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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 March 2025) | Viewed by 22110

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Dr. Yoshihisa Koyama

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Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Suita 565-0871, Japan
Interests: antioxidant therapy; hydrogen
Special Issues, Collections and Topics in MDPI journals

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

Manuscript Submission Information

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Keywords

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

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Published Papers (10 papers)

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Research

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23 pages, 3820 KiB

Open AccessArticle

A Study of Antioxidant, Antihyperlipidemic, and Anti-Glycation Effects of Alkylsulfonic Acids with Quinobenzothiazinyl Substituents: In Vitro and In Silico Investigations

by Kirthani Anamalay, Lee Qiao Er, Abbirami Balachandran, Patrick Nwabueze Okechukwu, Beata Morak-Młodawska, Merell P. Billacura, Charlie A. Lavilla, Jr., Anis Najwa Abdul Rani, Anand Gaurav, Adam Konefał and Małgorzata Jeleń

Antioxidants 2025, 14(4), 464; https://doi.org/10.3390/antiox14040464 - 12 Apr 2025

Viewed by 520

Abstract

Hyperlipidemia, marked by high levels of fats in the blood, is a major risk factor for non-communicable diseases such as type 2 diabetes, cardiovascular diseases, and cancer. It has been linked to the action of reactive oxygen species and the formation of advanced glycation end products. Current treatments for hyperlipidemia, like orlistat, simvastatin, and atorvastatin, often present undesirable side effects, prompting the need for new therapeutic agents that are safer, more effective, cost-efficient, and have fewer side effects. In this context, new compounds, specifically propano- and butanosulfonic acids with 9-substituted quinobenzothiazinyl substituents, were synthesized through reactions with 9-substituted quinobenzothiazines and propane sultone or butane sultone. These novel quinobenzothiazine derivatives were verified using ¹H NMR, ¹³C NMR, and HR-MS techniques. The research focused on assessing these compounds for their toxicity, ability to prevent glycation, antioxidant properties, and their potential to combat hyperlipidemia. Toxicity was evaluated on the 3T3 L1 fibroblast cell line using the MTT assay. The capacity to prevent glycation was tested with bovine serum albumin–methylglyoxal and bovine serum albumin–glucose systems. This study measured total reactive oxygen species in the 3T3 L1 cell line using 2′,7′-dichlorodihydrofluorescein diacetate staining, and antioxidant capacity was assessed through DPPH scavenging and metal ion chelation tests. The effectiveness against hyperlipidemia was determined by targeting cholesterol esterase and pancreatic lipase activities, with concentrations of the compounds 5 to 12 ranging from 0.0245 to 0.268 μM. Standard drugs such as orlistat, simvastatin, statins, and aminoguanidine were used as positive controls in various assays. Additionally, computational docking studies with AutoDock Vina were performed. The resulting findings indicated that the compounds were non-toxic to cells, effectively inhibited key enzymes related to hyperlipidemia, and showed significant antioxidant properties, including the prevention of advanced glycation end-product formation. Compounds 11 and 12 demonstrated the highest activity levels. These promising results highlight the potential of new quinobenzothiazine derivatives as lead compounds for the development of antihyperlipidemic drugs, although further research is necessary to confirm their efficacy and safety. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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19 pages, 3006 KiB

Open AccessArticle

Dichloromethane Extract from Amburana cearensis (Allemão) A.C. Sm. Seeds and Its Coumarin Reduce ROS Production and Protect PC12 Cells Against Glutamate Excitotoxicity and Oxygen-Glucose Deprivation

by Flávia Santos Sanches, Florisvaldo da Silva Ramos, Cinthia Cristina de O. S. Costa, Ravena Pereira do Nascimento, Bruno Solano de Freitas Souza, Maria de Fátima Dias Costa, Silvia Lima Costa, Paulo R. Ribeiro, Rafael Short Ferreira and Victor Diogenes Amaral da Silva

Antioxidants 2025, 14(4), 440; https://doi.org/10.3390/antiox14040440 - 5 Apr 2025

Viewed by 500

Abstract

Amburana cearensis is a plant native to Brazil used in folk medicine for the treatment of several pathological conditions including stroke. Previous research indicates that a dichloromethane extract of A. cearensis seeds (EDAC), rich in coumarins, protects neural cells against oxygen and glucose deprivation (OGD) and glutamate-induced stress. However, further studies are needed to elucidate the role of coumarin, in the protective effect of EDAC. Glutamatergic excitotoxicity is an important cause of neuronal loss involved in the pathogenesis of Alzheimer’s disease, Huntington’s disease, Parkinson’s disease, and ischemic stroke. Therefore, this study aimed to investigate the protective effects of coumarin isolated from EDAC against glutamate excitotoxicity in regulating MAPK pathway proteins and reactive oxygen species (ROS) production on PC12 cells. Furthermore, we aimed to investigate the protective effects of coumarin against cell death induced by OGD. We characterized the isolated compound from EDAC as coumarin by ¹H and ¹³C-NMR. Thus, PC12 cells were exposed to OGD or glutamate (20 mM) and/or treated with EDAC or coumarin (500 μg/mL) for 24 h. Subsequently, cell viability was assessed by propidium iodide staining or by MTT test. Furthermore, the expression of MAPK pathway proteins was investigated by Western blot analysis and the expression of cleaved caspase-3 by immunofluorescence. Furthermore, reactive oxygen species (ROS) production was assessed by 2′,7′-dichlorofluorescein diacetate and CellROX. We observed that EDAC and coumarin were able to protect PC12 cells against OGD conditions. Moreover, EDAC totally inhibited the glutamate toxicity in PC12 cells. Meanwhile, coumarin mitigated the glutamate toxicity. Both were able to downregulate the expression of ERK1/2 and phosphorylated ERK and inhibit caspase-3 activation. EDAC and coumarin also prevented the increase of ROS induced by treatment with H₂O₂ or glutamate. Our results evidenced that coumarin from A. cearensis is antioxidative and is an important cytoprotective compound in EDAC against glutamate excitotoxicity or OGD injury. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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15 pages, 2054 KiB

Open AccessArticle

Six-Day Fasting Causes Temporary Increases in Both Antioxidant Capacity and Oxidative Stress in Healthy Young Men: A Randomized Controlled Trial

by Marius Brazaitis, Katerina Židonienė, Nerijus Eimantas and Rima Solianik

Antioxidants 2025, 14(3), 269; https://doi.org/10.3390/antiox14030269 - 26 Feb 2025

Viewed by 1138

Abstract

The impact of prolonged fasting on human oxidative stress (OS) levels and antioxidant defence mechanisms remains poorly understood. The aim of this current study was to investigate the redox response to a 6-day fast in a cohort of healthy men. Twenty-six participants were randomly allocated to a 6-day complete fasting or a control trial. Sympathetic activity, substrate oxidation, redox status, blood glucose, ketones, and testosterone concentrations were assessed. Throughout the fasting period, ketone concentration and fat oxidation increased, and carbohydrate oxidation and glucose and testosterone concentrations decreased. Heart rate increased on fasting days 2 and 4 and returned to the pre-fasting level on fasting day 6. Malondialdehyde (MDA) concentration increased after fasting days 4 and 6, and this increase was accompanied by an increase in the total antioxidant capacity (TAC), but the TAC/MDA ratio remained constant. Notably, all fasting-evoked changes returned to the baseline values after resumption of the regular diet. Thus, prolonged fasting activated both antioxidant defence and OS, but the redox balance was maintained. Consistent with this response, ketone concentration and sympathetic nervous system activity increased, and testosterone concentration decreased. These variables returned to the pre-fasting state after resumption of the usual eating habits. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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20 pages, 10108 KiB

Open AccessArticle

Intense Caloric Restriction from Birth Protects the Heart Against Ischemia/Reperfusion Injury and Reduces Reactive Oxygen Species in Ovariectomized Rats

by Vinícius Lopes Cantuária, Cíntia Maria Rodrigues, Isabella Rocha Dias, Vinícius de Oliveira Ottone, Bruna Oliveira Costa, Lourdes Fernanda Godinho, Gabriela Silva, Marco Antônio Alves Schetino, Etel Rocha-Vieira, Marco Fabrício Dias-Peixoto and Kinulpe Honorato-Sampaio

Antioxidants 2025, 14(2), 169; https://doi.org/10.3390/antiox14020169 - 31 Jan 2025

Viewed by 855

Abstract

This study investigates the cardioprotective effects of intense caloric restriction (ICR) from birth in ovariectomized rats, a model of estrogen deficiency mimicking menopause. Our findings demonstrate that ICR significantly improved both basal and post-ischemic cardiac function, even in the absence of estrogens. The restricted animals exhibited enhanced cardiac contractility and relaxation, particularly after ischemia/reperfusion (I/R) injury, with superior functional recovery compared to control groups. Notably, ICR reduced key cardiometabolic risk factors, including blood pressure, heart rate, and adiposity, while improving glucose tolerance and insulin sensitivity. Additionally, while mitochondrial biogenesis remained unaffected, ICR preserved mitochondrial integrity by reducing the number of damaged mitochondria. This was linked to a reduction in oxidative stress, as evidenced by lower reactive oxygen species (ROS) production in the hearts of restricted animals. These results suggest that ICR offers a protective effect against cardiovascular dysfunction induced by estrogen depletion, potentially through enhanced antioxidant defenses and mitochondrial protection. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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17 pages, 2699 KiB

Open AccessArticle

Molecular Hydrogen Modulates T Cell Differentiation and Enhances Neuro-Regeneration in a Vascular Dementia Mouse Model

by Dain Lee, Hyunjun Jo and Jong-Il Choi

Antioxidants 2025, 14(1), 111; https://doi.org/10.3390/antiox14010111 - 20 Jan 2025

Cited by 1 | Viewed by 1296

Abstract

This study explores whether molecular hydrogen (H₂) administration can alleviate cognitive and immunological disturbances in a mouse model of vascular dementia (VaD). Adult male C57BL/6 mice underwent bilateral common carotid artery stenosis to induce VaD and were subsequently assigned to three groups: VaD, VaD with hydrogen-rich water treatment (VaD + H₂), and Sham controls. Behavioral assessments using open field and novel object recognition tests revealed that VaD mice exhibited anxiety-deficient behavior and memory impairment, both of which were reversed by H₂ treatment. Histological examinations showed pyknotic neuronal morphologies and elevated reactive oxygen species (ROS) in the VaD hippocampus, whereas H₂ administration mitigated these alterations. Furthermore, VaD-induced downregulation of BCL2 was reversed in the VaD + H₂ group, in parallel with increased IL-4 expression. Flow cytometric analyses revealed that VaD disrupted T regulatory cell homeostasis by significantly increasing their proportion, an effect reversed by H₂ treatment, thereby restoring immunological balance. Transcriptomic evaluations confirmed that VaD suppressed key neuroprotective and anti-inflammatory genes, while H₂ treatment restored or enhanced their expression. Collectively, these findings highlight the neuroprotective and immuno-modulatory potential of molecular hydrogen, suggesting that H₂ supplementation may promote neuronal resilience, modulate T cell differentiation, and support cognitive recovery in vascular dementia. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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17 pages, 3369 KiB

Open AccessArticle

N-Acetylcysteine Counteracts Immune Dysfunction and Autism-Related Behaviors in the Shank3b Mouse Model of Autism Spectrum Disorder

by Luca Pangrazzi, Enrica Cerilli, Luigi Balasco, Ginevra Matilde Dall’O’, Gabriele Chelini, Anna Pastore, Birgit Weinberger and Yuri Bozzi

Antioxidants 2024, 13(11), 1390; https://doi.org/10.3390/antiox13111390 - 14 Nov 2024

Cited by 3 | Viewed by 1347

Abstract

Autism spectrum disorder (ASD) includes a range of neurodevelopmental disabilities characterized by social interaction deficits, communication impairments, and repetitive behaviors. Previous studies have shown that pro-inflammatory conditions play a key role in ASD. Despite this, how oxidative stress and inflammation may contribute to ASD-related behaviors is still poorly understood. Here, we reported that increased levels of molecules related to inflammation are present in the cerebellum and peripheral blood (PB) of mice lacking Shank3b, an established model of syndromic ASD. In parallel, immune dysfunction was documented in the bone marrow (BM) and spleens of mutant mice. N-acetylcysteine (NAC) treatment rescued inflammation in the cerebellum and PB and impaired the production of pro-inflammatory molecules in the BM and spleen. In addition, social impairment was counteracted in NAC-treated Shank3b^−/− animals. Taken together, our results provide clear evidence of the key role of cerebellar oxidative stress and inflammation in the establishment of ASD-related behaviors. Furthermore, our findings underscore the importance of considering ASD as a systemic disorder. Full article

(This article belongs to the Special Issue Novel Antioxidant Mechanisms for Health and Diseases)

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30 pages, 5219 KiB

Open AccessArticle

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 2 | Viewed by 1889

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” 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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13 pages, 1647 KiB

Open AccessArticle

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 4 | Viewed by 1971

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 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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26 pages, 3701 KiB

Open AccessReview

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

Cited by 2 | Viewed by 3382

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 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

Open AccessReview

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 16 | Viewed by 7763

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 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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