The Role of Oxidative Stress in Environmental Toxicity—2nd Edition

A special issue of Antioxidants (ISSN 2076-3921).

Deadline for manuscript submissions: closed (10 December 2025) | Viewed by 4401

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Laboratorio de Toxicología Ambiental, Facultad de Química, Universidad Autónoma del Estado de México, Toluca 50120, Mexico
Interests: ecotoxicology; aquatic toxicology; emerging contaminants; ecopharmacovigilance; oxidative stress; teratogenesis; geno- and cytotoxic effects
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Special Issue Information

Dear Colleagues,

The interaction between living organisms and the ever-changing environment, marked by the presence of various pollutants with different origins, constitutes a crucial field of study for understanding environmental and public health. Within this framework, oxidative stress emerges as a fundamental and transversal mechanism in the toxicity induced by a wide range of environmental agents. This Special Issue, titled “The Role of Oxidative Stress in Environmental Toxicity”, is dedicated to the exploration of the intricate relationship between pollutant exposure and alterations in redox balance in biological systems.

Exposure to xenobiotics, ranging from heavy metals, pesticides, and ultrafine particles to persistent organic compounds such as pharmaceuticals, emerging contaminants, and endocrine disruptors, can trigger the excessive generation of reactive oxygen species (ROS) and reactive nitrogen species (RNS). When the production of these species overwhelms the organism’s antioxidant defense systems, a state of oxidative stress is established. This condition can lead to significant molecular damage, affecting lipids, proteins, and nucleic acids and ultimately compromising cellular integrity and function.

In this second edition, we welcome cutting-edge research that contributes to elucidating the ways in which oxidative stress acts as a unifying mechanism of toxicity for diverse classes of environmental pollutants. By deepening our understanding of the molecular and cellular processes underlying this response, we can develop more effective strategies for risk assessment, disease prevention, and the mitigation of the negative impacts of pollution on the health of both ecosystems and populations.

Prof. Dr. Hariz Islas Flores
Guest Editor

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Keywords

  • environmental pollutants
  • oxidative stress biomarkers
  • water/air/soil pollution
  • environmental toxicity
  • ROS and RNS

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Published Papers (2 papers)

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Research

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16 pages, 2586 KB  
Article
Copper-Induced Thyroid Disruption and Oxidative Stress in Schizopygopsis younghusbandi Larvae
by Liqiao Zhong, Chi Zhang, Fei Liu, Haitao Gao, Dengyan Di, Fan Yao, Baoshan Ma, Mingdian Liu and Xinbin Duan
Antioxidants 2026, 15(1), 112; https://doi.org/10.3390/antiox15010112 - 15 Jan 2026
Cited by 1 | Viewed by 670
Abstract
In recent years, heavy metal emissions in Lhasa have been increasing, which has an impact on the local water environment. The negative effects of copper (Cu2+) on aquatic ecosystems have attracted much attention, as even low concentrations of Cu2+ can [...] Read more.
In recent years, heavy metal emissions in Lhasa have been increasing, which has an impact on the local water environment. The negative effects of copper (Cu2+) on aquatic ecosystems have attracted much attention, as even low concentrations of Cu2+ can exert toxic effects on aquatic organisms. However, the impact of Cu2+ on native fish species from the Lhasa River remains poorly understood. In this study, Schizopygopsis younghusbandi (S. younghusbandi) larvae were exposed to Cu2+ at concentrations of 0. 5, 5, 50, and 500 μg/L for 7 or 14 days to evaluate its toxic effects on thyroid function and the antioxidant system. The results indicate that whole-body total thyroxine (T4) and triiodothyronine (T3) levels were significantly decreased following Cu2+ exposure. This decrease was accompanied by a marked increase in dio1 and dio2 gene expression and decreased expression of thyroid hormone synthesis genes (nis, tg, ttf1 and pax8) after exposure to Cu2+. Furthermore, the activity of superoxide dismutase (SOD), catalase (CAT), and glutathione reductase (GR) and the content of lipid peroxidation were increased, while the content of glutathione (GSH) was decreased. In addition, the survival rates and body lengths of S. younghusbandi larvae were significantly reduced following 7- and 14-day Cu2+ exposure. The Integrated Assessment of Biomarker Response (IBR) analysis further revealed dose- and time-dependent effects of Cu2+ on the larvae. In conclusion, the findings demonstrate that Cu2+ exposure induced disruption of thyroid endocrine and antioxidant systems and caused developmental toxicity in S. younghusbandi larvae. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity—2nd Edition)
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Review

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32 pages, 927 KB  
Review
Environmental Nephrotoxicity Across the Life Course: Oxidative Stress Mechanisms and Opportunities for Early Intervention
by Chien-Ning Hsu, Chih-Yao Hou, Yu-Wei Chen, Guo-Ping Chang-Chien, Shu-Fen Lin and You-Lin Tain
Antioxidants 2025, 14(10), 1205; https://doi.org/10.3390/antiox14101205 - 4 Oct 2025
Cited by 8 | Viewed by 3043
Abstract
Chronic kidney disease (CKD) affects nearly 10% of the global population, ranks among the top ten causes of death, and often progresses silently to end-stage disease without timely intervention. Increasing evidence indicates that many adult-onset cases originate in early life through adverse influences [...] Read more.
Chronic kidney disease (CKD) affects nearly 10% of the global population, ranks among the top ten causes of death, and often progresses silently to end-stage disease without timely intervention. Increasing evidence indicates that many adult-onset cases originate in early life through adverse influences on kidney development, a process termed kidney programming within the Developmental Origins of Health and Disease (DOHaD) framework. Environmental pollutants are now recognized as key drivers of kidney injury across the life course. Heavy metals, air pollutants, plastic contaminants such as bisphenol A, phthalates, and micro/nanoplastics—as well as biocontaminants like mycotoxins and aristolochic acid—and chronic light pollution can accumulate in kidney tissue or act systemically to impair function. These exposures promote oxidative stress, inflammation, and endothelial and circadian disruption, culminating in tubular injury, glomerular damage, and fibrosis. Notably, early-life exposures can induce epigenetic modifications that program lifelong susceptibility to CKD and related complications. Oxidative stress is central to these effects, mediating DNA, lipid, and protein damage while influencing developmental reprogramming during gestation. Preclinical studies demonstrate that antioxidant-based interventions may mitigate these processes, providing both renoprotective and reprogramming benefits. This review explores the mechanistic links between environmental pollutants, oxidative stress, and kidney disease and highlights antioxidant strategies as promising avenues for prevention and intervention in vulnerable populations. Full article
(This article belongs to the Special Issue The Role of Oxidative Stress in Environmental Toxicity—2nd Edition)
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