Redox Balance in Hematologic Diseases

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: 31 December 2024 | Viewed by 1744

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Lipids, Oxidation, and Cell Biology Group, Laboratory of Immunology (LIM19), Heart Institute (InCor), Hospital das Clínicas HCFMUSP, Faculdade de Medicina, Universidade de São Paulo, São Paulo, Brazil
Interests: oxysterol; cell proliferation; cell death; lipid oxidation; antioxidants; cancer; atherosclerosis; stem cell biology; regenerative medicine
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Special Issue Information

Dear Colleagues,

This Special Issue, “Redox Balance in Hematologic Diseases”, aims to be a forum of redox biology in the area of hematology. Acceptable paper types are novel research articles (short or full communications), methods, and review articles. Several areas are accepted: from chemical or biochemical mechanisms of redox biology (including oxidants and anti-oxidants, superoxide radical and hydrogen peroxide) if these include effects in relevant hematological models, to redox balance of blood, including in white and blood cells, platelets, endothelial cells, hematopoietic stem cells, hematological cell signaling, self-renewal and differentiation, in health and in hematological disorders, such as malignancies (leukemias, lymphomas, myelodysplastic syndrome), hemoglobinopathies or thrombosis.

Dr. Sérgio Paulo Bydlowski
Guest Editor

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Keywords

  • redox balance
  • oxidants
  • oxidative stress
  • hematology
  • hematological tumor
  • hemoglobinopathy
  • thrombosis
  • hemostasis

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Published Papers (1 paper)

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Research

15 pages, 2258 KiB  
Article
Targeted Metabolomics Highlights Dramatic Antioxidant Depletion, Increased Oxidative/Nitrosative Stress and Altered Purine and Pyrimidine Concentrations in Serum of Primary Myelofibrosis Patients
by Renata Mangione, Cesarina Giallongo, Andrea Duminuco, Enrico La Spina, Lucia Longhitano, Sebastiano Giallongo, Daniele Tibullo, Giuseppe Lazzarino, Miriam Wissam Saab, Arianna Sbriglione, Giuseppe A. Palumbo, Andrea Graziani, Amer M. Alanazi, Valentina Di Pietro, Barbara Tavazzi, Angela Maria Amorini and Giacomo Lazzarino
Antioxidants 2024, 13(4), 490; https://doi.org/10.3390/antiox13040490 - 19 Apr 2024
Cited by 1 | Viewed by 1411
Abstract
To date, little is known concerning the circulating levels of biochemically relevant metabolites (antioxidants, oxidative/nitrosative stress biomarkers, purines, and pyrimidines) in patients with primary myelofibrosis (PMF), a rare form of myeloproliferative tumor causing a dramatic decrease in erythropoiesis and angiogenesis. In this study, [...] Read more.
To date, little is known concerning the circulating levels of biochemically relevant metabolites (antioxidants, oxidative/nitrosative stress biomarkers, purines, and pyrimidines) in patients with primary myelofibrosis (PMF), a rare form of myeloproliferative tumor causing a dramatic decrease in erythropoiesis and angiogenesis. In this study, using a targeted metabolomic approach, serum samples of 22 PMF patients and of 22 control healthy donors were analyzed to quantify the circulating concentrations of hypoxanthine, xanthine, uric acid (as representative purines), uracil, β-pseudouridine, uridine (as representative pyrimidines), reduced glutathione (GSH), ascorbic acid (as two of the main water-soluble antioxidants), malondialdehyde, nitrite, nitrate (as oxidative/nitrosative stress biomarkers) and creatinine, using well-established HPLC method for their determination. Results showed that PMF patients have dramatic depletions of both ascorbic acid and GSH (37.3- and 3.81-times lower circulating concentrations, respectively, than those recorded in healthy controls, p < 0.0001), accompanied by significant increases in malondialdehyde (MDA) and nitrite + nitrate (4.73- and 1.66-times higher circulating concentrations, respectively, than those recorded in healthy controls, p < 0.0001). Additionally, PMF patients have remarkable alterations of circulating purines, pyrimidines, and creatinine, suggesting potential mitochondrial dysfunctions causing energy metabolism imbalance and consequent increases in these cell energy-related compounds. Overall, these results, besides evidencing previously unknown serum metabolic alterations in PMF patients, suggest that the determination of serum levels of the aforementioned compounds may be useful to evaluate PMF patients on hospital admission for adjunctive therapies aimed at recovering their correct antioxidant status, as well as to monitor patients’ status and potential pharmacological treatments. Full article
(This article belongs to the Special Issue Redox Balance in Hematologic Diseases)
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