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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 (20 October 2023) | Viewed by 25102

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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,

In 2021, the World Health Organization issued a new guideline on particulate matter such as PM2.5 and sounded a warning (WHO global air quality guidelines). There are various types of particles such as fine particle substances (PM2.5), industrial/pharmaceutical nanoparticles, and radiation α/β particles, and their properties are also different. Exposure to pollution containing these particulates is becoming more serious in many countries, including health effects. In particular, PM2.5 is involved in the cause of death in big cities and is said to be associated with cardiovascular disease, respiratory disease, and lung cancer. It is known that exposure to these substances induces inflammation at the exposed site and produces reactive oxygen species. Oxidative stress derived from PM affects various cells, and as a result, cell death is induced in some cells. In this process, acute and chronic inflammation is induced, establishing a mechanism by which they have additional biological effects.

Many studies have investigated the relationship between environmentally polluting particulates and health effects using cell-level experiments and animal experiments, but many parts have not yet been resolved. In this Special Issue, we will focus on the oxidative stress caused by these environmentally polluting particulates and provide topics that approach urgent issues.

Dr. Yasuhiro Yoshida
Guest Editor

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Keywords

particulate matter
inflammation
air pollution
oxidative stress

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Published Papers (11 papers)

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Editorial

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4 pages, 154 KiB

Open AccessEditorial

Oxidative Stress Induced by Air Pollution

by Yasuhiro Yoshida

Antioxidants 2024, 13(11), 1393; https://doi.org/10.3390/antiox13111393 - 15 Nov 2024

Cited by 2 | Viewed by 953

Abstract

In 2021, the World Health Organization issued new guidelines on particulate matter (PM), including PM2 [...] Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

Research

Jump to: Editorial

12 pages, 1097 KiB

Open AccessArticle

Occupational Exposure to Metal-Based Nanomaterials: A Possible Relationship between Chemical Composition and Oxidative Stress Biomarkers

by Valeria Bellisario, Giacomo Garzaro, Giulia Squillacioti, Marco Panizzolo, Federica Ghelli, Giuseppe Mariella, Roberto Bono, Irina Guseva Canu and Enrico Bergamaschi

Antioxidants 2024, 13(6), 676; https://doi.org/10.3390/antiox13060676 - 31 May 2024

Cited by 3 | Viewed by 1165

Abstract

Nanomaterials (NMs) are in high demand for a wide range of practical applications; however, comprehensively understanding the toxicity of these materials is a complex challenge, due to the limited availability of epidemiological evidence on the human health effects arising from workplace exposures. The aim of this work is to assess whether and how urinary metal concentrations could be reliable and useful in NM biomonitoring. In the framework of “NanoExplore Project” [EU LIFE17 Grant ENV/GR/000285], 43 not-exposed subjects and 40 exposed workers were recruited to measure exposure to NMs (PCN and LDSA) in the proximity of the workstations and biological biomarkers (urinary metal concentrations—Aluminum (Al), Silica (Si), Titanium (Ti), and Chromium (Cr); urinary OS biomarkers—TAP, Isop, and MDA). The results showed that Si and Ti were directly associated with NM exposure (both PCN and LDSA), as well as with OS biomarkers, especially in exposed workers. Moreover, the mediation analyses showed that Si could account for about 2.8% in the relationship between LDSA and OS biomarkers, possibly by decreasing OS antioxidant defenses in exposed people. In conclusion, our study provides evidence that occupational exposure to mixtures containing NMs can represent an underestimated hazard for exposed people, increasing the body burden and the oxidative balance. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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15 pages, 4088 KiB

Open AccessArticle

Inflammatory Cytokines and Chemokines Are Synergistically Induced in a ROS-Dependent Manner by a Co-Culture of Corneal Epithelial Cells and Neutrophil-like Cells in the Presence of Particulate Matter

by Zirui Zeng, Yasuhiro Yoshida, Duo Wang, Yuri Fujii, Mengyue Shen, Tatsuya Mimura and Yoshiya Tanaka

Antioxidants 2024, 13(4), 467; https://doi.org/10.3390/antiox13040467 - 16 Apr 2024

Cited by 3 | Viewed by 1981

Abstract

Ocular exposure to particulate matter (PM) causes local inflammation; however, the influence of neutrophils on PM-induced ocular inflammation is still not fully understood. In this study, we constructed a system to investigate the role of PM in ocular inflammation using a co-culture of human corneal epithelial cells (HCE-T) and differentiation-induced neutrophils (dHL-60). To investigate whether HCE-T directly endocytosed PM, we performed a holographic analysis, which showed the endocytosis of PM in HCE-T. The cytokines and chemokines produced by HCE-T were measured using an ELISA. HCE-T treated with PM produced IL-6 and IL-8, which were inhibited by N-Acetyl-L-cysteine (NAC), suggesting the involvement of ROS. Their co-culture with dHL-60 enhanced their production of IL-6, IL-8, and MCP-1. This suggests an inflammatory loop involving intraocular corneal epithelial cells and neutrophils. These cytokines and chemokines are mainly regulated by NF-κB. Therefore, this co-culture system was examined in the presence of an IKK inhibitor known to downregulate NF-κB activity. The IKK inhibitor dramatically suppressed the production of these factors in co-culture supernatants. The results suggest that the inflammatory loop observed in the co-culture is mediated through ROS and the transcription factor NF-κB. Thus, the co-culture system is considered a valuable tool for analyzing complex inflammations. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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14 pages, 2774 KiB

Open AccessArticle

Effects of Particulate Matter Inhalation during Exercise on Oxidative Stress and Mitochondrial Function in Mouse Skeletal Muscle

by Jinhan Park, Junho Jang, Byunghun So, Kanggyu Lee, Dongjin Yeom, Ziyi Zhang, Woo Shik Shin and Chounghun Kang

Antioxidants 2024, 13(1), 113; https://doi.org/10.3390/antiox13010113 - 17 Jan 2024

Cited by 1 | Viewed by 2562

Abstract

Particulate matter (PM) has deleterious consequences not only on the respiratory system but also on essential human organs, such as the heart, blood vessels, kidneys, and liver. However, the effects of PM inhalation on skeletal muscles have yet to be sufficiently elucidated. Female C57BL/6 or mt-Keima transgenic mice were randomly assigned to one of the following four groups: control (CON), PM exposure alone (PM), treadmill exercise (EX), or PM exposure and exercise (PME). Mice in the three-treatment group were subjected to treadmill running (20 m/min, 90 min/day for 1 week) and/or exposure to PM (100 μg/m³). The PM was found to exacerbate oxidative stress and inflammation, both at rest and during exercise, as assessed by the levels of proinflammatory cytokines, manganese-superoxide dismutase activity, and the glutathione/oxidized glutathione ratio. Furthermore, we detected significant increases in the levels of in vivo mitophagy, particularly in the PM group. Compared with the EX group, a significant reduction in the level of mitochondrial DNA was recorded in the PME group. Moreover, PM resulted in a reduction in cytochrome c oxidase activity and an increase in hydrogen peroxide generation. However, exposure to PM had no significant effect on mitochondrial respiration. Collectively, our findings in this study indicate that PM has adverse effects concerning both oxidative stress and inflammatory responses in skeletal muscle and mitochondria, both at rest and during exercise. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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17 pages, 1004 KiB

Open AccessArticle

Traffic Density Exposure, Oxidative Stress Biomarkers and Plasma Metabolomics in a Population-Based Sample: The Hortega Study

by Laura Sanchez-Rodriguez, Marta Galvez-Fernandez, Ayelén Rojas-Benedicto, Arce Domingo-Relloso, Nuria Amigo, Josep Redon, Daniel Monleon, Guillermo Saez, Maria Tellez-Plaza, Juan Carlos Martin-Escudero and Rebeca Ramis

Antioxidants 2023, 12(12), 2122; https://doi.org/10.3390/antiox12122122 - 15 Dec 2023

Cited by 3 | Viewed by 2041

Abstract

Exposure to traffic-related air pollution (TRAP) generates oxidative stress, with downstream effects at the metabolic level. Human studies of traffic density and metabolomic markers, however, are rare. The main objective of this study was to evaluate the cross-sectional association between traffic density in the street of residence with oxidative stress and metabolomic profiles measured in a population-based sample from Spain. We also explored in silico the potential biological implications of the findings. Secondarily, we assessed the contribution of oxidative stress to the association between exposure to traffic density and variation in plasma metabolite levels. Traffic density was defined as the average daily traffic volume over an entire year within a buffer of 50 m around the participants’ residence. Plasma metabolomic profiles and urine oxidative stress biomarkers were measured in samples from 1181 Hortega Study participants by nuclear magnetic resonance spectroscopy and high-performance liquid chromatography, respectively. Traffic density was associated with 7 (out of 49) plasma metabolites, including amino acids, fatty acids, products of bacterial and energy metabolism and fluid balance metabolites. Regarding urine oxidative stress biomarkers, traffic associations were positive for GSSG/GSH% and negative for MDA. A total of 12 KEGG pathways were linked to traffic-related metabolites. In a protein network from genes included in over-represented pathways and 63 redox-related candidate genes, we observed relevant proteins from the glutathione cycle. GSSG/GSH% and MDA accounted for 14.6% and 12.2% of changes in isobutyrate and the CH₂CH₂CO fatty acid moiety, respectively, which is attributable to traffic exposure. At the population level, exposure to traffic density was associated with specific urine oxidative stress and plasma metabolites. Although our results support a role of oxidative stress as a biological intermediary of traffic-related metabolic alterations, with potential implications for the co-bacterial and lipid metabolism, additional mechanistic and prospective studies are needed to confirm our findings. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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13 pages, 1279 KiB

Open AccessArticle

Effect of Particulate Matter 2.5 on Fetal Growth in Male and Preterm Infants through Oxidative Stress

by Sunwha Park, Eunjin Kwon, Gain Lee, Young-Ah You, Soo Min Kim, Young Min Hur, Sooyoung Jung, Yongho Jee, Mi Hye Park, Sung Hun Na, Young-Han Kim, Geum Joon Cho, Jin-Gon Bae, Soo-Jeong Lee, Sun Hwa Lee and Young Ju Kim

Antioxidants 2023, 12(11), 1916; https://doi.org/10.3390/antiox12111916 - 26 Oct 2023

Cited by 4 | Viewed by 2100 | Correction

Abstract

Particulate matter 2.5 (PM_2.5) levels are associated with adverse pregnancy outcomes. In this retrospective cohort study, we examined whether the concentration of indoor PM_2.5 affected pregnancy outcomes. Additionally, we evaluated biomarkers of pregnancy-related complications caused by fine dust. We collected clinical information and data based on residential addresses from the Air Korea database to assess PM_2.5 exposure levels. As a multicenter prospective cohort study, we measured the indoor PM_2.5 concentration and inflammatory and oxidative stress markers. The PM_2.5 concentration of the low-birth-weight (LBW) delivery group was 27.21 μg/m³, which was significantly higher than that of the normal-birth-weight (NBW) group (26.23 μg/m³) (p = 0.02). When the newborns were divided by sex, the PM_2.5 concentration of the LBW group was 27.89 μg/m³ in male infants, which was significantly higher than that of the NBW group (26.26 μg/m³) (p = 0.01). In the prospective study, 8-hydroxy-2-deoxyguanosine significantly increased in the high-concentration group (113.55 ng/mL, compared with 92.20 ng/mL in the low-concentration group); in the high-concentration group, the rates of preterm birth (PTB) and small size for gestational age significantly increased (p < 0.01, p = 0.01). This study showed an association between PM_2.5, oxidative stress, and fetal growth, with the PTB group being more vulnerable. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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17 pages, 3579 KiB

Open AccessArticle

Codium fragile Suppressed Chronic PM_2.5-Exposed Pulmonary Dysfunction via TLR/TGF-β Pathway in BALB/c Mice

by Tae Yoon Kim, Jong Min Kim, Hyo Lim Lee, Min Ji Go, Seung Gyum Joo, Ju Hui Kim, Han Su Lee, Won Min Jeong, Dong Yeol Lee, Hyun-Jin Kim and Ho Jin Heo

Antioxidants 2023, 12(9), 1743; https://doi.org/10.3390/antiox12091743 - 10 Sep 2023

Cited by 7 | Viewed by 2270

Abstract

This study investigated the ameliorating effect of the aqueous extract of Codium fragile on PM_2.5-induced pulmonary dysfunction. The major compounds of Codium fragile were identified as palmitic acid, stearic acid, and oleamide using GC/MS² and hexadecanamide, oleamide, and 13-docosenamide using UPLC-Q-TOF/MS^E. Codium fragile improved pulmonary antioxidant system deficit by regulating SOD activities and reducing GSH levels and MDA contents. It suppressed pulmonary mitochondrial dysfunction by regulating ROS contents and mitochondrial membrane potential levels. It regulated the inflammatory protein levels of TLR4, MyD88, p-JNK, p-NF-κB, iNOS, Caspase-1, TNF-α, and IL-1β. In addition, it improved the apoptotic protein expression of BCl-2, BAX, and Caspase-3 and attenuated the fibrous protein expression of TGF-β1, p-Smad-2, p-Smad-3, MMP-1, and MMP-2. In conclusion, this study suggests that Codium fragile might be a potential material for functional food or pharmaceuticals to improve lung damage by regulating oxidative stress inflammation, cytotoxicity, and fibrosis via the TLR/TGF-β1 signaling pathway. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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16 pages, 5419 KiB

Open AccessArticle

3-Bromo-4,5-dihydroxybenzaldehyde Protects Keratinocytes from Particulate Matter 2.5-Induced Damages

by Ao-Xuan Zhen, Mei-Jing Piao, Kyoung-Ah Kang, Pincha-Devage-Sameera-Madushan Fernando, Herath-Mudiyanselage-Udari-Lakmini Herath, Suk-Ju Cho and Jin-Won Hyun

Antioxidants 2023, 12(6), 1307; https://doi.org/10.3390/antiox12061307 - 20 Jun 2023

Cited by 7 | Viewed by 2096

Abstract

Cellular senescence can be activated by several stimuli, including ultraviolet radiation and air pollutants. This study aimed to evaluate the protective effect of marine algae compound 3-bromo-4,5-dihydroxybenzaldehyde (3-BDB) on particulate matter 2.5 (PM_2.5)-induced skin cell damage in vitro and in vivo. The human HaCaT keratinocyte was pre-treated with 3-BDB and then with PM_2.5. PM_2.5-induced reactive oxygen species (ROS) generation, lipid peroxidation, mitochondrial dysfunction, DNA damage, cell cycle arrest, apoptotic protein expression, and cellular senescence were measured using confocal microscopy, flow cytometry, and Western blot. The present study exhibited PM_2.5-generated ROS, DNA damage, inflammation, and senescence. However, 3-BDB ameliorated PM_2.5-induced ROS generation, mitochondria dysfunction, and DNA damage. Furthermore, 3-BDB reversed the PM_2.5-induced cell cycle arrest and apoptosis, reduced cellular inflammation, and mitigated cellular senescence in vitro and in vivo. Moreover, the mitogen-activated protein kinase signaling pathway and activator protein 1 activated by PM_2.5 were inhibited by 3-BDB. Thus, 3-BDB suppressed skin damage induced by PM_2.5. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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15 pages, 3508 KiB

Open AccessArticle

Clionasterol-Rich Fraction of Caulerpa racemosa against Particulate Matter-Induced Skin Damage via Inhibition of Oxidative Stress and Apoptosis-Related Signaling Pathway

by N. M. Liyanage, D. P. Nagahawatta, Thilina U. Jayawardena, H. H. A. C. K. Jayawardhana, Hyo-Geun Lee, Young-Sang Kim and You-Jin Jeon

Antioxidants 2022, 11(10), 1941; https://doi.org/10.3390/antiox11101941 - 28 Sep 2022

Cited by 10 | Viewed by 2798

Abstract

The increasing airborne particulate matter (PM) consisting of environmental contaminants such as dust, aerosols, and fibers has become a global concern by causing oxidative stress that leads to apoptosis and skin damage. The current study evaluated the protective effect of Caulerpa racemosa (CR) against PM-induced skin damage using human keratinocytes and a zebrafish model. The clionasterol-rich hexane fraction (CRHF2) of CR exhibited superior protective activity through downregulating intracellular reactive oxygen species levels and mitochondrial ROS levels, as well as the PM-induced increase in apoptotic body formation and upregulation of apoptotic signaling pathway proteins, along with sub-G1 cell accumulation dose-dependently. Furthermore, in vivo results showed that CRHF2 potentially downregulates PM-induced cell death, ROS, and NO production in the zebrafish model. Hence, the results evidenced that the protective effect of CRHF2 is caused by inhibiting oxidative stress and mitochondrial-mediated apoptosis in cells. Therefore, C. racemosa has the potential to be used in the development of pharmaceuticals to attenuate PM-induced skin diseases. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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11 pages, 1013 KiB

Open AccessArticle

Body Mass Index Modulates the Impact of Short-Term Exposure to Air Particulate Matter on High-Density Lipoprotein Function

by Alice Ossoli, Chiara Favero, Luisella Vigna, Angela Cecilia Pesatori, Valentina Bollati and Monica Gomaraschi

Antioxidants 2022, 11(10), 1938; https://doi.org/10.3390/antiox11101938 - 28 Sep 2022

Cited by 3 | Viewed by 2063

Abstract

Air particulate matter (PM) exposure has been associated with increased cardiovascular risk, especially in obesity. By triggering inflammation and oxidative stress, PM could impact atheroprotection by high-density lipoproteins (HDL). The aim of the study was to assess the relationship between short-term exposure to PM and HDL function, and the modifying effect of body mass index (BMI). Daily exposures to PM₁₀ and PM_2.5 of 50 subjects with overweight/obesity and 41 healthy volunteers with BMI < 30 kg/m² were obtained from fixed monitoring stations. HDL function was assessed as promotion of nitric oxide (NO) release by endothelial cells and reduction in cholesterol in macrophages. HDL-induced NO release progressively declined with the increase in BMI. No association was found between HDL function and PM exposure, but a modifying effect of BMI was observed. The positive association between PM₁₀ exposure at day −1 and NO production found at normal BMI values was lost in participants with higher BMI. Similar results were obtained for the reduction in macrophage cholesterol. The loss of the compensatory response of HDL function to PM exposure at increasing BMI levels could contribute to the endothelial dysfunction induced by PM and help to explain the susceptibility of subjects with obesity to air pollution. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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18 pages, 2566 KiB

Open AccessArticle

Oxidative Stress, Cytotoxic and Inflammatory Effects of Urban Ultrafine Road-Deposited Dust from the UK and Mexico in Human Epithelial Lung (Calu-3) Cells

by Jessica Hammond, Barbara A. Maher, Tomasz Gonet, Francisco Bautista and David Allsop

Antioxidants 2022, 11(9), 1814; https://doi.org/10.3390/antiox11091814 - 14 Sep 2022

Cited by 14 | Viewed by 3173

Abstract

Road-deposited dust (RD) is a pervasive form of particulate pollution identified (typically via epidemiological or mathematical modelling) as hazardous to human health. Finer RD particle sizes, the most abundant (by number, not mass), may pose greater risk as they can access all major organs. Here, the first in vitro exposure of human lung epithelial (Calu-3) cells to 0–300 µg/mL of the ultrafine (<220 nm) fraction of road dust (UF-RDPs) from three contrasting cities (Lancaster and Birmingham, UK, and Mexico City, Mexico) resulted in differential oxidative, cytotoxic, and inflammatory responses. Except for Cd, Na, and Pb, analysed metals were most abundant in Mexico City UF-RDPs, which were most cytotoxic. Birmingham UF-RDPs provoked greatest ROS release (only at 300 µg/mL) and greatest increase in pro-inflammatory cytokine release. Lancaster UF-RDPs increased cell viability. All three UF-RDP samples stimulated ROS production and pro-inflammatory cytokine release. Mass-based PM limits seem inappropriate given the location-specific PM compositions and health impacts evidenced here. A combination of new, biologically relevant metrics and localised regulations appears critical to mitigating the global pandemic of health impacts of particulate air pollution and road-deposited dust. Full article

(This article belongs to the Special Issue Oxidative Stress Induced by Air Pollution)

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