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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: 20 December 2024 | Viewed by 6287

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 (4 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 989
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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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
Viewed by 1242
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 1049
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 5 | Viewed by 2111
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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