Assistant
Laboratory of Reliability and Quality Control in Laboratory Hematology (HemQcR), Department of Biomedical Sciences, School of Health and Welfare Sciences, University of West Attica (UniWA), 122 43 Egaleo, 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 Colleague,

In several pathophysiological conditions, oxidative stress leads to the impairment of the functionality of blood cells and the emergence of oxidative markers. At the same time, the formed elements of blood are equipped with antioxidant systems and contribute to the balance of several molecules with antioxidant potential in plasma. Redox balance lies at the core of cellular and systems homeostasis and is maintained by a network of intertwined pathways, with a key cross-talk process between energy and redox metabolism, organelle biology, and proteostasis. The redox equilibrium is known to regulate and affect hematopoiesis, the immunometabolism of white blood cells, and red cell functions, among others; therefore, fluctuations in the blood cell redox status contribute to the etiopathology of several diseases, or represent early markers of pathological states. Understanding how oxidative stress impacts blood cell physiology and functionality is crucial to identify novel biomarkers and intervenable mechanisms for promising new therapies in many diseases. Moreover, several currently available iatrogenic and pharmacological interventions alter the oxidative status of blood cells, contributing to the complex puzzle of blood cells and redox homeostasis in health and disease.

This Special Issue aims to gather contributions that enhance our knowledge regarding the redox-related features of blood components and the impact of blood redox disequilibrium on pathophysiological backgrounds.

Potential topics include, but are not limited to, the following:

  • Oxidative stress and hematopoiesis;
  • Blood redox parameters in disease states;
  • Oxidation and antioxidant systems in mitochondria-devoid, iron and oxygen-loaded red blood cells;
  • Role of oxidative stress and redox systems in platelet activation and coagulopathy;
  • Role of hypoxia in mitochondrial oxidant stress in the etiopathology of diseases;
  • Role of iatrogenic (e.g., blood storage; extracorporeal membrane oxygenation) or other exposures (e.g., exercise, smoking, etc.) in oxidant stress generation and mitigation in blood cells;
  • Effect of xenometabolites (including bacterial metabolites or drugs, e.g., common chemotherapeutic agents) on blood cell redox status;
  • Redox therapies, including novel drug delivery systems;
  • Role of aging and inflammation in blood cell oxidant stress.

Prof. Dr. Angelo D'Alessandro
Guest Editor

Dr. Alkmini T. Anastasiadi
Guest Editor Assistant

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

Published Papers (7 papers)

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Research

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21 pages, 3634 KiB  
Article
Nrf2 Plays a Key Role in Erythropoiesis during Aging
by Serge Cedrick Toya Mbiandjeu, Angela Siciliano, Alessandro Mattè, Enrica Federti, Massimiliano Perduca, Davide Melisi, Immacolata Andolfo, Angela Amoresano, Achille Iolascon, Maria Teresa Valenti, Francesco Turrini, Michele Bovi, Arianna Pisani, Antonio Recchiuti, Domenico Mattoscio, Veronica Riccardi, Luca Dalle Carbonare, Carlo Brugnara, Narla Mohandas and Lucia De Franceschi
Antioxidants 2024, 13(4), 454; https://doi.org/10.3390/antiox13040454 - 12 Apr 2024
Viewed by 487
Abstract
Aging is characterized by increased oxidation and reduced efficiency of cytoprotective mechanisms. Nuclear factor erythroid-2-related factor (Nrf2) is a key transcription factor, controlling the expression of multiple antioxidant proteins. Here, we show that Nrf2−/− mice displayed an age-dependent anemia, due to the [...] Read more.
Aging is characterized by increased oxidation and reduced efficiency of cytoprotective mechanisms. Nuclear factor erythroid-2-related factor (Nrf2) is a key transcription factor, controlling the expression of multiple antioxidant proteins. Here, we show that Nrf2−/− mice displayed an age-dependent anemia, due to the combined contributions of reduced red cell lifespan and ineffective erythropoiesis, suggesting a role of Nrf2 in erythroid biology during aging. Mechanistically, we found that the expression of antioxidants during aging is mediated by activation of Nrf2 function by peroxiredoxin-2. The absence of Nrf2 resulted in persistent oxidation and overactivation of adaptive systems such as the unfolded protein response (UPR) system and autophagy in Nrf2−/− mouse erythroblasts. As Nrf2 is involved in the expression of autophagy-related proteins such as autophagy-related protein (Atg) 4-5 and p62, we found impairment of late phase of autophagy in Nrf2−/− mouse erythroblasts. The overactivation of the UPR system and impaired autophagy drove apoptosis of Nrf2−/− mouse erythroblasts via caspase-3 activation. As a proof of concept for the role of oxidation, we treated Nrf2−/− mice with astaxanthin, an antioxidant, in the form of poly (lactic-co-glycolic acid) (PLGA)-loaded nanoparticles (ATS-NPs) to improve its bioavailability. ATS-NPs ameliorated the age-dependent anemia and decreased ineffective erythropoiesis in Nrf2−/− mice. In summary, we propose that Nrf2 plays a key role in limiting age-related oxidation, ensuring erythroid maturation and growth during aging. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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14 pages, 2942 KiB  
Article
Ascorbic Acid Protects Bone Marrow from Oxidative Stress and Transient Elevation of Corticosterone Caused by X-ray Exposure in Akr1a-Knockout Mice
by Tomoki Bo, Hidekazu Nohara, Ken-ichi Yamada, Satoshi Miyata and Junichi Fujii
Antioxidants 2024, 13(2), 152; https://doi.org/10.3390/antiox13020152 - 25 Jan 2024
Viewed by 1110
Abstract
Bone marrow cells are the most sensitive to exposure to X-rays in the body and are selectively damaged even by doses that are generally considered permissive in other organs. Ascorbic acid (Asc) is a potent antioxidant that is reported to alleviate damages caused [...] Read more.
Bone marrow cells are the most sensitive to exposure to X-rays in the body and are selectively damaged even by doses that are generally considered permissive in other organs. Ascorbic acid (Asc) is a potent antioxidant that is reported to alleviate damages caused by X-ray exposure. However, rodents can synthesize Asc, which creates difficulties in rigorously assessing its effects in such laboratory animals. To address this issue, we employed mice with defects in their ability to synthesize Asc due to a genetic ablation of aldehyde reductase (Akr1a-KO). In this study, concentrations of white blood cells (WBCs) were decreased 3 days after exposure to X-rays at 2 Gy and then gradually recovered. At approximately one month, the recovery rate of WBCs was delayed in the Akr1a-KO mouse group, which was reversed via supplementation with Asc. Following exposure to X-rays, Asc levels decreased in plasma, bone marrow cells, and the liver during an early period, and then started to increase. X-ray exposure stimulated the pituitary gland to release adrenocorticotropic hormone (ACTH), which stimulated corticosterone secretion. Asc released from the liver, which was also stimulated by ACTH, appeared to be recruited to the bone marrow. Since corticosterone in high doses is injurious, these collective results imply that Asc protects bone marrow via its antioxidant capacity against ROS produced via exposure to X-rays and the cytotoxic action of transiently elevated corticosterone. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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14 pages, 1785 KiB  
Article
Alterations in Antioxidant Status and Erythrocyte Properties in Children with Autism Spectrum Disorder
by Tomas Jasenovec, Dominika Radosinska, Katarina Jansakova, Maria Kopcikova, Aleksandra Tomova, Denisa Snurikova, Norbert Vrbjar and Jana Radosinska
Antioxidants 2023, 12(12), 2054; https://doi.org/10.3390/antiox12122054 - 28 Nov 2023
Viewed by 799
Abstract
Erythrocytes are responsible for the transport of oxygen within the organism, which is particularly important for nerve tissues. Erythrocyte quality has been shown to be deteriorated in oxidative stress conditions. In this study, we measured the same series of oxidative stress markers in [...] Read more.
Erythrocytes are responsible for the transport of oxygen within the organism, which is particularly important for nerve tissues. Erythrocyte quality has been shown to be deteriorated in oxidative stress conditions. In this study, we measured the same series of oxidative stress markers in plasma and erythrocytes to compare the differences between neurotypical children (controls) and children with autism spectrum disorder (ASD). We also focused on erythrocyte properties including their deformability, osmotic resistance, Na,K-ATPase activity, nitric oxide levels and free radical levels in children with ASD and controls. Greater oxidative damage to proteins and lipids was observed in the erythrocytes than in the plasma of ASD subjects. Additionally, antioxidant enzymes were more active in plasma samples from ASD children than in their erythrocytes. Significantly higher nitric oxide level and Na,K-ATPase enzyme activity were detected in erythrocytes of ASD individuals in comparison with the controls. Changes in oxidative status could at least partially contribute to the deterioration of erythrocyte morphology, as more frequent echinocyte formation was detected in ASD individuals. These alterations are most probably responsible for worsening the erythrocyte deformability observed in children with ASD. We can conclude that abnormalities in antioxidant status and erythrocyte properties could be involved in the pathomechanisms of ASD and eventually contribute to its clinical manifestations. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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15 pages, 1674 KiB  
Article
Stratification of βSβ+ Compound Heterozygotes Based on L-Glutamine Administration and RDW: Focusing on Disease Severity
by Aimilia Giannaki, Hara Τ. Georgatzakou, Sotirios P. Fortis, Alkmini T. Anastasiadi, Efthimia G. Pavlou, Efrosyni G. Nomikou, Maria P. Drandaki, Angeliki Kotsiafti, Aikaterini Xydaki, Christina Fountzoula, Effie G. Papageorgiou, Vassilis L. Tzounakas and Anastasios G. Kriebardis
Antioxidants 2023, 12(11), 1982; https://doi.org/10.3390/antiox12111982 - 08 Nov 2023
Viewed by 897
Abstract
Sickle cell disease (SCD) is heterogeneous in terms of manifestation severity, even more so when in compound heterozygosity with beta-thalassemia. The aim of the present study was to stratify βSβ+ patient blood samples in a severity-dependent manner. Blood from thirty-two [...] Read more.
Sickle cell disease (SCD) is heterogeneous in terms of manifestation severity, even more so when in compound heterozygosity with beta-thalassemia. The aim of the present study was to stratify βSβ+ patient blood samples in a severity-dependent manner. Blood from thirty-two patients with HbS/β-thalassemia compound heterozygosity was examined for several parameters (e.g., hemostasis, inflammation, redox equilibrium) against healthy controls. Additionally, SCD patients were a posteriori (a) categorized based on the L-glutamine dose and (b) clustered into high-/low-RDW subgroups. The patient cohort was characterized by anemia, inflammation, and elevated coagulation. Higher-dose administration of L-glutamine was associated with decreased markers of inflammation and oxidation (e.g., intracellular reactive oxygen species) and an altered coagulation profile. The higher-RDW group was characterized by increased hemolysis, elevated markers of inflammation and stress erythropoiesis, and oxidative phenomena (e.g., membrane-bound hemoglobin). Moreover, the levels of hemostasis parameters (e.g., D-Dimers) were greater compared to the lower-RDW subgroup. The administration of higher doses of L-glutamine along with hydroxyurea seems to attenuate several features in SCD patients, probably by enhancing antioxidant power. Moreover, anisocytosis may alter erythrocytes’ coagulation processes and hemolytic propensity. This results in the disruption of the redox and pro-/anti-inflammatory equilibria, creating a positive feedback loop by inducing stress erythropoiesis and, thus, the occurrence of a mixed erythrocyte population. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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20 pages, 6667 KiB  
Article
Red Blood Cells from Individuals with Lesch–Nyhan Syndrome: Multi-Omics Insights into a Novel S162N Mutation Causing Hypoxanthine-Guanine Phosphoribosyltransferase Deficiency
by Julie A. Reisz, Monika Dzieciatkowska, Daniel Stephenson, Fabia Gamboni, D. Holmes Morton and Angelo D’Alessandro
Antioxidants 2023, 12(9), 1699; https://doi.org/10.3390/antiox12091699 - 31 Aug 2023
Cited by 1 | Viewed by 1478
Abstract
Lesch–Nyhan syndrome (LN) is an is an X-linked recessive inborn error of metabolism that arises from a deficiency of purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). The disease manifests severely, causing intellectual deficits and other neural abnormalities, hypercoagulability, uncontrolled self-injury, and gout. While allopurinol [...] Read more.
Lesch–Nyhan syndrome (LN) is an is an X-linked recessive inborn error of metabolism that arises from a deficiency of purine salvage enzyme hypoxanthine-guanine phosphoribosyltransferase (HPRT). The disease manifests severely, causing intellectual deficits and other neural abnormalities, hypercoagulability, uncontrolled self-injury, and gout. While allopurinol is used to alleviate gout, other symptoms are less understood, impeding treatment. Herein, we present a high-throughput multi-omics analysis of red blood cells (RBCs) from three pediatric siblings carrying a novel S162N HPRT1 mutation. RBCs from both parents—the mother, a heterozygous carrier, and the father, a clinically healthy control—were also analyzed. Global metabolite analysis of LN RBCs shows accumulation of glycolytic intermediates upstream of pyruvate kinase, unsaturated fatty acids, and long chain acylcarnitines. Similarly, highly unsaturated phosphatidylcholines are also elevated in LN RBCs, while free choline is decreased. Intracellular iron, zinc, selenium, and potassium are also decreased in LN RBCs. Global proteomics documented changes in RBC membrane proteins, hemoglobin, redox homeostasis proteins, and the enrichment of coagulation proteins. These changes were accompanied by elevation in protein glutamine deamidation and methylation in the LN children and carrier mother. Treatment with allopurinol incompletely reversed the observed phenotypes in the two older siblings currently on this treatment. This unique data set provides novel opportunities for investigations aimed at potential therapies for LN-associated sequelae. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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12 pages, 2342 KiB  
Article
Molecular Study on Twin Cohort with Discordant Birth Weight
by Payal Chakraborty, Hajnalka Orvos and Edit Hermesz
Antioxidants 2023, 12(7), 1370; https://doi.org/10.3390/antiox12071370 - 30 Jun 2023
Viewed by 1352
Abstract
The increased rate of twinning has pointed out newer challenges in clinical practices related to gestational complications, intrauterine growth restriction, perinatal mortality, and comorbidities. As a twin pregnancy progresses, the increased demand for oxygen supply can easily disrupt the redox homeostasis balance and [...] Read more.
The increased rate of twinning has pointed out newer challenges in clinical practices related to gestational complications, intrauterine growth restriction, perinatal mortality, and comorbidities. As a twin pregnancy progresses, the increased demand for oxygen supply can easily disrupt the redox homeostasis balance and further impose a greater challenge for the developing fetuses. A substantial birth-weight difference acts as an indicator of a deficit in oxygenation or blood flow to one of the fetuses, which might be related to a low bioavailable nitric oxide level. Therefore, in this study, we focused on networks involved in the adjustment of oxygen supply, like the activation of inducible and endothelial nitric oxide synthase (NOS3) along with free radical and lipid peroxide formation in mature twin pairs with high birth-weight differences. The selected parameters were followed by immunofluorescence staining, fluorescence-activated cell sorting analysis, and biochemical measurements in the umbilical cord vessels and fetal red blood cells. Based on our data set, it is clear that the lower-weight siblings are markedly exposed to persistent intrauterine hypoxic conditions, which are connected to a decreased level in NOS3 activation. Furthermore, the increased level of peroxynitrite aggravates lipid peroxidation and induces morphological and functional damage and loss in redox homeostasis. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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Review

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22 pages, 3556 KiB  
Review
Targeting Cysteine Oxidation in Thrombotic Disorders
by Moua Yang and Roy L. Silverstein
Antioxidants 2024, 13(1), 83; https://doi.org/10.3390/antiox13010083 - 09 Jan 2024
Viewed by 1620
Abstract
Oxidative stress increases the risk for clinically significant thrombotic events, yet the mechanisms by which oxidants become prothrombotic are unclear. In this review, we provide an overview of cysteine reactivity and oxidation. We then highlight recent findings on cysteine oxidation events in oxidative [...] Read more.
Oxidative stress increases the risk for clinically significant thrombotic events, yet the mechanisms by which oxidants become prothrombotic are unclear. In this review, we provide an overview of cysteine reactivity and oxidation. We then highlight recent findings on cysteine oxidation events in oxidative stress-related thrombosis. Special emphasis is on the signaling pathway induced by a platelet membrane protein, CD36, in dyslipidemia, and by protein disulfide isomerase (PDI), a member of the thiol oxidoreductase family of proteins. Antioxidative and chemical biology approaches to target cysteine are discussed. Lastly, the knowledge gaps in the field are highlighted as they relate to understanding how oxidative cysteine modification might be targeted to limit thrombosis. Full article
(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)
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