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Oxidative Stress Induced by Air Pollution, 2nd Edition

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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: 15 March 2025 | Viewed by 3789

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Dr. Yasuhiro Yoshida

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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
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Dear Colleagues,

Over the recent decades, rapid industrialization and urbanization have significantly increased the levels of air pollution, presenting a multifaceted challenge to global public health. One of the critical consequences of exposure to various air pollutants is the induction of oxidative stress, a complex imbalance between the production of reactive oxygen species (ROS) and the body's ability to detoxify or repair the resulting damage. This phenomenon has emerged as a pivotal link between air pollution and a myriad of adverse health outcomes, ranging from respiratory diseases to cardiovascular disorders and beyond.

Building upon the fruitful first edition, this second edition will further unravel the complex interplay between air pollution and oxidative stress. By assembling a collection of cutting-edge studies, this Special Issue seeks to deepen our understanding of the intricate pathways through which air pollutants contribute to oxidative stress and, consequently, influence the development and progression of various diseases.

Dr. Yasuhiro Yoshida
Guest Editor

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Keywords

particulate matter
air pollution
oxidative stress
reactive oxygen species
inflammation

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Published Papers (4 papers)

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Research

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21 pages, 4339 KiB

Open AccessArticle

A Combined Extract from Dioscorea bulbifera and Zingiber officinale Mitigates PM_2.5-Induced Respiratory Damage by NF-κB/TGF-β1 Pathway

by In Young Kim, Hyo Lim Lee, Hye Ji Choi, Yeong Hyeon Ju, Yu Mi Heo, Hwa Rang Na, Dong Yeol Lee, Won Min Jeong and Ho Jin Heo

Antioxidants 2024, 13(12), 1572; https://doi.org/10.3390/antiox13121572 - 20 Dec 2024

Viewed by 514

Abstract

This research evaluated the protective role of a combined extract of Dioscorea bulbifera and Zingiber officinale (DBZO) against respiratory dysfunction caused by particulate matter (PM_2.5) exposure in BALB/c mice. The bioactive compounds identified in the DBZO are catechin, astragalin, 6-gingerol, 8-gingerol, and 6-shogaol. DBZO ameliorated cell viability and reactive oxygen species (ROS) production in PM_2.5-stimulated A549 and RPMI 2650 cells. In addition, it significantly alleviated respiratory dysfunction in BALB/c mice exposed to PM_2.5. DBZO improved the antioxidant systems in lung tissues by modulating malondialdehyde (MDA) content, as well as levels of reduced glutathione (GSH) and superoxide dismutase (SOD). Likewise, DBZO restored mitochondrial dysfunction by improving ROS levels, mitochondrial membrane potential, and ATP production. Moreover, DBZO modulated the levels of neutrophils, eosinophils, monocytes, and lymphocytes (specifically CD4⁺, CD8⁺, and CD4⁺IL-4⁺ T cells) in blood and IgE levels in serum. DBZO was shown to regulate the c-Jun N-terminal kinase (JNK) pathway, nuclear factor kappa B (NF-κB) pathway, and transforming growth factor β (TGF-β)/suppressor of mothers against decapentaplegic (Smad) pathway. Histopathological observation indicated that DBZO mitigates the increase in alveolar septal thickness. These findings indicate that DBZO is a promising natural agent for improving respiratory health. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 2nd Edition)

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14 pages, 1240 KiB

Open AccessArticle

Association Between Oxidative Potential of Particulate Matter Collected by Personal Samplers and Systemic Inflammation Among Asthmatic and Non-Asthmatic Adults

by Miguel Santibáñez, Juan José Ruiz-Cubillán, Andrea Expósito, Juan Agüero, Juan Luis García-Rivero, Beatriz Abascal, Carlos Antonio Amado, Laura Ruiz-Azcona, Marcos Lopez-Hoyos, Juan Irure, Yolanda Robles, Ana Berja, Esther Barreiro, Adriana Núñez-Robainas, José Manuel Cifrián and Ignacio Fernandez-Olmo

Antioxidants 2024, 13(12), 1464; https://doi.org/10.3390/antiox13121464 - 28 Nov 2024

Viewed by 621

Abstract

With the rationale that the oxidative potential of particulate matter (PM-OP) may induce oxidative stress and inflammation, we conducted the ASTHMA-FENOP study in which 44 asthmatic patients and 37 matched controls wore a personal sampler for 24 h, allowing the collection of fine and coarse PM fractions separately, to determine PM-OP by the dithiothreitol (DTT) and ascorbic acid (AA) methods. The levels of Interleukin 6 (IL-6) and the IL-6/IL-10 ratio, as indicators of pro- and anti-inflammatory statuses, were determined by calculating the mean differences (MDs), odds ratios (ORs) and p-trends adjusted for sex, age, study level and body mass index. Positive associations for IL-6 levels in the form of adjusted MDs and ORs were obtained for all PM-OP metrics, reaching statistical significance for both OP-DTT and OP-AA in the fine fraction, with adjusted OR = 5.66; 95%CI (1.46 to 21.92) and 3.32; 95%CI (1.07 to 10.35), respectively, along with statistically significant dose–response patterns when restricting to asthma and adjusted also for clinical variables (adjusted p-trend = 0.029 and 0.01). Similar or stronger associations and dose–response patterns were found for the IL-6/IL-10 ratio. In conclusion, our findings on the effect of PM-OP on systemic inflammation support that asthma is a heterogeneous disease at the molecular level, with PM-OP potentially playing an important role. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 2nd Edition)

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17 pages, 7392 KiB

Open AccessArticle

Photobiomodulation Mitigates PM_2.5-Exacerbated Pathologies in a Mouse Model of Allergic Asthma

by Jisu Park, Bo-Young Kim, Eun Jung Park, Yong-Il Shin and Ji Hyeon Ryu

Antioxidants 2024, 13(8), 1003; https://doi.org/10.3390/antiox13081003 - 19 Aug 2024

Cited by 2 | Viewed by 1546

Abstract

Exposure to particulate matter (PM), especially PM_2.5, is known to exacerbate asthma, posing a significant public health risk. This study investigated the asthma-reducing effects of photobiomodulation (PBM) in a mice model mimicking allergic airway inflammation exacerbated by PM_2.5 exposure. The mice received sensitization with ovalbumin (OVA) and were subsequently treated with PM_2.5 at a dose of 0.1 mg/kg every 3 days, for 9 times over 3 weeks during the challenge. PBM, using a 610 nm wavelength LED, was applied at 1.7 mW/cm² to the respiratory tract via direct skin contact for 20 min daily for 19 days. Results showed that PBM significantly reduced airway hyperresponsiveness, plasma immunoglobulin E (IgE) and OVA-specific IgE, airway inflammation, T-helper type 2 cytokine, histamine and tryptase in bronchoalveolar lavage fluid (BALF), and goblet cell hyperplasia in PM_2.5-exposed asthmatic mice. Moreover, PBM alleviated subepithelial fibrosis by reducing collagen deposition, airway smooth muscle mass, and expression of fibrosis-related genes. It mitigated reactive oxygen species generation, oxidative stress, endoplasmic reticulum stress, apoptotic cell death, ferroptosis, and modulated autophagic signals in the asthmatic mice exposed to PM_2.5. These findings suggest that PBM could be a promising intervention for PM_2.5-induced respiratory complications in patients with allergic asthma. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 2nd Edition)

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Figure 1
Inhibitory effects of PBM on the induction of airway hyperresponsiveness (AHR) and plasma IgE in a PM2.5-exposed asthma exacerbation model. (A) Establishment of an allergic asthma exacerbation mouse model induced by PM2.5 exposure. A timeline describing the asthma exacerbation model induction and PBM treatment. (B) Measurement of body weight, thymus-to-body-weight ratio, and spleen-to-body-weight ratio on the final day of the experiment. (C) Assessment of AHR to methacholine (MCh) at concentrations of 25 and 50 mg/mL. (D) Measurement of total immunoglobulin E (IgE) and ovalbumin (OVA)-specific IgE in plasma. Data are shown as the mean ± SEM (n = 8). * p < 0.05 compared with control. † p < 0.05 compared with PM + OVA. i.n., intranasal injection; i.p., intraperitoneal injection; BW, body weight; PM, particulate matter; OVA, ovalbumin; PBM, photobiomodulation; DEX, dexamethasone. Full article ">Figure 2
Inhibitory effects of PBM on the elevation of allergic airway inflammation and goblet cell metaplasia in a PM2.5-exposed asthma exacerbation model. (A) Measurement of total and differential inflammatory cell counts (macrophage, neutrophils, lymphocytes, and eosinophils) in bronchoalveolar lavage fluid (BALF). (B) Evaluation of Th2 cytokines including interleukin (IL)-4, IL-5, and IL-13 in BALF. (C) Assessment of histamine and mast cell tryptase in BALF. (D) Representative images of H&E staining revealed the infiltration of inflammatory cells in lung tissues. Scale bar represents 200 µm (up) and 100 µm (down). The bar graphs represent the summarized score of inflammation. (E) Goblet cells secreting mucus in lung tissues were identified using PAS staining. The bar graphs represent the number of PAS-reactive airway epithelial cells. Scale bar represents 50 µm. The bar graphs represent the summarized scores of PAS-positive mucus-producing cells. Data are shown as the mean ± SEM (n = 8). * p < 0.05 compared with control. † p < 0.05 compared with PM + OVA. ‡ p < 0.05 compared with PM + OVA + PBM. Full article ">Figure 3
Inhibitory effects of PBM on the elevation of subepithelial fibrosis in a PM2.5-exposed asthma exacerbation model. Representative histological images showing (A) lung collagen fiber (Masson’s trichrome staining) and (B) collagen deposition (Sirius Red staining) in the lung tissues. Scale bar represents 100 µm. The bar graphs represent the summarized scores of collagen fiber deposition (n = 8). (C) Representative images of α-smooth muscle actin (α-SMA) and FITC expression, as determined by immunohistochemistry, in bronchioles of similar size. Scale bar represents 20 µm. The bar graphs represent the area of α-SMA staining per micrometer length of the bronchiolar basement membrane (µm2/µm; n = 6). (D) Detection of the mRNA levels of Acta2, Tgfb1, Col1a1, and Col3a1 in lung tissues using qRT-PCR (n = 4). Data are shown as the mean ± SEM. * p < 0.05 compared with control. † p < 0.05 compared with PM + OVA. Full article ">Figure 4
Inhibitory effects of PBM on the ROS-mediated ER stress in a PM2.5-exposed asthma exacerbation model. (A) Representative lung sections were stained with antibody specific for 8-hydroxy-2′-deoxyguanosine (8-OHdG). Bar graphs represent the quantification of positive areas of 8-OHdG in each experimental group (n = 4). Scale bar represents 100 µm. (B) ROS levels in lung tissue were measured in relative fluorescence units (RFU). (C) Protein expression of superoxide dismutase 1 (SOD1) and peroxiredoxin 4 (PRDX4). (D) ER stress markers (PERK, eIF2α, ATF4, and CHOP) in lung tissues by Western blotting. β-actin was used as a loading control. Bar graphs represent the quantification protein expression (n = 3). Data are shown as the mean ± SEM. * p < 0.05 compared with control. † p < 0.05 compared with PM + OVA. Full article ">Figure 5
Inhibitory effects of PBM on the cell death in a PM2.5-exposed asthma exacerbation model. (A) Representative immunofluorescence for TUNEL (green) and DAPI (blue) staining. Scale bar represents 50 µm. Bar graphs represent TUNEL (+)/DAPI (+) cells in the lung tissues (n = 3). (B) Apoptotic markers in lung tissues. Bar graphs represent the quantification protein expression (n = 3). Bar graphs represent the quantification protein expression (n = 3). Data are shown as the mean ± SEM. * p < 0.05 compared with control. † p < 0.05 compared with PM + OVA. Full article ">Figure 6
Inhibitory effects of PBM on the ferroptosis and autophagic signals in a PM2.5-exposed asthma exacerbation model. (A) Deposition of iron in lung tissue using Perls Prussian blue staining in lung tissues (n = 6). Scale bar represents 20 µm. (B) Malondialdehyde (MDA) concentration in lung tissue (n = 6). (C) Glutathione (GSH) concentration in lung tissue (n = 6). (D) Ca2+ levels in lung tissue (n = 5). (E) 4-Hydroxynonenal (4-HNE) levels in lung tissue (n = 6). (F) Ferroptosis markers in lung tissue (n = 3). (G) Autophagy markers in lung tissues. Bar graphs represent the quantification protein expression (n = 3). Data are shown as the mean ± SEM. * p < 0.05 compared to control. † p < 0.05 compared to PM + OVA. Full article ">Figure 7
Schematic representation of the anti-asthmatic effects of photobiomodulation (PBM) therapy on PM2.5 exposure-induced allergic asthma in a mouse model. PBM therapy reduces AHR, inflammation, Th2 cytokines, goblet cell hyperplasia, and subepithelial fibrosis in a PM2.5-exacerbated allergic asthma mouse model. PBM therapy also decreases oxidative and ER stress, apoptosis, and ferroptosis, while modulating autophagy in asthmatic mice exposed to PM2.5. These findings suggest PBM’s potential as an adjunct to asthma treatment in patients exposed to environmental pollutants. Abbreviations: DEX, dexamethasone; OVA, ovalbumin; PBM, photobiomodulation; PM, particulate matter, PM2.5, PM with a diameter < 2.5 μm. Full article ">

Review

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15 pages, 782 KiB

Open AccessReview

Deciphering the Liaison Between Fine Particulate Matter Pollution, Oxidative Stress, and Prostate Cancer: Where Are We Now?

by Chiang-Wen Lee, Yao-Chang Chiang, Thi Thuy Tien Vo, Zih-Chan Lin, Miao-Ching Chi, Mei-Ling Fang, Kuo-Ti Peng, Ming-Horng Tsai and I-Ta Lee

Antioxidants 2024, 13(12), 1505; https://doi.org/10.3390/antiox13121505 - 10 Dec 2024

Viewed by 493

Abstract

Prostate cancer (PCa), a highly prevalent cancer in men worldwide, is projected to rise in the coming years. As emerging data indicate the carcinogenic effects of fine particulate matter (PM2.5) in lung cancer and other site-specific cancers, there is an urgent need to evaluate the relationship between this environmental risk factor and PCa as a potential target for intervention. The present review provides up-to-date evidence about the impact of airborne PM2.5 pollution on the initiation and progression of PCa. Examining the composition and characteristics of PM2.5 reveals its ability to induce toxic effects, inflammatory injuries, and oxidative damages. Additionally, PM2.5 can attach to endocrine-disrupting chemicals implicated in prostatic carcinogenesis. Considering the potential significance of oxidative stress in the risk of the disease, our review underlines the protective strategies, such as antioxidant-based approaches, for individuals exposed to increased PM2.5 levels. Moreover, the findings call for further research to understand the associations and mechanisms linking PM2.5 exposure to PCa risk as well as to suggest appropriate measures by policymakers, scientific researchers, and healthcare professionals in order to address this global health issue. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution, 2nd Edition)

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