Antioxidant Therapies for Oxidative Stress-Related Diseases in Newborns

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: closed (1 April 2024) | Viewed by 1711

Special Issue Editors


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Department of Clinical and Experimental Medicine, Neonatal Intensive Care Unit, University of Messina, 98125 Messina, Italy
Interests: pediatrics; intensive care; oxidative stress; antioxidants
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Guest Editor
Neonatology Unit, University Hospital, Department of Medicine and Surgery, University of Parma, 43126 Parma, Italy
Interests: pediatrics; intensive care; oxidative stress; antioxidants
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Pediatric Unit, Department of Human and Pediatric Pathology "Gaetano Barresi", University of Messina, Street Consolare Valeria, 198124 Messina, Italy
Interests: pediatrics; pulmonology; allergy
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Special Issue Information

Dear Colleagues, 

Oxidative stress is a condition caused by an imbalance between antioxidant and oxidative factors, with severe consequences on our organism, leading to cell apoptosis and necrosis, cellular ageing and an increased incidence in neonatal, autoimmune, respiratory, neuronal and cancer diseases, also in children and adolescents. The involvement of oxidative stress in pediatric diseases is an important issue, but oxidative stress status in young populations and appropriate methods for its detection is to be elucidated.

In the context of pediatric diseases, specific biomarkers for oxidative stress-mediated injury have been investigated in the field of pediatric medicine, and, in parallel, there are currently numerous clinical trials involving the administration of antioxidants in various conditions.

Nevertheless, studies are urgently requested to understand the relationship between oxidative stress and pediatric diseases; a better knowledge of this issue supports future therapeutic strategies.

Globally, this Special Issue will accept high-quality research papers and original articles that have immediate relevance to clinical practice and multi-disciplinary perspectives reflecting the nature of modern treatment. This Special Issue will provide a multi-disciplinary focus for publishing original papers, reviews and commentary on the biochemistry and pathophysiology of oxidative stress, antioxidant defence systems and clinically applicable biomarkers in several clinical conditions, such as neonatal, respiratory and neuronal diseases. Finally, this Special Issue will accept clinical trials evaluating the efficacy and safety of antioxidants for oxidative stress-related diseases.  

Prof. Dr. Eloisa Gitto
Prof. Dr. Serafina Perrone
Dr. Sara Manti
Guest Editors

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Published Papers (2 papers)

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Research

24 pages, 5551 KiB  
Article
Obesogenic Diet in Mice Leads to Inflammation and Oxidative Stress in the Mother in Association with Sex-Specific Changes in Fetal Development, Inflammatory Markers and Placental Transcriptome
by Alejandro A. Candia, Samantha C. Lean, Cindy X. W. Zhang, Daniel R. McKeating, Anna Cochrane, Edina Gulacsi, Emilio A. Herrera, Bernardo J. Krause and Amanda N. Sferruzzi-Perri
Antioxidants 2024, 13(4), 411; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox13040411 - 28 Mar 2024
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Abstract
Background: Obesity during pregnancy is related to adverse maternal and neonatal outcomes. Factors involved in these outcomes may include increased maternal insulin resistance, inflammation, oxidative stress, and nutrient mishandling. The placenta is the primary determinant of fetal outcomes, and its function can be [...] Read more.
Background: Obesity during pregnancy is related to adverse maternal and neonatal outcomes. Factors involved in these outcomes may include increased maternal insulin resistance, inflammation, oxidative stress, and nutrient mishandling. The placenta is the primary determinant of fetal outcomes, and its function can be impacted by maternal obesity. The aim of this study on mice was to determine the effect of obesity on maternal lipid handling, inflammatory and redox state, and placental oxidative stress, inflammatory signaling, and gene expression relative to female and male fetal growth. Methods: Female mice were fed control or obesogenic high-fat/high-sugar diet (HFHS) from 9 weeks prior to, and during, pregnancy. On day 18.5 of pregnancy, maternal plasma, and liver, placenta, and fetal serum were collected to examine the immune and redox states. The placental labyrinth zone (Lz) was dissected for RNA-sequencing analysis of gene expression changes. Results: the HFHS diet induced, in the dams, hepatic steatosis, oxidative stress (reduced catalase, elevated protein oxidation) and the activation of pro-inflammatory pathways (p38-MAPK), along with imbalanced circulating cytokine concentrations (increased IL-6 and decreased IL-5 and IL-17A). HFHS fetuses were asymmetrically growth-restricted, showing sex-specific changes in circulating cytokines (GM-CSF, TNF-α, IL-6 and IFN-γ). The morphology of the placenta Lz was modified by an HFHS diet, in association with sex-specific alterations in the expression of genes and proteins implicated in oxidative stress, inflammation, and stress signaling. Placental gene expression changes were comparable to that seen in models of intrauterine inflammation and were related to a transcriptional network involving transcription factors, LYL1 and PLAG1. Conclusion: This study shows that fetal growth restriction with maternal obesity is related to elevated oxidative stress, inflammatory pathways, and sex-specific placental changes. Our data are important, given the marked consequences and the rising rates of obesity worldwide. Full article
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17 pages, 8537 KiB  
Article
Selenium Deficiency Exacerbates Hyperoxia-Induced Lung Injury in Newborn C3H/HeN Mice
by Lora C. Bailey-Downs, Laura G. Sherlock, Michaela N. Crossley, Aristides Rivera Negron, Paul T. Pierce, Shirley Wang, Hua Zhong, Cynthia Carter, Kathryn Burge, Jeffrey V. Eckert, Lynette K. Rogers, Peter F. Vitiello and Trent E. Tipple
Antioxidants 2024, 13(4), 391; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox13040391 - 25 Mar 2024
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Abstract
Extremely preterm infants are often treated with supraphysiological oxygen, which contributes to the development of bronchopulmonary dysplasia (BPD). These same infants exhibit compromised antioxidant capacities due in part to selenium (Se) deficiency. Se is essential for basal and inducible antioxidant responses. The present [...] Read more.
Extremely preterm infants are often treated with supraphysiological oxygen, which contributes to the development of bronchopulmonary dysplasia (BPD). These same infants exhibit compromised antioxidant capacities due in part to selenium (Se) deficiency. Se is essential for basal and inducible antioxidant responses. The present study utilized a perinatal Se deficiency (SeD) mouse model to identify the combined effects of newborn hyperoxia exposure and SeD on alveolarization and antioxidant responses, including the identification of affected developmental pathways. Se-sufficient (SeS) and SeD C3H/HeN breeding pairs were generated, and pups were exposed to room air or 85% O2 from birth to 14 d. Survival, antioxidant protein expression, and RNA seq analyses were performed. Greater than 40% mortality was observed in hyperoxia-exposed SeD pups. Surviving SeD pups had greater lung growth deficits than hyperoxia-exposed SeS pups. Gpx2 and 4 protein and Gpx activity were significantly decreased in SeD pups. Nrf2-regulated proteins, Nqo1 and Gclc were increased in SeD pups exposed to hyperoxia. RNA seq revealed significant decreases in the Wnt/β-catenin and Notch pathways. Se is a biologically relevant modulator of perinatal lung development and antioxidant responses, especially in the context of hyperoxia exposure. The RNA seq analyses suggest pathways essential for normal lung development are dysregulated by Se deficiency. Full article
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