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Antioxidants
Special Issues
Oxidative Stress Induced by Air Pollution, 3rd Edition
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Oxidative Stress Induced by Air Pollution, 3rd 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: 20 July 2026 | Viewed by 2933

Special Issue Editor

Dr. Yasuhiro Yoshida

E-Mail Website
Guest Editor
Department of Immunology and Parasitology, University of Occupational and Environmental Health, 1-1 Iseigaoka, Yahatanishi-ku, Kitakyushu 807-8555, Japan
Interests: IL-1 signaling; NF-κB; particulate matter; neutrophil
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Over recent decades, rapid industrialization and urbanization have significantly increased air pollution levels, posing a multifaceted challenge to global public health. One of the most critical consequences of exposure to air pollutants is the induction of oxidative stress—an imbalance between the production of reactive oxygen species (ROSs) and the body’s capacity to detoxify these molecules or repair the resulting damage. This process has emerged as a key mechanistic link between air pollution and a wide range of adverse health outcomes, including respiratory diseases, cardiovascular disorders, and other systemic conditions.

Building on the success of the first and second editions, this third edition will further explore the complex interplay between air pollution and oxidative stress. By bringing together a collection of cutting-edge studies, this Special Issue aims to deepen our understanding of the molecular and cellular pathways through which air pollutants drive oxidative stress and, in turn, influence the onset and progression of diverse diseases.

Dr. Yasuhiro Yoshida
Guest Editor

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

  • particulate matter
  • air pollution
  • oxidative stress
  • reactive oxygen species
  • inflammation

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Published Papers (3 papers)

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Research

24 pages, 11261 KB  
Article
Inhibition of EPAC1 Prevents Neuronal Death Mediated by Diesel Exhaust Particles in Ferroptotic Cell Death Conditions
by Hong Yan, Leshan Zhang, Ana L. Manzano-Covarrubias, Phoeja S. Gadjdjoe, Anja Land, Christina H. J. T. M. van der Veen, Teresa Mitchell-Garcia, Heba A. Fayyaz, Marco Venema, Christoffer Åberg, Marieke van der Hart, Frank Lezoualc’h, Xiaodong Cheng, Amalia M. Dolga and Martina Schmidt
Antioxidants 2026, 15(5), 566; https://doi.org/10.3390/antiox15050566 - 29 Apr 2026
Viewed by 301
Abstract
Air pollution is a growing hazard to global health. Epidemiological studies have reported a potential role of air pollutant exposure in the development or aggravation of neurodegenerative diseases. However, the underlying mechanisms are ill-defined. Ferroptosis is an iron- and reactive oxygen species (ROS)-dependent [...] Read more.
Air pollution is a growing hazard to global health. Epidemiological studies have reported a potential role of air pollutant exposure in the development or aggravation of neurodegenerative diseases. However, the underlying mechanisms are ill-defined. Ferroptosis is an iron- and reactive oxygen species (ROS)-dependent form of cell death that drives neuronal loss in neurodegenerative diseases. Our previous studies reported the involvement of adenosine 3′,5′-cyclic monophosphate (cAMP) and EPAC (exchange protein directly activated by cAMP) in ferroptotic cell death. Here, we investigated the effects of diesel exhaust particles (DEP) in mouse hippocampal (HT22) neuronal cells. Our data showed that toxicity induced by RSL3 (50–75 nM), a ferroptosis inducer, was significantly increased by the addition of DEP (100 μg/mL). Pharmacological inhibition of EPAC1 (CE3F4 30 μM or AM-001 30 μM) and soluble adenylyl cyclase (sAC; TDI-10229 1 μM or TDI-11861 0.1 μM) prevented enhanced ferroptotic HT22 cell death caused by DEP, while pharmacological modulation of EPAC2, protein kinase A (PKA), phosphodiesterases (PDEs), or transmembrane AC did not. DEP in combination with RSL3 exposure increased intracellular calcium levels and induced lysosomal de-acidification. Furthermore, inhibition of EPAC1 prevented mitochondrial ROS (MitoSOX) and lipid peroxidation (BODIPY C11 and MDA levels) after DEP and RSL3 co-exposure. Collectively, EPAC1 may serve as a novel target for the treatment or prevention of neurodegenerative diseases accelerated by air pollution. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 3rd Edition)
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21 pages, 4266 KB  
Article
Traffic-Related Emissions Induce Angiotensin II-Dependent Oxidative Stress in the Hippocampus of ApoE-Null Male Mice
by Tyler D. Armstrong, Usa Suwannasual, Analana Stanley, Bailee Johnson, Victoria L. Youngblood, Isabella Santiago, Mickaela Cook, Sophia M. Giasolli and Amie K. Lund
Antioxidants 2026, 15(2), 161; https://doi.org/10.3390/antiox15020161 - 25 Jan 2026
Viewed by 1137
Abstract
Traffic-related air pollution (TRAP) is known to contribute to oxidative stress in the central nervous system (CNS) and has been linked to increased risk of Alzheimer’s disease (AD). Alterations in the renin–angiotensin system (RAS), specifically increased angiotensin II (Ang II) signaling via the [...] Read more.
Traffic-related air pollution (TRAP) is known to contribute to oxidative stress in the central nervous system (CNS) and has been linked to increased risk of Alzheimer’s disease (AD). Alterations in the renin–angiotensin system (RAS), specifically increased angiotensin II (Ang II) signaling via the angiotensin II type 1 (AT1) receptor, are implicated in increased oxidative stress in the CNS via activation of NADPH oxidase (NOX). As exposure to TRAP may further elevate AD risk, we investigated whether exposure to inhaled mixed gasoline and diesel vehicle emissions (MVE) promotes RAS-dependent expression of factors that contribute to AD pathophysiology in an apolipoprotein E-deficient (ApoE−/−) mouse model. Male ApoE−/− mice (6–8 weeks old) on a high-fat diet were treated with either an ACE inhibitor (captopril, 4 mg/kg/day) or water and exposed to filtered air (FA) or MVE (200 µg PM/m3) for 30 days. MVE exposure elevated plasma Ang II, inflammation, and oxidative stress in the hippocampus, associated with increased levels of Aph-1 homolog B (APH1B), a gamma-secretase subunit, and beta-secretase 1 (BACE1), involved in Aβ production. Each of these endpoints was normalized with ACEi treatment. These findings indicate that TRAP exposure in ApoE−/− mice drives a RAS- and NOX-dependent oxidative and inflammatory response and shifts Aβ processing towards an amyloidogenic profile before overt Aβ deposition, suggesting a potential therapeutic approach for air pollution-induced AD risk. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 3rd Edition)
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17 pages, 2128 KB  
Article
Angiotensin-Converting Enzyme (ACE) Inhibitors and Statins Mitigate Negative Cardiovascular and Pulmonary Effects of Particulate Matter in a Mouse Exposure Model
by Tristan Junglas, Andreas Daiber, Ivana Kuntic, Arijan Valar, Jiayin Zheng, Matthias Oelze, Lea Strohm, Henning Ubbens, Omar Hahad, Maria Teresa Bayo Jimenez, Thomas Münzel and Marin Kuntic
Antioxidants 2026, 15(1), 106; https://doi.org/10.3390/antiox15010106 - 13 Jan 2026
Viewed by 1139
Abstract
Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollution-mediated damage of the heart and vessels. The present study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular [...] Read more.
Particulate matter (PM) is a significant contributor to air pollution-associated negative health effects, and cardiovascular disease patients are more susceptible to air pollution-mediated damage of the heart and vessels. The present study investigated the protective effects against PM-induced cardiovascular damage by classic cardiovascular drugs, as used for the standard therapy of cardiovascular disease patients. Male C57BL/6J mice were exposed to ambient PM2.5 (<2.5 µm) for 3 days with or without treatment with the cholesterol-lowering drug atorvastatin (20 mg/kg/d) or the angiotensin-converting enzyme (ACE) inhibitor captopril (50 mg/kg/d). Both drugs mitigated PM2.5-induced systolic blood pressure increases and partially prevented endothelial dysfunction, as reflected by a mixed effect on endothelial nitric oxide synthase phosphorylation. Both drugs ameliorated reactive oxygen species (ROS) formation and phagocytic nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX-2) expression in the vasculature of PM2.5-exposed mice. Pulmonary ROS levels showed a minor improvement by the treatments, whereas Nox2 mRNA expression was not diminished. Only captopril showed some anti-inflammatory effects in the heart and lung of PM2.5-exposed mice, whereas both drugs failed to reduce systemic inflammation measured in plasma. These findings offer new insights into potential mitigation strategies for PM2.5-induced cardiovascular complications, particularly for patients at higher cardiovascular risk, like those with coronary artery or ischemic heart disease or hypertension. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 3rd Edition)
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