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Antioxidants
Special Issues
The Mechanism of Oxidative Stress Caused by PM2.5
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The Mechanism of Oxidative Stress Caused by PM2.5

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 (30 November 2022) | Viewed by 5830

Special Issue Editor

Prof. Dr. Wenjun Ding

E-Mail Website
Guest Editor
College of Life Sciences, University of Chinese Academy of Sciences, Beijing, China
Interests: environment and health; diabetes mellitus; obesity; oxidative stress
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Numerous epidemiologic studies have demonstrated that short- and long-term exposure to airborne fine particulate matter (PM) with aerodynamic diameter ≤ 2.5 μm (PM2.5) is closely associated with adverse health effects. PM2.5 exposure can induce airway damage, cardiovascular impairments, neurodegenerative disorders, exacerbation of diabetes mellitus and reproductive damage. Although the mechanisms underlying these adverse health effects are not fully understood, PM2.5-induced oxidative stress has been considered as a key mechanism of PM2.5-mediated toxicities. For example, PM2.5 exposure may lead to induction or increased levels of intracellular reactive oxygen species (ROS) and contribute to systemic oxidative stress. PM2.5-induced oxidative stress can activate inflammatory responses. PM2.5 can impair antioxidant defense and decrease the antioxidant capacity of exposed cells. On the other hand, PM2.5-induced ROS may cause toxic effects on cells via reacting to biomacromolecules, such as lipids, proteins, and DNA, impairing their structure and function and ultimately increasing damage to the target cells and tissues.

This Special Issue aims to collect papers dealing with all aspects of the mechanisms by which PM2.5-induced oxidative stress and its constituents act in producing the observed health effects; papers describing intricate signal pathways which are involved in the cellular responses to PM2.5 will be especially welcome.

Prof. Dr. Wenjun Ding
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • PM2.5
  • oxidative stress
  • toxic effects

Published Papers (2 papers)

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Research

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14 pages, 2856 KiB  
Article
Ageing Significantly Alters the Physicochemical Properties and Associated Cytotoxicity Profiles of Ultrafine Particulate Matters towards Macrophages
by Xu Yan, Yucai Chen, Li Ma, Yongchun Liu, Yu Qi and Sijin Liu
Antioxidants 2022, 11(4), 754; https://doi.org/10.3390/antiox11040754 - 10 Apr 2022
Cited by 3 | Viewed by 2178
Abstract
There are still significant concerns about the detrimental effects and health risks of particulate matters (PMs) on the respiratory system. Notably, a largely overlooked knowledge gap is whether the environmental ageing process would change the physicochemical properties of PMs as well as the [...] Read more.
There are still significant concerns about the detrimental effects and health risks of particulate matters (PMs) on the respiratory system. Notably, a largely overlooked knowledge gap is whether the environmental ageing process would change the physicochemical properties of PMs as well as the toxic influences of PMs on macrophages. Here, we applied ambient treatment of model PMs to mimic the real O3-induced ageing process and investigated ageing-determined cytotoxicity profile changes of PMs towards macrophages. The consequent distinct bioreactivity and toxicity towards macrophages are largely attributed to the changes of species of surface O-functional groups. Importantly, we unveiled the specific interactions between aged PMs and macrophages due to the variant contents of the surface carboxyl group, resulting in the divergent inflammatory activations and immune balance in the lung. Collectively, this study unearths the significance of ageing in altering particle cytotoxicity, and also provides additional understandings for consecutive investigations on the adverse effects of air pollution on the respiratory system. Full article
(This article belongs to the Special Issue The Mechanism of Oxidative Stress Caused by PM2.5)
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Review

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23 pages, 1212 KiB  
Review
Microglial Activation and Oxidative Stress in PM2.5-Induced Neurodegenerative Disorders
by Jie Song, Keyang Han, Ya Wang, Rongrong Qu, Yuan Liu, Shaolan Wang, Yinbiao Wang, Zhen An, Juan Li, Hui Wu and Weidong Wu
Antioxidants 2022, 11(8), 1482; https://doi.org/10.3390/antiox11081482 - 29 Jul 2022
Cited by 17 | Viewed by 3015
Abstract
Fine particulate matter (PM2.5) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM2.5 on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous [...] Read more.
Fine particulate matter (PM2.5) pollution remains a prominent environmental problem worldwide, posing great threats to human health. The adverse effects of PM2.5 on the respiratory and cardiovascular systems have been extensively studied, while its detrimental effects on the central nervous system (CNS), specifically neurodegenerative disorders, are less investigated. Neurodegenerative disorders are characterized by reduced neurogenesis, activated microglia, and neuroinflammation. A variety of studies involving postmortem examinations, epidemiological investigations, animal experiments, and in vitro cell models have shown that PM2.5 exposure results in neuroinflammation, oxidative stress, mitochondrial dysfunction, neuronal apoptosis, and ultimately neurodegenerative disorders, which are strongly associated with the activation of microglia. Microglia are the major innate immune cells of the brain, surveilling and maintaining the homeostasis of CNS. Upon activation by environmental and endogenous insults, such as PM exposure, microglia can enter an overactivated state that is featured by amoeboid morphology, the over-production of reactive oxygen species, and pro-inflammatory mediators. This review summarizes the evidence of microglial activation and oxidative stress and neurodegenerative disorders following PM2.5 exposure. Moreover, the possible mechanisms underlying PM2.5-induced microglial activation and neurodegenerative disorders are discussed. This knowledge provides certain clues for the development of therapies that may slow or halt the progression of neurodegenerative disorders induced by ambient PM. Full article
(This article belongs to the Special Issue The Mechanism of Oxidative Stress Caused by PM2.5)
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