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Antioxidants
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From Field to Cell: Redox Mechanisms of Chemical Stressor Toxicity...
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From Field to Cell: Redox Mechanisms of Chemical Stressor Toxicity in Biological Systems

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 September 2026 | Viewed by 6876

Special Issue Editors

Dr. Marco G. Alves

E-Mail Website
Guest Editor
Institute of Biomedicine (iBiMED), Department of Medical Sciences, University of Aveiro, 3810-193 Aveiro, Portugal
Interests: metabolism; mitochondria; omics; andrology; oxidative stress
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Ariane Zamoner

E-Mail Website
Guest Editor
Department of Biochemistry, Federal University of Santa Catarina, Florianópolis, SC, Brazil
Interests: redox mechanisms in biological systems; environmental toxicology and health; molecular mechanisms of disease; chemical stressor toxicity; reproductive endocrinology and toxicology; drug discovery and development; interdisciplinary approaches in biosciences
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Antioxidants announces a Special Issue focusing on the intricate relationship between redox biology, redox signaling, and the toxicology of chemical stressors, including pesticides, environmental pollutants, and lifestyle. This issue aims to shed light on how redox processes are influenced by external chemical cues and how this impacts different biological systems. Chemical stressors have the potential to trigger intricate biochemical reactions that disrupt the redox balance, essential for sustaining cellular homeostasis and optimal functionality.

This Special Issue invites scientists to contribute articles and comprehensive reviews exploring the mechanisms of redox signaling affected by chemical stressors. We are particularly interested in studies revealing how these agents alter redox processes, impact cellular signaling pathways, and contribute to toxicity in different biological systems.

We encourage submissions that cover a range of topics, including but not limited to the identification of new chemical stressors affecting redox balance, mechanistic insights into redox-mediated toxicity, and the implications of redox biology in environmental toxicology. This issue aims to provide a platform for interdisciplinary dialogue and advance our understanding of redox processes in environmental health.

Dr. Marco G. Alves
Prof. Dr. Ariane Zamoner
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-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

  • redox biology
  • environmental toxicology
  • chemical stressors
  • pesticides
  • redox signaling

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Published Papers (2 papers)

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Research

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21 pages, 1013 KB  
Article
Alterations in Adenylate Nucleotide Metabolism and Associated Lipid Peroxidation and Protein Oxidative Damage in Rat Kidneys Under Combined Acetaminophen Toxicity and Protein Deficiency
by Oksana M. Voloshchuk, Halyna P. Kopylchuk, Maria S. Ursatyy, Karolina A. Kovalchuk and Oleksii Skorokhod
Antioxidants 2026, 15(1), 105; https://doi.org/10.3390/antiox15010105 - 13 Jan 2026
Cited by 3 | Viewed by 897
Abstract
Acetaminophen (APAP) overdose is a major cause of acute liver failure and can be fatal, often without early symptoms. Protein deficiency, arising from illness or inadequate diet, impairs growth, immunity, and tissue repair. Both conditions can harm the kidneys, yet the impact of [...] Read more.
Acetaminophen (APAP) overdose is a major cause of acute liver failure and can be fatal, often without early symptoms. Protein deficiency, arising from illness or inadequate diet, impairs growth, immunity, and tissue repair. Both conditions can harm the kidneys, yet the impact of energy imbalance on renal physiology remains unclear. In this study, APAP toxicity and a low-protein diet induced behavioral suppression and tissue damage, as evidenced by reduced whole-body, liver, and kidney weights in rats. In kidney mitochondria of rats exposed to only toxic APAP doses, ATP levels declined sharply while ADP and AMP increased. AMP deaminase and ATPases’ activities rose about twofold and 1.5-fold, respectively, whereas cytosolic 5′-nucleotidase activity fell nearly threefold, suggesting compensatory responses to disrupted energy balance. The strongest reductions in ATP and the greatest increases in AMP and ATPase activity occurred in APAP-intoxicated rats fed a low-protein diet. This combination also intensified lipid peroxidation and oxidative protein damage, evidenced by elevated TBARS, reduced protein SH-groups, and increased protein carbonyls. Overall, APAP intoxication with protein deficiency disrupts renal energy metabolism, leading to mitochondrial dysfunction and structural kidney injury. Nutritional status therefore critically influences drug-induced nephrotoxicity, and antioxidant strategies may help prevent damage under metabolic stress. Full article
(This article belongs to the Special Issue From Field to Cell: Redox Mechanisms of Chemical Stressor Toxicity in Biological Systems)
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Review

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33 pages, 4466 KB  
Review
Critical Review of Glyphosate-Induced Oxidative and Hormonal Testicular Disruption
by Sara R. Branco, Marco G. Alves, Pedro Fontes Oliveira and Ariane Zamoner
Antioxidants 2025, 14(9), 1036; https://doi.org/10.3390/antiox14091036 - 22 Aug 2025
Cited by 4 | Viewed by 4342
Abstract
Glyphosate, the active ingredient in many herbicides, has been extensively used in agricultural practices worldwide, leading to environmental persistence of the herbicide and its main metabolite, aminomethylphosphonic acid (AMPA), particularly in water and soil. Despite a short half-life in biological fluids, frequent detection [...] Read more.
Glyphosate, the active ingredient in many herbicides, has been extensively used in agricultural practices worldwide, leading to environmental persistence of the herbicide and its main metabolite, aminomethylphosphonic acid (AMPA), particularly in water and soil. Despite a short half-life in biological fluids, frequent detection of glyphosate and AMPA in urine samples suggests ongoing human exposure. Evidence indicates that glyphosate and AMPA may exert endocrine-disrupting effects on testicular function. Glyphosate exposure may disrupt the hypothalamic–pituitary–gonadal axis, impacting serum testosterone levels and other key hormones involved in spermatogenesis and fertility. It has also been shown to impair key cellular processes within the male reproductive system, including oxidative stress, mitochondrial dysfunction, and hormone biosynthesis. These findings raise concerns about the herbicide’s ability to compromise sperm production, structure, and motility, which are crucial factors for male fertility. This review examines the mechanisms underlying glyphosate-induced testicular toxicity, emphasizing endocrine disruption, oxidative stress, and mitochondrial dysfunction, and highlights the need for further studies on long-term effects across different life stages and genetic backgrounds. Glyphosate-induced testicular toxicity can be counteracted by antioxidant agents, which emerge as promising therapeutic strategies in need of further investigation. Full article
(This article belongs to the Special Issue From Field to Cell: Redox Mechanisms of Chemical Stressor Toxicity in Biological Systems)
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