Oxidative Stress and Antioxidants in Hypoxia and Human Pathophysiology Settings, 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: 30 November 2025 | Viewed by 1783

Special Issue Editors


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Guest Editor
1. Departamento de Medicina Interna Oriente, Facultad de Medicina, Universidad de Chile, Santiago 7500922, Chile
2. Unidad de Paciente Crítico, Hospital del Salvador, Santiago 7500922, Chile
Interests: cardiovascular physiology and pathophysiology; animal models of intermittent hypoxia; cardiotoxicity; internal medicine; clinical trial
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Health Sciences Institute, Universidad de O’Higgins, Rancagua 282000, Chile
Interests: hypoxia; cardiovascular dysfunction; cerebrovascular function

Special Issue Information

Dear Colleagues,

Hypoxic (HI) injury involves the worsening of organ dysfunction and cell death due to reduced blood flow, often caused by organ targeting or increased oxygen demand. While restoring blood flow is crucial to save ischemic tissues, reperfusion can cause additional damage, leading to reversible and irreversible changes in tissue and organ function. This is the basic pathophysiology of ischemia-reperfusion (IR) injury, particularly oxidative stress and cell death mechanisms. During reperfusion, local inflammation and oxidative stress increase, causing secondary injury. IR injury affects various organs, including the heart, lungs, kidneys, and brain, and neuroendocrine system, may induce systemic damage, potentially leading to multisystem organ and metabolic dysfunction. Similar responses occur in humans, especially in patients with acute and chronic hypoxia, intermittent hypoxia and hyperoxia expositions. Additionally, in certain cancers, like breast and colon, oxidative stress and hypoxia can lead to distant effects, such as cardio and lung toxicity. Finally, recent evidence suggests the implications of HI and oxidative stress in exercise preconditioning associated with Hyperbaric Oxygen Therapy (HBOT), and their clinical applications.

This Special Issue builds on the success of the First Edition, which features more than 10 interesting papers. In this Second Edition, we will continue to gather research articles and reviews that cover, but are not limited to, the following topics:

  • Current concepts of pathophysiology and therapies in cardiac HI and pharmacological preconditioning;
  • Current concepts of pathophysiology and therapies in HI signaling in skeletal muscle physiology;
  • Current concepts of cancer therapy related-cardiac dysfunction in breast cancer and cancer survivors, oxidative stress mechanisms;
  • Role of oxidative stress in metabolic syndrome and pregnancy disorders associated with obesity;
  • Role of hypoxia in cardiovascular and renal programming: mechanisms and potential therapeutic targets with antioxidants;
  • Effects of hypoxia on the programming of brain and blood–brain barrier antioxidant homeostasis;
  • Epigenetic mechanisms involved in cardio-cerebral oxidative stress;
  • Role of microRNAs in regulating cardiac HI injury in animal and clinical settings;
  • Role of exercise and oxidative stress in hypoxia/hyperoxia cycle in hyperbaric oxygen therapy.

Dr. Rodrigo L. Castillo
Dr. Alejandro Gonzalez-Candia
Guest Editors

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Keywords

  • tissue hypoxia
  • reperfusion injury
  • hypoxic preconditioning
  • oxidative stress
  • antioxidants
  • hypoxic programing
  • microRNA
  • clinical hypoxic settings

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Published Papers (1 paper)

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Research

21 pages, 5705 KiB  
Article
Effects of DHEA and DHEAS in Neonatal Hypoxic–Ischemic Brain Injury
by Elena Mayer, Ira Winkler, Eva Huber, Martina Urbanek, Ursula Kiechl-Kohlendorfer, Elke Griesmaier and Anna Posod
Antioxidants 2024, 13(12), 1542; https://doi.org/10.3390/antiox13121542 - 16 Dec 2024
Cited by 1 | Viewed by 1214
Abstract
Neonatal brain injury remains a significant issue with limited treatment options. This study investigates the potential of the endogenous neurosteroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) as neuroprotective agents, building on evidence of their mechanisms in adult brain injury models. The primary [...] Read more.
Neonatal brain injury remains a significant issue with limited treatment options. This study investigates the potential of the endogenous neurosteroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) as neuroprotective agents, building on evidence of their mechanisms in adult brain injury models. The primary objective was to evaluate their neuroprotective and anti-oxidative properties in a mouse model of neonatal hypoxic–ischemic brain injury. Using the modified Rice–Vannucci model, brain injury was induced in 7-day-old mouse pups, followed by treatment with various concentrations of DHEA and DHEAS (0.1, 1, and 10 µg/g body weight) via intraperitoneal injection after a 2 h recovery period. Mice were sacrificed after 24 hours for analysis of somatometry, brain injury, apoptosis, microglial activation, and oxidative stress markers (NOX2, 4-HNE, 8-OHdG), along with the anti-oxidant marker SOD1. While no statistically significant effects of DHEA or DHEAS were observed at the tested doses and time points, the absence of toxic or adverse effects highlights their safety profile. These findings provide a foundation for further research into optimizing dosing strategies, timing, and delivery methods. Future studies should refine these variables to maximize neuroprotective efficacy, investigate DHEA(S)’ exact mechanisms of action, and explore their potential for clinical application in neonatal care. Full article
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