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Antioxidants
Special Issues
One Health and Oxidative Stress: Environmental Drivers, Molecular Pathways, and...
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One Health and Oxidative Stress: Environmental Drivers, Molecular Pathways, and Disease Risk

A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 30 November 2026 | Viewed by 2070

Editors

Dr. Francesca Gorini

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Guest Editor
Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy
Interests: environmental pollution; environmental epidemiology; endocrine disruptors; thyroid diseases; thyroid cancer
Special Issues, Collections and Topics in MDPI journals
Dr. Andrea Borghini

E-Mail Website
Guest Editor
Institute of Clinical Physiology, National Research Council, 56124 Pisa, Italy
Interests: molecular epidemiology; cardiovascular disease; genetics; cellular mechanisms; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Alessandro Tonacci

E-Mail Website
Guest Editor
Institute of Clinical Physiology, National Research Council, Pisa, Italy
Interests: biomedical signal processing; artificial intelligence; consumer technology; sensoriality
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The One Health concept is based around the tight interconnection between human, animal, and ecosystem health, particularly in the context of rapidly changing environmental exposures. A growing body of evidence indicates that many environmental stressors—including air pollutants, micro- and nanoplastics, pesticides, endocrine disruptors, and emerging contaminants—exert their harmful effects through oxidative stress, mitochondrial dysfunction, epigenetic alterations, and redox-sensitive signaling pathways. These mechanisms are increasingly implicated in major non-communicable diseases, such as cardiovascular disease, cancer, metabolic disorders, and neurodegeneration, with profound implications for public and planetary health.

This Special Issue will explore the role of oxidative stress and antioxidant responses in mediating the health impacts of environmental exposures within a long-lasting, human-centered One Health framework. We welcome contributions that address, but are not limited to, the following topics:

  • Integration of mechanistic toxicology, environmental chemistry, and epidemiology;
  • Investigationsintomolecular and cellular mechanisms underlying the health effects of environmental stressors;
  • Assessment of shared risks across humans and ecosystems;
  • Evaluation of endogenous and exogenous (dietary or pharmacological) antioxidants as modulators of toxicity and disease risk;
  • Methodological advances in assessing oxidative stress in environmental and One Health research;
  • Novel methodological insights for measurements and data analysisand interrelationships between stressors, toxicity,and disease risks.

We invite original research articles, reviews, and conceptual or perspective papers. By bringing together multidisciplinary contributions, this Special Issue will provide a comprehensive and translational overview of how environmental drivers of oxidative stress affect health across species and systems and how antioxidant defenses may mitigate these effects. Ultimately, our goal is to support evidence-based strategies for prevention, risk assessment, and policy development aligned with the One Health vision. 

Dr. Francesca Gorini
Dr. Andrea Borghini
Dr. Alessandro Tonacci
Guest Editors

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

  • one health
  • environmental exposures
  • environmental epidemiology
  • cardiovascular disease
  • cancer
  • mitochondrial dysfunction
  • epigenetics
  • oxidative stress
  • antioxidants
  • toxicology

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Further information on MDPI's Special Issue policies can be found here.

Published Papers (2 papers)

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Review

32 pages, 2121 KB  
Review
Environmental Exposure to Micro- and Nanoplastics: Linking Cardiovascular Disease and Cancer Through Shared Biological Pathways—A Critical Review
by Andrea Borghini, Mariangela Palazzo, Alessandro Tonacci, Fabrizio Minichilli, Haotian Wu and Francesca Gorini
Antioxidants 2026, 15(7), 786; https://doi.org/10.3390/antiox15070786 - 24 Jun 2026
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Abstract
Micro- and nanoplastics (MPs/NPs) are ubiquitous environmental contaminants increasingly detected in air, food, drinking water, and human tissues, raising concerns about their potential long-term health effects. Accumulating evidence indicates that these particles can enter the human body, cross biological barriers, and elicit cellular [...] Read more.
Micro- and nanoplastics (MPs/NPs) are ubiquitous environmental contaminants increasingly detected in air, food, drinking water, and human tissues, raising concerns about their potential long-term health effects. Accumulating evidence indicates that these particles can enter the human body, cross biological barriers, and elicit cellular and molecular responses relevant to disease development. This review synthesizes current mechanistic evidence linking MP/NP exposure to cardiovascular disease (CVD) and cancer, two leading global causes of morbidity and mortality that share interconnected pathogenic pathways. Key mechanisms include chronic inflammation, oxidative stress, gut microbiota dysbiosis, genotoxicity, and epigenetic alterations, all of which are widely implicated in both conditions. However, the available evidence is still largely derived from in vitro and animal studies, with limited human epidemiological data. Important uncertainties remain regarding real-world exposure characterization, dose–response relationships, and long-term clinical outcomes, underscoring the need for standardized analytical approaches, validated exposure and effect biomarkers, and large-scale longitudinal studies to clarify causal associations for both cancer and CVD. Taken together, current evidence suggests that MPs/NPs may represent emerging environmental contributors to shared pathogenic pathways linking CVD and cancer; however, establishing causality in humans will require well-designed longitudinal studies that integrate exposure assessment and clinical outcomes. Full article
(This article belongs to the Special Issue One Health and Oxidative Stress: Environmental Drivers, Molecular Pathways, and Disease Risk)
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26 pages, 2345 KB  
Review
From Parallel Programming to Bidirectional Crosstalk: The Brain–Kidney Axis in Cardiovascular–Kidney–Metabolic Syndrome
by Chien-Ning Hsu and You-Lin Tain
Antioxidants 2026, 15(6), 769; https://doi.org/10.3390/antiox15060769 - 19 Jun 2026
Viewed by 868
Abstract
Cardiovascular–kidney–metabolic (CKM) syndrome is a systemic, interdependent disorder arising from the convergence of metabolic dysfunction, chronic kidney disease, and cardiovascular pathology. Anchored in the Developmental Origins of Health and Disease (DOHaD) framework, this review advances a “parallel hit” model, primarily based on evidence [...] Read more.
Cardiovascular–kidney–metabolic (CKM) syndrome is a systemic, interdependent disorder arising from the convergence of metabolic dysfunction, chronic kidney disease, and cardiovascular pathology. Anchored in the Developmental Origins of Health and Disease (DOHaD) framework, this review advances a “parallel hit” model, primarily based on evidence from experimental animal studies, particularly rodent models, posited that early-life environmental insults concurrently program structural and functional vulnerabilities in both renal and central nervous system hubs. These early perturbations prime susceptibility long before clinical manifestations emerge. CKM progression is conceptualized as a two-stage trajectory, with an initial phase of parallel programming affecting kidney and brain development, followed by a transition to maladaptive bidirectional crosstalk. In the later phase, heightened efferent sympathetic outflow and aberrant afferent renal signaling—potentiated by uremic toxin accumulation, neuroinflammation, and blood–brain barrier disruption—drive a self-perpetuating cycle that accelerates cardiorenal and metabolic injury. Key integrative mechanisms, including oxidative stress, chronic low-grade inflammation, mitochondrial dysfunction, and gut microbiota dysbiosis, serve as convergent pathways linking early-life exposures to adult CKM phenotypes. These pathways not only sustain disease progression but also represent actionable therapeutic targets. Importantly, this framework underscores the translational potential of early-life “reprogramming” strategies. Interventions such as precision nutrition, antioxidant supplementation, microbiota-directed therapies (including prebiotics, probiotics, and postbiotics), and mechanism-based pharmacotherapies may mitigate or reverse maladaptive programming. However, much of the current mechanistic evidence remains preclinical, and further human studies are needed to validate these pathways and therapeutic approaches. Collectively, this dual-hub paradigm reframes CKM syndrome as a life-course continuum rather than a late-stage comorbidity cluster, emphasizing the necessity of early, mechanism-driven interventions to stabilize the brain–kidney axis and improve long-term cardiovascular–kidney–metabolic outcomes. Full article
(This article belongs to the Special Issue One Health and Oxidative Stress: Environmental Drivers, Molecular Pathways, and Disease Risk)
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