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Antioxidants
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Developmental Origins of Health and Disease: Antioxidants as Strategy for...
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Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment

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

Deadline for manuscript submissions: 30 June 2026 | Viewed by 15641

Special Issue Editors

Dr. Silvia M. Arribas

E-Mail Website
Guest Editor
Department of Physiology, Faculty of Medicine, Universidad Autonoma de Madrid, C/Arzobispo Morcillo 2, 28029 Madrid, Spain
Interests: fetal programming; hypertension; oxidative stress biomarkers; nutrition; confocal microscopy
Special Issues, Collections and Topics in MDPI journals
Dr. David Ramiro-Cortijo

E-Mail Website
Guest Editor
Department of Phsyiology, Faculty of Medicine, Universidad Autonoma de Madrid, 28049 Madrid, Spain
Interests: breast milk; inflammation; prematurity; fetal programming; oxidative status; obstetrical complications; pregnant physiology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Disease development originates early in life, with mounting evidence highlighting the detrimental impact of adverse fetal environments on future health. Exposure to nutritional imbalances, hypoxia, toxic substances, obstetric complications, and psychological stress during pregnancy are well-documented to yield negative consequences for the offspring. These stressors exert their influence from the periconceptional period through the first 1000 days of life, underscoring their widespread reach.

Oxidative stress emerges as a common thread linking adverse early-life environments to disease development. Disruptions in redox equilibrium, stemming from either excessive oxidant production or inadequate antioxidant defenses, have been observed in humans and experimental animals exposed to these stressors during critical developmental windows. Oxidative stress contributes to germline damage, obstetric complications, and prematurity-related morbidity and underlies many common programmed diseases. Yet, the molecular changes tying these associations together remain largely unknown, including the mechanisms through which reactive oxygen species (ROS) and other oxidants modulate specific genes and their interplay with epigenetic modifications. Conversely, endogenous antioxidants sometimes prove insufficient, prompting an exploration into potential treatments. Understanding the capacity and safety of interventions to prevent or mitigate the effects of fetal programming is paramount.

We cordially invite submissions of your latest research or review articles to this Special Issue, aimed at elucidating the role of oxidative stress in the developmental origins of disease and exploring the potential therapeutic applications of antioxidants for prevention or treatment.

Dr. Silvia M. Arribas
Dr. David Ramiro-Cortijo
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

  • oxidative stress
  • pregnancy
  • germline damage
  • obstetric complications
  • fetal programming

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Published Papers (6 papers)

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Research

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28 pages, 2784 KB  
Article
Prenatal Melatonin Modulates Cardiovascular Function and Oxidative Stress in Guinea Pig Neonates Under Normoxic and Hypoxic Gestation
by Adolfo A. Paz, Tamara A. Jiménez, Pedro Herrera, Josefa Carreño, Damaris Cornejo, Julieta Ibarra-González, Javiera N. Ponce, Felipe A. Beñaldo, Mario Salamanca, Rodrigo Jeria, Esteban G. Figueroa, Alejandro González-Candia and Emilio A. Herrera
Antioxidants 2026, 15(2), 162; https://doi.org/10.3390/antiox15020162 - 25 Jan 2026
Cited by 1 | Viewed by 812
Abstract
Introduction: Gestational hypoxia (GH) increases the risk of cardiovascular diseases by inducing oxidative stress and vascular dysfunction. This study investigates whether prenatal melatonin can mitigate these effects in guinea pigs. Methods: Pregnant guinea pigs were exposed to normoxia or hypoxia and [...] Read more.
Introduction: Gestational hypoxia (GH) increases the risk of cardiovascular diseases by inducing oxidative stress and vascular dysfunction. This study investigates whether prenatal melatonin can mitigate these effects in guinea pigs. Methods: Pregnant guinea pigs were exposed to normoxia or hypoxia and treated with melatonin (1 mg/kg/day). Echocardiography, vascular reactivity, and molecular assays were used to assess cardiovascular structure, function, and redox balance in neonates. Results: GH reduced neonatal birth weight and altered left ventricular (LV) development, resulting in increased LV systolic function and aortic blood flow velocity. Melatonin treatment reversed these effects, restoring endothelial-dependent vasodilation and decreasing oxidative stress in the LV and thoracic aorta. Catalase antioxidant enzyme activity was elevated in melatonin-treated hypoxic neonates. Unexpectedly, melatonin treatment altered cardiac structure in normoxic pregnancies, increasing LV length and decreasing LV myocardial nuclei density. Conclusions: Prenatal melatonin partially modulates GH-induced endothelial dysfunction and oxidative stress, offering potential therapeutic value. However, its effects under normoxic conditions deserve caution, emphasizing the need for targeted use only in pregnancies with evident hypoxic and oxidative stress conditions. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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19 pages, 1640 KB  
Article
Exploratory Evaluation of Circulating Microbiota-Derived Corisin Levels in Women with Adverse Pregnancy Outcomes
by Maya Kato, Masafumi Nii, Kuniaki Toriyabe, Yuya Tamaishi, Sho Takakura, Shoichi Magawa, Taro Yasuma, Corina N. D’Alessandro-Gabazza, Hajime Fujimoto, Masaaki Toda, Isaac Cann, Tetsu Kobayashi, Esteban C. Gabazza, Eiji Kondo and Tomoaki Ikeda
Antioxidants 2025, 14(6), 670; https://doi.org/10.3390/antiox14060670 - 31 May 2025
Viewed by 1602
Abstract
Preterm birth and low birth weight remain major contributors to neonatal morbidity and mortality, yet the underlying mechanisms are not fully understood. Maternal microbiota has been implicated in adverse pregnancy outcomes, but key mediators remain unidentified. We previously showed that the microbiota-derived peptide [...] Read more.
Preterm birth and low birth weight remain major contributors to neonatal morbidity and mortality, yet the underlying mechanisms are not fully understood. Maternal microbiota has been implicated in adverse pregnancy outcomes, but key mediators remain unidentified. We previously showed that the microbiota-derived peptide corisin induces epithelial apoptosis via mitochondrial membrane depolarization and reactive oxygen species accumulation. In this retrospective preliminary study, we evaluated the association between maternal serum corisin levels and pregnancy outcomes in 84 eligible women. Among them, 10 experienced preterm birth, and 22 delivered low-birth-weight infants. Corisin levels were significantly elevated in these groups compared with women with full-term, normal-weight deliveries. Preterm birth was associated with increased tissue factor, while low birth weight correlated with higher thrombin–antithrombin complex and soluble thrombomodulin and lower fibrinogen levels. Corisin concentrations showed negative correlations with maternal BMI, birth weight and length, and estimated fetal weight. Positive correlations were observed between corisin, myeloperoxidase, and several coagulation markers. These preliminary findings suggest that elevated maternal corisin levels are associated with adverse pregnancy outcomes and may reflect underlying mechanisms involving oxidative stress and coagulation activation. Further investigation is warranted to clarify its potential role as a microbiota-derived biomarker in pregnancy complications. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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Review

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26 pages, 1854 KB  
Review
Oxidative Stress-Related Metabolomic Alterations in Pregnancy: Evidence from Exposure to Air Pollution, Metals/Metalloid, and Tobacco Smoke
by Alica Pizent
Antioxidants 2025, 14(12), 1442; https://doi.org/10.3390/antiox14121442 - 30 Nov 2025
Cited by 2 | Viewed by 1859
Abstract
Developmental programming, shaped by environmental and lifestyle stressors during prenatal life, is increasingly recognized as a major contributor to non-communicable diseases (NCDs) later in life. Oxidative stress, one of key mechanisms linking these stressors to fetal metabolomic reprogramming and disease pathogenesis, leaves measurable [...] Read more.
Developmental programming, shaped by environmental and lifestyle stressors during prenatal life, is increasingly recognized as a major contributor to non-communicable diseases (NCDs) later in life. Oxidative stress, one of key mechanisms linking these stressors to fetal metabolomic reprogramming and disease pathogenesis, leaves measurable metabolomic signatures that reflect disrupted redox balance. Alterations in glucose, lipid, and amino acid metabolism and antioxidant response could reveal the main pathways driving NCD development. This review summarizes epidemiological studies that have investigated biochemical responses of the prenatal exposure to metals, air pollution, and tobacco smoke and e-cigarette vapor in maternal–placental–fetal compartments using a metabolomic approach. Summarized studies indicate that maternal exposure to metals primarily disrupts amino acid pathways related to one-carbon metabolism, glutathione synthesis, and oxidative stress defense, while air pollution, particularly fine particulate matter, mainly affects lipid oxidation, fatty acid β-oxidation, and amino acid and carbohydrate metabolism. Tobacco smoke and e-cigarette vapor induce widespread disturbances involving reduced citric acid cycle intermediates, altered acylcarnitines and phospholipids, and impaired antioxidant capacity, collectively promoting oxidative damage and inflammatory signaling. The identification of these metabolome alterations might contribute to a deeper understanding of the toxicity and biological impact of environmental stressors on offspring health. These results may eventually lead to the identification of early biomarkers and to the development of therapeutic strategies aimed at reducing NCD risk. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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24 pages, 587 KB  
Review
Uric Acid and Preeclampsia: Pathophysiological Interactions and the Emerging Role of Inflammasome Activation
by Celia Arias-Sánchez, Antonio Pérez-Olmos, Virginia Reverte, Isabel Hernández, Santiago Cuevas and María Teresa Llinás
Antioxidants 2025, 14(8), 928; https://doi.org/10.3390/antiox14080928 - 29 Jul 2025
Cited by 10 | Viewed by 5332
Abstract
Preeclampsia (PE) is a multifactorial hypertensive disorder unique to pregnancy and a leading cause of maternal and fetal morbidity and mortality worldwide. Its pathogenesis involves placental dysfunction and an exaggerated maternal inflammatory response. Uric acid (UA), traditionally regarded as a marker of renal [...] Read more.
Preeclampsia (PE) is a multifactorial hypertensive disorder unique to pregnancy and a leading cause of maternal and fetal morbidity and mortality worldwide. Its pathogenesis involves placental dysfunction and an exaggerated maternal inflammatory response. Uric acid (UA), traditionally regarded as a marker of renal impairment, is increasingly recognized as an active contributor to the development of PE. Elevated UA levels are associated with oxidative stress, endothelial dysfunction, immune activation, and reduced renal clearance. Clinically, UA is measured in the second and third trimesters to assess disease severity and guide obstetric management, with higher levels correlating with early-onset PE and adverse perinatal outcomes. Its predictive accuracy improves when combined with other clinical and biochemical markers, particularly in low-resource settings. Mechanistically, UA and its monosodium urate crystals can activate the NLRP3 inflammasome, a cytosolic multiprotein complex of the innate immune system. This activation promotes the release of IL-1β and IL-18, exacerbating placental, vascular, and renal inflammation. NLRP3 inflammasome activation has been documented in placental tissues, immune cells, and kidneys of women with PE and is associated with hypertension, proteinuria, and endothelial injury. Experimental studies indicate that targeting UA metabolism or inhibiting NLRP3 activation, using agents such as allopurinol, metformin, or MCC950, can mitigate the clinical and histopathological features of PE. These findings support the dual role of UA as both a biomarker and a potential therapeutic target in the management of the disease. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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22 pages, 1077 KB  
Review
Oxidative Stress in Maternal and Offspring Kidney Disease and Hypertension: A Life-Course Perspective
by Pei-Chen Lu, You-Lin Tain, Ying-Jui Lin and Chien-Ning Hsu
Antioxidants 2025, 14(4), 387; https://doi.org/10.3390/antiox14040387 - 26 Mar 2025
Cited by 4 | Viewed by 1921
Abstract
Kidney disease and hypertension are interconnected, prevalent conditions that affect both pregnant women and children. Oxidative stress occurs when reactive oxygen species or reactive nitrogen species exceed the capacity of antioxidant systems. It plays a critical role in kidney development, resulting in kidney [...] Read more.
Kidney disease and hypertension are interconnected, prevalent conditions that affect both pregnant women and children. Oxidative stress occurs when reactive oxygen species or reactive nitrogen species exceed the capacity of antioxidant systems. It plays a critical role in kidney development, resulting in kidney programming and increased risks for kidney disease and hypertension across the life course. Animal models have significantly advanced our understanding of oxidative stress-related kidney programming, the molecular mechanisms involved, and early-life antioxidant interventions to prevent kidney disease. This review critically examines the influence of perinatal oxidative stress on kidney development, highlighting its long-term effects on kidney outcomes and susceptibility to hypertension. It also explores the potential of antioxidant-based interventions in preventing kidney disease and hypertension. Furthermore, the review addresses the existing gap between insights gained from animal models and their translation into clinical practices, emphasizing the challenges and opportunities for future research in this area. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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Other

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31 pages, 500 KB  
Systematic Review
Oxidative Stress and Down Syndrome: A Systematic Review
by Goran Slivšek, Sandra Mijač, Ivan Dolanc, Marija Fabijanec, Silvija Petković, Renato Mautner, Karmen Lončarek, Josip Kranjčić, Alenka Boban Blagaić, Marin Marinović, Ksenija Vitale, Donatella Verbanac, Miran Čoklo and Jadranka Vraneković
Antioxidants 2025, 14(7), 816; https://doi.org/10.3390/antiox14070816 - 2 Jul 2025
Cited by 4 | Viewed by 3109
Abstract
Down syndrome (DS), the most common human aneuploidy, is associated with oxidative stress, which contributes to morphological abnormalities, immune dysfunction, cognitive impairment and accelerated ageing. This article aims to provide an overview of the studies on oxidative stress in DS, in particular the [...] Read more.
Down syndrome (DS), the most common human aneuploidy, is associated with oxidative stress, which contributes to morphological abnormalities, immune dysfunction, cognitive impairment and accelerated ageing. This article aims to provide an overview of the studies on oxidative stress in DS, in particular the investigation of endogenous and exogenous antioxidants, with a focus on endogenous systems. A literature search in MEDLINE and Scopus based on the PRISMA 2020 criteria revealed 41 relevant studies that mainly analysed blood samples (plasma or serum) and occasionally saliva or urine. The findings suggest that oxidative stress in DS is multifactorial and results from an imbalance of superoxide dismutase activity, overexpression of genes on chromosome 21, mitochondrial dysfunction and inflammation. Despite extensive studies over the decades, new sources and mechanisms for oxidative stress in DS continue to emerge, further highlighting the complexity of DS. The recognition that oxidative stress is a hallmark of DS emphasises the need to develop more sensitive and specific methods to detect it and to investigate the associated metabolic pathways in DS in more detail. The expansion of in vivo studies could facilitate the development of targeted interventions aimed at mitigating oxidative damage and ultimately improving outcomes for individuals with DS. Full article
(This article belongs to the Special Issue Developmental Origins of Health and Disease: Antioxidants as Strategy for Prevention and Treatment)
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