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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 (10 July 2024) | Viewed by 20617

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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 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

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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.

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Keywords

blood
redox status
antioxidants
oxidative stress
redox therapy
oxidative stress biomarkers

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Published Papers (11 papers)

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Editorial

Jump to: Research, Review

4 pages, 168 KiB

Open AccessEditorial

E Pluribus, Unum: Emergent Redox Harmony from the Chaos of Blood Cells

by Alkmini T. Anastasiadi and Angelo D’Alessandro

Antioxidants 2024, 13(9), 1151; https://doi.org/10.3390/antiox13091151 - 23 Sep 2024

Viewed by 606

Abstract

Blood cells play a fundamental role in maintaining systemic homeostasis, by responding dynamically to various physiological and environmental stimuli [...] Full article

(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)

Research

Jump to: Editorial, Review

19 pages, 1734 KiB

Open AccessArticle

Erythrocyte Oxidative Status in People with Obesity: Relation to Tissue Losses, Glucose Levels, and Weight Reduction

by Beata Szlachta, Anna Birková, Beáta Čižmárová, Anna Głogowska-Gruszka, Paulina Zalejska-Fiolka, Maria Dydoń and Jolanta Zalejska-Fiolka

Antioxidants 2024, 13(8), 960; https://doi.org/10.3390/antiox13080960 - 7 Aug 2024

Viewed by 816

Abstract

Background: This study aimed to investigate the impact of reductions in various body mass components on the erythrocyte oxidative status and glycemic state of people with obesity (PWO). Methods: A total of 53 PWO followed a six-month individualized low-calorie diet with exercise, during which anthropometric, biochemical, and oxidative parameters were measured. The participants were divided into groups based on weight (W), visceral fat area (VFA), total body water (TBW), and skeletal muscle mass (SMM) losses, as well as normoglycemia (NG) and hyperglycemia (HG). Results: Weight reduction normalized glycemia and influenced erythrocyte enzyme activity. Regardless of the tissue type lost (VFA, TBW, or SMM), glutathione peroxidase activity decreased in all groups, accompanied by an increase in glutathione reductase activity. Lipofuscin (LPS) and malondialdehyde (MDA) concentrations decreased regardless of the type of tissue lost. The α-/γ-tocopherol ratio increased in those losing >10% body weight, >15% VFA, and >5% TBW. In the NG group, compared to the HG group, there was a decrease in glutathione peroxidase and an increase in glutathione reductase, with these changes being stronger in the HG group. The LPS and MDA concentrations decreased in both groups. Significant correlations were observed between glucose reduction and changes in catalase, retinol, and α-tocopherol, as well as between VFA reduction and changes in vitamin E, L-LPS, and the activities of L-GR and L-GST. Conclusions: This analysis highlights the complex interactions between glucose metabolism, oxidative state, and erythrocyte membrane integrity, crucial for understanding diabetes and its management. This study shows the significant metabolic adaptability of erythrocytes in response to systemic changes induced by obesity and hyperglycemia, suggesting potential therapeutic targets to improve metabolic health in obese individuals. Full article

(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)

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21 pages, 3634 KiB

Open AccessArticle

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

Cited by 1 | Viewed by 1684

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 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

Open AccessArticle

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

Cited by 1 | Viewed by 1797

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 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

Open AccessArticle

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

Cited by 1 | Viewed by 1317

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 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

Open AccessArticle

Stratification of β^Sβ⁺ 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 - 8 Nov 2023

Cited by 1 | Viewed by 1320

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 β^Sβ⁺ 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

Open AccessArticle

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 3 | Viewed by 2255

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 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

Open AccessArticle

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 1798

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 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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16 pages, 2841 KiB

Open AccessReview

Vitamin C-Dependent Uptake of Non-Heme Iron by Enterocytes, Its Impact on Erythropoiesis and Redox Capacity of Human Erythrocytes

by Xia Pan, Martin Köberle and Mehrdad Ghashghaeinia

Antioxidants 2024, 13(8), 968; https://doi.org/10.3390/antiox13080968 - 9 Aug 2024

Viewed by 2316

Abstract

In the small intestine, nutrients from ingested food are absorbed and broken down by enterocytes, which constitute over 95% of the intestinal epithelium. Enterocytes demonstrate diet- and segment-dependent metabolic flexibility, enabling them to take up large amounts of glutamine and glucose to meet their energy needs and transfer these nutrients into the bloodstream. During glycolysis, ATP, lactate, and H⁺ ions are produced within the enterocytes. Based on extensive but incomplete glutamine oxidation large amounts of alanine or lactate are produced. Lactate, in turn, promotes hypoxia-inducible factor-1α (Hif-1α) activation and Hif-1α-dependent transcription of various proton channels and exchangers, which extrude cytoplasmic H⁺-ions into the intestinal lumen. In parallel, the vitamin C-dependent and duodenal cytochrome b-mediated conversion of ferric iron into ferrous iron progresses. Finally, the generated electrochemical gradient is utilized by the divalent metal transporter 1 for H⁺-coupled uptake of non-heme Fe²⁺-ions. Iron efflux from enterocytes, subsequent binding to the plasma protein transferrin, and systemic distribution supply a wide range of cells with iron, including erythroid precursors essential for erythropoiesis. In this review, we discuss the impact of vitamin C on the redox capacity of human erythrocytes and connect enterocyte function with iron metabolism, highlighting its effects on erythropoiesis. Full article

(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)

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18 pages, 744 KiB

Open AccessReview

The Role of Ergothioneine in Red Blood Cell Biology: A Review and Perspective

by Tiffany A. Thomas, Richard O. Francis, James C. Zimring, Joseph P. Kao, Travis Nemkov and Steven L. Spitalnik

Antioxidants 2024, 13(6), 717; https://doi.org/10.3390/antiox13060717 - 13 Jun 2024

Cited by 1 | Viewed by 2423

Abstract

Oxidative stress can damage tissues and cells, and their resilience or susceptibility depends on the robustness of their antioxidant mechanisms. The latter include small molecules, proteins, and enzymes, which are linked together in metabolic pathways. Red blood cells are particularly susceptible to oxidative stress due to their large number of hemoglobin molecules, which can undergo auto-oxidation. This yields reactive oxygen species that participate in Fenton chemistry, ultimately damaging their membranes and cytosolic constituents. Fortunately, red blood cells contain robust antioxidant systems to enable them to circulate and perform their physiological functions, particularly delivering oxygen and removing carbon dioxide. Nonetheless, if red blood cells have insufficient antioxidant reserves (e.g., due to genetics, diet, disease, or toxin exposure), this can induce hemolysis in vivo or enhance susceptibility to a “storage lesion” in vitro, when blood donations are refrigerator-stored for transfusion purposes. Ergothioneine, a small molecule not synthesized by mammals, is obtained only through the diet. It is absorbed from the gut and enters cells using a highly specific transporter (i.e., SLC22A4). Certain cells and tissues, particularly red blood cells, contain high ergothioneine levels. Although no deficiency-related disease has been identified, evidence suggests ergothioneine may be a beneficial “nutraceutical.” Given the requirements of red blood cells to resist oxidative stress and their high ergothioneine content, this review discusses ergothioneine’s potential importance in protecting these cells and identifies knowledge gaps regarding its relevance in enhancing red blood cell circulatory, storage, and transfusion quality. Full article

(This article belongs to the Special Issue Blood Cells and Redox Homeostasis in Health and Disease)

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22 pages, 3556 KiB

Open AccessReview

Targeting Cysteine Oxidation in Thrombotic Disorders

by Moua Yang and Roy L. Silverstein

Antioxidants 2024, 13(1), 83; https://doi.org/10.3390/antiox13010083 - 9 Jan 2024

Cited by 2 | Viewed by 2430

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 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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