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Antioxidants
Special Issues
Oxidative Stress and Environmental Toxicology
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Oxidative Stress and Environmental Toxicology

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 (15 April 2025) | Viewed by 13939

Special Issue Editor

Dr. Ken-ichiro Tanaka

E-Mail Website
Guest Editor
Research Institute of Pharmaceutical Sciences, Faculty of Pharmacy, Musashino University, Nishitokyo 2028585, Japan
Interests: air pollution; metallothionein; oxidative stress; fibroblasts; idiopathic pulmonary fibrosis

Special Issue Information

Dear Colleagues,

Humans are exposed to air pollutants such as fine particulate matter (PM2.5), toxic metals such as cadmium and arsenic, and pesticides in the environment, and in many cases, these induce health problems. In addition, these toxic substances induce the excessive production of reactive oxygen species (ROS) through their own properties as radicals or by acting on our human tissues and cells. For example, it has been confirmed in cellular and animal experiments as well as clinical studies that air pollutants such as PM2.5 induce excessive ROS production, which in turn induces lung injury and cardiovascular damage. Therefore, discovering the detailed mechanisms of oxidative stress induced by toxic substances and how to prevent it is a critical issue for maintaining our health.

As Guest Editor, I invite you to contribute to the Special Issue on “Oxidative Stress and Environmental Toxicology”. Original articles and reviews will be published online in Antioxidants.

Dr. Ken-ichiro Tanaka
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

  • air pollutants
  • toxic metals
  • environmental toxicology
  • ROS

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Published Papers (6 papers)

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Research

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25 pages, 7480 KiB  
Article
Heavy Metal Exposure-Mediated Dysregulation of Sphingolipid Metabolism
by Shaheer Ahmad, Sierra Single, Yuelong Liu, Kenneth P. Hough, Yong Wang, Victor J. Thannickal, Mohammad Athar, Kayla F. Goliwas and Jessy S. Deshane
Antioxidants 2024, 13(8), 978; https://doi.org/10.3390/antiox13080978 - 12 Aug 2024
Viewed by 1727
Abstract
Exposure to heavy metals (HMs) is often associated with inflammation and cell death, exacerbating respiratory diseases including asthma. Most inhaled particulate HM exposures result in the deposition of HM-bound fine particulate matter, PM2.5, in pulmonary cell populations. While localized high concentrations [...] Read more.
Exposure to heavy metals (HMs) is often associated with inflammation and cell death, exacerbating respiratory diseases including asthma. Most inhaled particulate HM exposures result in the deposition of HM-bound fine particulate matter, PM2.5, in pulmonary cell populations. While localized high concentrations of HMs may be a causative factor, existing studies have mostly evaluated the effects of systemic or low-dose chronic HM exposures. This report investigates the impact of local high concentrations of specific HMs (NaAsO2, MnCl2, and CdCl2) on sphingolipid homeostasis and oxidative stress, as both play a role in mediating responses to HM exposure and have been implicated in asthma. Utilizing an in vitro model system and three-dimensional ex vivo human tissue models, we evaluated the expression of enzymatic regulators of the salvage, recycling, and de novo synthesis pathways of sphingolipid metabolism, and observed differential modulation in these enzymes between HM exposures. Sphingolipidomic analyses of specific HM-exposed cells showed increased levels of anti-apoptotic sphingolipids and reduced pro-apoptotic sphingolipids, suggesting activation of the salvage and de novo synthesis pathways. Differential sphingolipid regulation was observed within HM-exposed lung tissues, with CdCl2 exposure and NaAsO2 exposure activating the salvage and de novo synthesis pathway, respectively. Additionally, using spatial transcriptomics and quantitative real-time PCR, we identified HM exposure-induced transcriptomic signatures of oxidative stress in epithelial cells and human lung tissues. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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Review

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33 pages, 1735 KiB  
Review
Ambient Air Pollution and Congenital Heart Disease: Updated Evidence and Future Challenges
by Francesca Gorini and Alessandro Tonacci
Antioxidants 2025, 14(1), 48; https://doi.org/10.3390/antiox14010048 - 3 Jan 2025
Viewed by 1401
Abstract
Congenital heart disease (CHD) represents the major cause of infant mortality related to congenital anomalies globally. The etiology of CHD is mostly multifactorial, with environmental determinants, including maternal exposure to ambient air pollutants, assumed to contribute to CHD development. While particulate matter (PM) [...] Read more.
Congenital heart disease (CHD) represents the major cause of infant mortality related to congenital anomalies globally. The etiology of CHD is mostly multifactorial, with environmental determinants, including maternal exposure to ambient air pollutants, assumed to contribute to CHD development. While particulate matter (PM) is responsible for millions of premature deaths every year, overall ambient air pollutants (PM, nitrogen and sulfur dioxide, ozone, and carbon monoxide) are known to increase the risk of adverse pregnancy outcomes. In this literature review, we provide an overview regarding the updated evidence related to the association between maternal exposure to outdoor air pollutants and CHD occurrence, also exploring the underlying biological mechanisms from human and experimental studies. With the exception of PM, for which there is currently moderate evidence of its positive association with overall CHD risk following exposure during the periconception and throughout pregnancy, and for ozone which shows a signal of association with increased risk of pooled CHD and certain CHD subtypes in the periconceptional period, for the other pollutants, the data are inconsistent, and no conclusion can be drawn about their role in CHD onset. Future epidemiological cohort studies in countries with different degree of air pollution and experimental research on animal models are warranted to gain a comprehensive picture of the possible involvement of ambient air pollutants in CHD etiopathogenesis. While on the one hand this information could also be useful for timely intervention to reduce the risk of CHD, on the other hand, it is mandatory to scale up the use of technologies for pollutant monitoring, as well as the use of Artificial Intelligence for data analysis to identify the non-linear relationships that will eventually exist between environmental and clinical variables. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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22 pages, 2228 KiB  
Review
Bisphenol A and Its Emergent Substitutes: State of the Art of the Impact of These Plasticizers on Oxidative Stress and Its Role in Vascular Dysfunction
by José R. Palacios-Valladares, Yesenia I. Martinez-Jimenez, Vanessa Morillon-Torres, Omar B. Rivera-Maya, Rocio Gómez and Emma S. Calderon-Aranda
Antioxidants 2024, 13(12), 1468; https://doi.org/10.3390/antiox13121468 - 29 Nov 2024
Cited by 1 | Viewed by 1759
Abstract
The “One Health approach” has evidenced the significant impact of xenobiotic exposure to health, and humans are a relevant target for their toxic effects. Bisphenol A (BPA) exerts a ubiquitous exposure source in all ecosystems. Given its endocrine-disrupting and harmful consequences on health, [...] Read more.
The “One Health approach” has evidenced the significant impact of xenobiotic exposure to health, and humans are a relevant target for their toxic effects. Bisphenol A (BPA) exerts a ubiquitous exposure source in all ecosystems. Given its endocrine-disrupting and harmful consequences on health, several countries have enforced new regulations to reduce exposure to BPA. Cardiovascular diseases (CVDs) are complex conditions that lead to higher mortality worldwide, where family history, lifestyle, and environmental factors, like BPA exposure, have a remarkable contribution. This chemical compound is the most widely used in plastic and epoxy resin manufacturing and has been associated with effects on human health. Therefore, new-generation bisphenols (NGBs) are replacing BPA use, arguing that they do not harm health. Nonetheless, the knowledge about whether NGBs are secure options is scanty. Although BPA’s effects on several organs and systems have been documented, the role of BPA and NGBs in CVDs has yet to be explored. This review’s goals are focused on the processes of endothelial activation (EA)–endothelial dysfunction (ED), a cornerstone of CVDs development, bisphenols’ (BPs) effects on these processes through oxidant and antioxidant system alteration. Despite the scarce evidence on pro-oxidant effects associated with NGBs, our review demonstrated a comparable harmful effect on BPA. The results from the present review suggest that the biological mechanisms to explain BPs cardiotoxic effects are the oxidant stress ↔ inflammatory response ↔ EA ↔ ED → atherosclerotic plate → coagulation promotion. Other effects contributing to CVD development include altered lipid metabolism, ionic channels, and the activation of different intracellular pathways, which contribute to ED perpetuation in a concerted manner. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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44 pages, 2718 KiB  
Review
Metal Toxicity and Dementia Including Frontotemporal Dementia: Current State of Knowledge
by Francesca Gorini and Alessandro Tonacci
Antioxidants 2024, 13(8), 938; https://doi.org/10.3390/antiox13080938 - 1 Aug 2024
Cited by 3 | Viewed by 2782
Abstract
Frontotemporal dementia (FTD) includes a number of neurodegenerative diseases, often with early onset (before 65 years old), characterized by progressive, irreversible deficits in behavioral, linguistic, and executive functions, which are often difficult to diagnose due to their similar phenotypic characteristics to other dementias [...] Read more.
Frontotemporal dementia (FTD) includes a number of neurodegenerative diseases, often with early onset (before 65 years old), characterized by progressive, irreversible deficits in behavioral, linguistic, and executive functions, which are often difficult to diagnose due to their similar phenotypic characteristics to other dementias and psychiatric disorders. The genetic contribution is of utmost importance, although environmental risk factors also play a role in its pathophysiology. In fact, some metals are known to produce free radicals, which, accumulating in the brain over time, can induce oxidative stress, inflammation, and protein misfolding, all of these being key features of FTD and similar conditions. Therefore, the present review aims to summarize the current evidence about the environmental contribution to FTD―mainly dealing with toxic metal exposure―since the identification of such potential environmental risk factors can lead to its early diagnosis and the promotion of policies and interventions. This would allow us, by reducing exposure to these pollutants, to potentially affect society at large in a positive manner, decreasing the burden of FTD and similar conditions on affected individuals and society overall. Future perspectives, including the application of Artificial Intelligence principles to the field, with related evidence found so far, are also introduced. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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13 pages, 748 KiB  
Review
Is Cadmium Genotoxicity Due to the Induction of Redox Stress and Inflammation? A Systematic Review
by Khulud Badawi, Basma M. El Sharazly, Ola Negm, Raheela Khan and Wayne G. Carter
Antioxidants 2024, 13(8), 932; https://doi.org/10.3390/antiox13080932 - 1 Aug 2024
Cited by 2 | Viewed by 1712
Abstract
The transition metal cadmium (Cd) is toxic to humans and can induce cellular redox stress and inflammation. Cd is a recognized carcinogen, but the molecular mechanisms associated with its genotoxicity and carcinogenicity are not defined. Therefore, a systematic review was undertaken to examine [...] Read more.
The transition metal cadmium (Cd) is toxic to humans and can induce cellular redox stress and inflammation. Cd is a recognized carcinogen, but the molecular mechanisms associated with its genotoxicity and carcinogenicity are not defined. Therefore, a systematic review was undertaken to examine the scientific literature that has covered the molecular mechanism of Cd genotoxicity and its relationship to cellular redox stress and inflammation. An electronic database search of PubMed, Scopus, and the Web of Science Core Collection was conducted to retrieve the studies that had investigated if Cd genotoxicity was directly linked to the induction of redox stress and inflammation. Studies included exposure to Cd via in vitro and in vivo routes of administration. Of 214 publications retrieved, 10 met the inclusion criteria for this review. Preclinical studies indicate that Cd exposure causes the induction of reactive oxygen species (ROS) and, via concomitant activity of the transcription factor NF-κβ, induces the production of pro-inflammatory cytokines and a cytokine profile consistent with the induction of an allergic response. There is limited information regarding the impact of Cd on cellular signal transduction pathways, and the relationship of this to genotoxicity is still inconclusive. Nevertheless, pre-incubation with the antioxidants, N-acetylcysteine or sulforaphane, or the necroptosis inhibitor, necrostatin-1, reduces Cd toxicity; indicative that these agents may be a beneficial treatment adjunct in cases of Cd poisoning. Collectively, this review highlights that Cd-induced toxicity and associated tissue pathology, and ultimately the carcinogenic potential of Cd, may be driven by redox stress and inflammatory mechanisms. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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27 pages, 817 KiB  
Review
Nitrooxidative Stress and Neuroinflammation Caused by Air Pollutants Are Associated with the Biological Markers of Neurodegenerative Diseases
by Abraham Alberto Ramírez-Mendoza, María Luisa Mendoza-Magaña, Mario Alberto Ramírez-Herrera, Zamira Helena Hernández-Nazara and José Alfredo Domínguez-Rosales
Antioxidants 2024, 13(3), 326; https://doi.org/10.3390/antiox13030326 - 7 Mar 2024
Cited by 11 | Viewed by 2991
Abstract
Millions of people around the world are exposed to air pollutants, such as particulate matter 2.5 (PM2.5) and ozone (O3). Such exposure usually does not exclude these two types of pollutants and their harmful effects could be additive or [...] Read more.
Millions of people around the world are exposed to air pollutants, such as particulate matter 2.5 (PM2.5) and ozone (O3). Such exposure usually does not exclude these two types of pollutants and their harmful effects could be additive or synergistic. O3 is a highly oxidizing gas that reacts with the cellular environment just as PM2.5, triggering nitrooxidative damage. Once nitrooxidative stress overcomes the endogenous antioxidant system, an acute neuroinflammatory process is generated, and once it becomes chronic, it favors the formation of neurodegenerative disease markers. The presence of these markers becomes potentially dangerous in people who have a genetic predisposition and are at a higher risk of developing neurodegenerative diseases such as Alzheimer’s and Parkinson’s. Our experimental approach for nitrooxidative damage and neuroinflammation caused by air pollutants has focused on the exposure of rats to O3 in an isolated chamber. The hippocampus is the most studied brain structure because of its neuronal connectivity network with the olfactory epithelium, its weak antioxidant defense, and its fundamental roll in cognitive processes. However, other brain structures may exhibit a different degree of damage upon exposure to O3 and PM2.5, making their involvement an important factor in developing other CNS diseases. The age spectrum for augmented sensibility to air pollutants seems to mostly affect the pre-postnatal (autism spectrum) period and the elderly (neurodegenerative). Thus, a new approach could be the estimation of the damage caused by PM2.5 and O3 through a controlled exposure paradigm to determine the extent of damage caused by both pollutants. Full article
(This article belongs to the Special Issue Oxidative Stress and Environmental Toxicology)
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