Novel Antioxidant Mechanisms for Health and 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: 10 March 2025 | Viewed by 9443

Special Issue Editor


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Guest Editor
Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, 2-2 Yamada-oka, Suita 565-0871, Osaka, Japan
Interests: antioxidant therapy; hydrogen

Special Issue Information

Dear Colleagues,

Antioxidant therapy effectively addresses oxidative-stress-related diseases. These conditions arise from the depletion of endogenous antioxidants, which leads to oxidative stress. Therefore, supplementation with exogenous antioxidants, including vitamins and polyphenols, has been suggested. However, some studies report potential drawbacks, such as neutralizing beneficial reactive oxygen species (ROS) or requiring excessive doses for effectiveness, making clinical application challenging. Oxidative stress plays a role in various contexts, from pathological conditions to fatigue and the side effects of anticancer drugs. Therefore, rapid and precise replenishment of antioxidants that specifically counteract harmful ROS is crucial.

Emerging approaches to antioxidant treatment offer new perspectives. Nutrigenomics-based treatments aim to enhance the body's antioxidant capacity by influencing gene expression through dietary choices. Nano-antioxidant therapy employs inorganic substances to continuously generate antioxidants within the body. There are also treatments that increase the production of antioxidants by regulating the microbiome. These treatments are innovative antioxidant therapies that differ from those used in the past, aiming to enhance the body's antioxidant capacity by modifying the internal environment. The objective of this Special Issue is to delve into these novel antioxidant treatments to gain a better understanding of the new mechanisms that regulate antioxidant activity in the body. We hope that this Special Issue will lead to the discovery of new antioxidant treatments for oxidative-stress-related diseases.

Dr. Yoshihisa Koyama
Guest Editor

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Keywords

  • antioxidant therapy
  • reactive oxygen species
  • oxidative stress
  • nano-antioxidant therapy
  • nutrigenomics
  • microbiome

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Published Papers (4 papers)

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Research

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30 pages, 5219 KiB  
Article
Apocynin Prevents Cigarette Smoke-Induced Anxiety-Like Behavior and Preserves Microglial Profiles in Male Mice
by Rana Alateeq, Alina Akhtar, Simone N. De Luca, Stanley M. H. Chan and Ross Vlahos
Antioxidants 2024, 13(7), 855; https://doi.org/10.3390/antiox13070855 - 16 Jul 2024
Cited by 1 | Viewed by 1084
Abstract
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally and is primarily caused by cigarette smoking (CS). Neurocognitive comorbidities such as anxiety and cognitive impairments are common among people with COPD. CS-induced lung inflammation and oxidative stress may “spill-over” [...] Read more.
Chronic obstructive pulmonary disease (COPD) is the third leading cause of death globally and is primarily caused by cigarette smoking (CS). Neurocognitive comorbidities such as anxiety and cognitive impairments are common among people with COPD. CS-induced lung inflammation and oxidative stress may “spill-over” into the systemic circulation, driving the onset of these comorbidities. We investigated whether a prophylactic treatment with the NADPH Oxidase 2 (NOX2) inhibitor, apocynin, could prevent CS-induced neurocognitive impairments. Adult male BALB/c mice were exposed to CS (9 cigarettes/day, 5 days/week) or room air (sham) for 8 weeks with co-administration of apocynin (5 mg/kg, intraperitoneal injection once daily) or vehicle (0.01% DMSO in saline). Following 7 weeks of CS exposure, mice underwent behavioral testing to assess recognition and spatial memory (novel object recognition and Y maze, respectively) and anxiety-like behaviors (open field and elevated plus maze). Mice were then euthanized, and blood, lungs, and brains were collected. Apocynin partially improved CS-induced lung neutrophilia and reversed systemic inflammation (C-reactive protein) and oxidative stress (malondialdehyde). Apocynin exerted an anxiolytic effect in CS-exposed mice, which was associated with restored microglial profiles within the amygdala and hippocampus. Thus, targeting oxidative stress using apocynin can alleviate anxiety-like behaviors and could represent a novel strategy for managing COPD-related anxiety disorders. Full article
(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)
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14 pages, 1647 KiB  
Article
TNFRSF1B Signaling Blockade Protects Airway Epithelial Cells from Oxidative Stress
by Javier Checa, Pau Fiol, Marta Guevara and Josep M. Aran
Antioxidants 2024, 13(3), 368; https://doi.org/10.3390/antiox13030368 - 18 Mar 2024
Cited by 1 | Viewed by 1463
Abstract
Progressive respiratory airway destruction due to unresolved inflammation induced by periodic infectious exacerbation episodes is a hallmark of cystic fibrosis (CF) lung pathology. To clear bacteria, neutrophils release high amounts of reactive oxygen species (ROS), which inflict collateral damage to the neighboring epithelial [...] Read more.
Progressive respiratory airway destruction due to unresolved inflammation induced by periodic infectious exacerbation episodes is a hallmark of cystic fibrosis (CF) lung pathology. To clear bacteria, neutrophils release high amounts of reactive oxygen species (ROS), which inflict collateral damage to the neighboring epithelial cells causing oxidative stress. A former genome-wide small interfering RNA (siRNA) screening in CF submucosal gland cells, instrumental for mucociliary clearance, proposed tumor necrosis factor receptor superfamily member 1B (TNFRSF1B; TNFR2) as a potential hit involved in oxidative stress susceptibility. Here, we demonstrate the relevance of TNFRSF1B transcript knock-down for epithelial cell protection under strong oxidative stress conditions. Moreover, a blockade of TNFR signaling through its ligand lymphotoxin-α (LTA), overexpressed in airway epithelial cells under oxidative stress conditions, using the anti-tumor necrosis factor (TNF) biologic etanercept significantly increased the viability of these cells from a toxic oxidizing agent. Furthermore, bioinformatic analyses considering our previous RNA interference (RNAi) screening output highlight the relevance of TNFRSF1B and of other genes within the TNF pathway leading to epithelial cell death. Thus, the inhibition of the LTα3-TNFR2 axis could represent a useful therapeutic strategy to protect the respiratory airway epithelial lining from the oxidative stress challenge because of recurrent infection/inflammation cycles faced by CF patients. Full article
(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)
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Review

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26 pages, 3701 KiB  
Review
Modulatory Impact of Oxidative Stress on Action Potentials in Pathophysiological States: A Comprehensive Review
by Chitaranjan Mahapatra, Ravindra Thakkar and Ravinder Kumar
Antioxidants 2024, 13(10), 1172; https://doi.org/10.3390/antiox13101172 - 26 Sep 2024
Viewed by 1630
Abstract
Oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, significantly affects cellular function and viability. It plays a pivotal role in modulating membrane potentials, particularly action potentials (APs), essential for properly functioning excitable [...] Read more.
Oxidative stress, characterized by an imbalance between the production of reactive oxygen species (ROS) and the body’s antioxidant defenses, significantly affects cellular function and viability. It plays a pivotal role in modulating membrane potentials, particularly action potentials (APs), essential for properly functioning excitable cells such as neurons, smooth muscles, pancreatic beta cells, and myocytes. The interaction between oxidative stress and AP dynamics is crucial for understanding the pathophysiology of various conditions, including neurodegenerative diseases, cardiac arrhythmias, and ischemia-reperfusion injuries. This review explores how oxidative stress influences APs, focusing on alterations in ion channel biophysics, gap junction, calcium dynamics, mitochondria, and Interstitial Cells of Cajal functions. By integrating current research, we aim to elucidate how oxidative stress contributes to disease progression and discuss potential therapeutic interventions targeting this interaction. Full article
(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)
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15 pages, 838 KiB  
Review
The Impact of Curcumin, Resveratrol, and Cinnamon on Modulating Oxidative Stress and Antioxidant Activity in Type 2 Diabetes: Moving beyond an Anti-Hyperglycaemic Evaluation
by Michalina Banaszak, Ilona Górna, Dagmara Woźniak, Juliusz Przysławski and Sławomira Drzymała-Czyż
Antioxidants 2024, 13(5), 510; https://doi.org/10.3390/antiox13050510 - 24 Apr 2024
Cited by 3 | Viewed by 4510
Abstract
Research indicates that up to half of the population resorts to dietary supplements for managing diseases such as type 2 diabetes rather than changing their nutritional habits. These supplements not only aim to have an anti-hyperglycaemic effect but also seek to reduce oxidative [...] Read more.
Research indicates that up to half of the population resorts to dietary supplements for managing diseases such as type 2 diabetes rather than changing their nutritional habits. These supplements not only aim to have an anti-hyperglycaemic effect but also seek to reduce oxidative stress to prevent diabetes complications. This systematic literature systematic review aims to evaluate the efficacy of curcumin, resveratrol, and cinnamon in modulating oxidative stress and antioxidant activity in individuals with type 2 diabetes. Data were collected from PubMed, Web of Sciences, and Scopus databases regarding the impact of curcumin, resveratrol, and cinnamon on total antioxidant capacity (TAC), malondialdehyde (MDA), tumour necrosis factor α (TNF-α), interleukin 6 (IL-6), and high-sensitivity C-reactive protein (hs-CRP) levels for this review. Effect sizes for each study were calculated using Cohen’s or Hedges’s d coefficient. Parameters of oxidative stress and inflammatory status, such as TAC, MDA, TNF-α, IL-6, and hs-CRP, improved following phytochemicals. Additionally, curcumin, resveratrol, and cinnamon exhibited regulatory effects on carbohydrate metabolism by reducing glucose, insulin, and glycated haemoglobin concentrations and lipid metabolism by lowering total cholesterol (TC), low-density lipoprotein (LDL), and triglycerides (TG) and increasing high-density lipoprotein (HDL). Incorporating curcumin, resveratrol, and cinnamon into diets may be beneficial for maintaining organism homeostasis and improving metabolic control in individuals with type 2 diabetes. However, the conflicting results reported in the literature highlight the need for further detailed investigations into the effectiveness of phytochemical use for type 2 diabetes. Full article
(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)
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