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14.7
8.2
Journals
Antioxidants
Special Issues
Oxidative Stress Induced by Environmental Pollutants
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Oxidative Stress Induced by Environmental Pollutants

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: 28 February 2027 | Viewed by 596

Editor

Dr. Amie K. Lund

E-Mail Website
Guest Editor
Advanced Environmental Research Institute, Department of Biological Sciences, University of North Texas, Denton, TX 76203, USA
Interests: environmental pollution exposure-mediated contributions to diseases; cardiovascular disease; obesity; neurovascular/blood-brain barrier (BBB) disorders; dementia-related disorders; exposure related outcomes on the microbiota profiles and diversity in the lung and intestine

Special Issue Information

Dear Colleagues,

A substantial body of epidemiological and laboratory-based research has established a strong correlation between exposure to environmental pollutants and adverse human health outcomes. Environmental pollutants encompass a wide array of chemical, gaseous, particulate matter (PM), and biological compounds introduced into air, water, or soil. Many of these substances disrupt cellular redox balance, resulting in the generation of reactive oxygen species (ROS) and subsequent oxidative stress. When ROS generated by pollutants exceeds the capacity of antioxidant defenses, oxidative stress causes damage to DNA, proteins, and lipids. This process initiates chronic inflammation, tissue dysfunction, and disease. Oxidative stress resulting from exposure to environmental pollutants has been associated with the development of numerous chronic diseases, including cancer, neurodegenerative disorders, cardiovascular and respiratory diseases, and metabolic disorders, amongst others.

This Special Issue aims to build upon previous editions that primarily addressed outcomes related to air pollution by seeking novel research findings from a wider spectrum of environmental pollutant sources. By broadening the scope, this Special Issue seeks to enhance understanding of how exposure to diverse environmental contaminants induces oxidative stress that contributes to the pathophysiology of human diseases, thereby supporting the development of potential therapeutic interventions and public health strategies.

Dr. Amie K. Lund
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 250 words) can be sent to the Editorial Office for assessment.

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-anonymized 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

  • environmental pollutants
  • redox balance
  • reactive oxygen species
  • chronic diseases

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Published Papers (1 paper)

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Research

14 pages, 3081 KB  
Article
Seminal Vesicle Abnormalities and Exploratory miR-664-5p and FOXO Findings in Aged Mice Following Long-Term Butyl Benzyl Phthalate Exposure
by Seonhwa Hwang, Hyun Bon Kang, Dae Hyun Kim, Hyung Hoi Kim and Min Hi Park
Antioxidants 2026, 15(8), 1021; https://doi.org/10.3390/antiox15081021 - 17 Aug 2026
Viewed by 193
Abstract
Butyl benzyl phthalate (BBP), a widely used endocrine-disrupting chemical, has been associated with reproductive toxicity; however, its long-term effects during aging remain poorly understood. In the present study, we examined the effects of prolonged BBP exposure on the male reproductive system using naturally [...] Read more.
Butyl benzyl phthalate (BBP), a widely used endocrine-disrupting chemical, has been associated with reproductive toxicity; however, its long-term effects during aging remain poorly understood. In the present study, we examined the effects of prolonged BBP exposure on the male reproductive system using naturally aged C57BL/6J mice. Mice received BBP at 169 μg/kg/day in drinking water for 10 or 22 months and were analyzed at 24 months of age. No significant differences in body weight, food intake, or water consumption were observed among the experimental groups. Representative gross images showed apparent distension and dark-red discoloration of the seminal vesicles in BBP-exposed aged mice. Compared with Young mice, the BBP-exposed aged groups showed higher expression of IL-1β, IL-6, TNFα, SOD1, and SOD2 and lower CAT expression in the seminal vesicle. H2DCFDA fluorescence showed a non-significant increasing trend. Because an untreated age-matched Old group was not included in the seminal vesicle analyses, the effects of aging and BBP could not be distinguished. In contrast, the testis showed limited changes in inflammatory cytokine-, antioxidant enzyme-, and steroidogenesis-related gene expression and in H2DCFDA fluorescence relative to the untreated Old group. Exploratory miRNA sequencing of pooled testicular RNA and comparison with a TM3 Leydig cell dataset identified miR-664-5p as a candidate showing higher relative abundance in both datasets. TargetScan analysis predicted binding sites for miR-664-5p in FOXO1 and FOXO3. In BBP-treated TM3 cells, FOXO3 protein expression was decreased, and FOXO6 expression was increased, whereas FOXO1 showed no consistent dose-dependent change. These molecular findings do not establish direct regulation of FOXO proteins by miR-664-5p or explain the seminal vesicle findings. Full article
(This article belongs to the Special Issue Oxidative Stress Induced by Environmental Pollutants)
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