Search for Articles:
Title / Keyword
Author / Affiliation / Email
Journal
Article Type
 
 
Advanced Search
 
Section
Special Issue
Volume
Issue
Number
Page
 
8.8
7.0
Journals
Antioxidants
Special Issues
Oxidative Stress in Newborns and Children
share announcement

Oxidative Stress in Newborns and Children

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 (31 October 2021) | Viewed by 23540

Special Issue Editors

Prof. Dr. Giuseppe Buonocore

E-Mail Website
Guest Editor
Department of Molecular and Developmental Medicine, General Hospital "Santa Maria alle Scotte", University of Siena, Siena, Italy
Interests: evaluation of new antioxidant drugs; role of oxidative stress in perinatal diseases; free radicals, proteomics and metabolomics; ethics and research in neonatology
Special Issues, Collections and Topics in MDPI journals
Prof. Dr. Serafina Perrone

E-Mail Website
Guest Editor
Department of Medicine and Surgery, University of Parma, 43121 Parma, Italy
Interests: oxidative stress; newborn; antioxidants
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Efforts to understand and prevent oxidative-stress-mediated diseases are worthwhile because of the huge number of newborn infants and children involved and the enormous cost to society.

The pathophysiology of oxidative-stress-mediated injury along life is complex and multifactorial, with oxidants playing a pivotal role because due to their involvement in the final common pathway for multiple converging events.

Antioxidant therapies may be considered to decrease organ damage. The mechanisms by which antioxidants exert protection are not fully understood. Antioxidants can act at different steps of the damage: scavenging reactive oxygen species, reducing the production of free radicals, altering antiradical defenses, increasing the antioxidant levels, and adding lipophilic antioxidants into cell membranes. Additionally, some antioxidants exhibit anti-inflammatory and anti-apoptotic properties as well.

To date, interesting research has been carried out, representing milestones for implementation of novel, reliable oxidative stress biomarkers and the discovery of functional pathways underlying free radical mediated diseases and their early identification and prevention.

Many compounds are ready for clinical trials, since their beneficial effects against oxidative stress have been proven in experimental animal studies. The next challenging goal will be to define yet unrecognized biological therapeutic targets and linking of oxidative stress biomarkers to relevant standard indices and long-term outcomes.

We invite you to submit your latest research results or review articles to this Special Issue, which will bring together current research related to oxidative stress in newborns and children and the action that antioxidant therapies have.

We look forward to your contribution.

Prof. Dr. Giuseppe Buonocore
Prof. Dr. Serafina Perrone
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 100 words) can be sent to the Editorial Office for announcement on this website.

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.

Published Papers (7 papers)

Download All Papers
Order results
Result details
Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:

Research

Jump to: Review

15 pages, 3085 KiB  
Article
Endothelial Adenosine Monophosphate-Activated Protein Kinase-Alpha1 Deficiency Potentiates Hyperoxia-Induced Experimental Bronchopulmonary Dysplasia and Pulmonary Hypertension
by Ahmed Elsaie, Renuka T. Menon, Amrit K. Shrestha, Sharada H. Gowda, Nidhy P. Varghese, Roberto J. Barrios, Cynthia L. Blanco, Girija G. Konduri and Binoy Shivanna
Antioxidants 2021, 10(12), 1913; https://doi.org/10.3390/antiox10121913 - 29 Nov 2021
Cited by 7 | Viewed by 2072
Abstract
Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase (AMPK) α1 in neonatal murine lungs; however, whether this phenomenon potentiates or mitigates lung [...] Read more.
Bronchopulmonary dysplasia and pulmonary hypertension, or BPD-PH, are serious chronic lung disorders of prematurity, without curative therapies. Hyperoxia, a known causative factor of BPD-PH, activates adenosine monophosphate-activated protein kinase (AMPK) α1 in neonatal murine lungs; however, whether this phenomenon potentiates or mitigates lung injury is unclear. Thus, we hypothesized that (1) endothelial AMPKα1 is necessary to protect neonatal mice against hyperoxia-induced BPD-PH, and (2) AMPKα1 knockdown decreases angiogenesis in hyperoxia-exposed neonatal human pulmonary microvascular endothelial cells (HPMECs). We performed lung morphometric and echocardiographic studies on postnatal day (P) 28 on endothelial AMPKα1-sufficient and -deficient mice exposed to 21% O2 (normoxia) or 70% O2 (hyperoxia) from P1–P14. We also performed tubule formation assays on control- or AMPKα1-siRNA transfected HPMECs, exposed to 21% O2 or 70% O2 for 48 h. Hyperoxia-mediated alveolar and pulmonary vascular simplification, pulmonary vascular remodeling, and PH were significantly amplified in endothelial AMPKα1-deficient mice. AMPKα1 siRNA knocked down AMPKα1 expression in HPMECs, and decreased their ability to form tubules in normoxia and hyperoxia. Furthermore, AMPKα1 knockdown decreased proliferating cell nuclear antigen expression in hyperoxic conditions. Our results indicate that AMPKα1 is required to reduce hyperoxia-induced BPD-PH burden in neonatal mice, and promotes angiogenesis in HPMECs to limit lung injury. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

13 pages, 843 KiB  
Article
Influence of Oxidative Stress Generated by Smoking during Pregnancy on Glutathione Status in Mother-Newborn Pairs
by Magdalena Chełchowska, Joanna Gajewska, Jadwiga Ambroszkiewicz, Joanna Mazur, Mariusz Ołtarzewski and Tomasz M. Maciejewski
Antioxidants 2021, 10(12), 1866; https://doi.org/10.3390/antiox10121866 - 24 Nov 2021
Cited by 8 | Viewed by 1972
Abstract
Glutathione plays a key role in maintaining a physiological balance between prooxidants and antioxidants in the human body. Therefore, we examined the influence of maternal smoking as a source of oxidative stress measured by total oxidant capacity (TOC) on reduced glutathione (GSH), oxidized [...] Read more.
Glutathione plays a key role in maintaining a physiological balance between prooxidants and antioxidants in the human body. Therefore, we examined the influence of maternal smoking as a source of oxidative stress measured by total oxidant capacity (TOC) on reduced glutathione (GSH), oxidized glutathione (GSSG), glutathione peroxidase (GPx-3), and reductase (GR) amount in maternal and umbilical cord blood in 110 (45 smoking and 65 non-smoking) mother-newborn pairs. Concentrations of glutathione status markers and TOC were evaluated by competitive inhibition enzyme immunoassay technique. Plasma TOC levels were significantly higher and the GSH/GSSG ratio, which is considered an index of the cell’s redox status, were significantly lower in smoking women and their offspring than in non-smoking pairs. Decreased GR levels were found in smoking mothers and their newborns compared with similar non-smoking groups. Although plasma GPx-3 concentrations were similar in both maternal groups, in the cord blood of newborns exposed to tobacco smoke in utero they were reduced compared with the levels observed in children of tobacco abstinent mothers. Oxidative stress generated by tobacco smoke impairs glutathione homeostasis in both the mother and the newborn. The severity of oxidative processes in the mother co-existing with the reduced potential of antioxidant systems may have a negative effect on the oxidative-antioxidant balance in the newborn. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

14 pages, 4757 KiB  
Article
Newborns of Mothers with Venous Disease during Pregnancy Show Increased Levels of Lipid Peroxidation and Markers of Oxidative Stress and Hypoxia in the Umbilical Cord
by Miguel A. Ortega, Lara Sánchez-Trujillo, Coral Bravo, Oscar Fraile-Martinez, Cielo García-Montero, Miguel A. Saez, Miguel A. Alvarez-Mon, Felipe Sainz, Melchor Alvarez-Mon, Julia Bujan, Juan A. De Leon-Luis and Natalio García-Honduvilla
Antioxidants 2021, 10(6), 980; https://doi.org/10.3390/antiox10060980 - 18 Jun 2021
Cited by 14 | Viewed by 2160
Abstract
Chronic venous disease (CVD) encompasses a set of disorders of the venous system that have a high prevalence in Western societies and are associated with significant sociohealth costs. Pregnancy is a period in which different hormonal and haemodynamic changes occur that lead to [...] Read more.
Chronic venous disease (CVD) encompasses a set of disorders of the venous system that have a high prevalence in Western societies and are associated with significant sociohealth costs. Pregnancy is a period in which different hormonal and haemodynamic changes occur that lead to significant changes in the cardiovascular system, increasing the risk of developing venous problems, especially during the third trimester of gestation. In turn, CVD involves a series of local and systemic alterations that can have negative repercussions in pregnancy. In this context, the role of oxidative stress in the pathophysiology of this condition has been shown to significantly affect other vascular structures during pregnancy, such as the placenta. However, the effects of oxidative stress on the umbilical cord in women with CVD have not yet been fully elucidated. Thus, the objective of this study was to analyse the gene and protein expression of the enzymes NOX-1, NOX-2 and iNOS, which are involved in the production of reactive oxygen and nitrogen species, respectively. Similarly, the presence of hypoxia-inducible factor 1-alpha (HIF-1α) in the umbilical cord in women with CVD was compared to that of pregnant control women, and the levels of the lipid peroxidation marker malonyldialdehyde (MDA) in cord tissue and blood was also analysed. Our results support a significant increase in the enzymes NOX-1, NOX-2 and iNOS and HIF-1α and MDA in the umbilical cord tissue and blood of women with CVD. For the first time, our work demonstrates an increase in oxidative stress and cellular damage in the umbilical cords of pregnant women who develop this condition, deepening the understanding of the consequences of CVD during pregnancy. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

11 pages, 945 KiB  
Article
Oxidative Stress and Alterations of Paraoxonases in Atopic Dermatitis
by Oriana Simonetti, Tiziana Bacchetti, Gianna Ferretti, Elisa Molinelli, Giulio Rizzetto, Luisa Bellachioma and Annamaria Offidani
Antioxidants 2021, 10(5), 697; https://doi.org/10.3390/antiox10050697 - 28 Apr 2021
Cited by 20 | Viewed by 2265
Abstract
Background: previous studies reported the involvement of reactive oxygen species (ROS) and lipid peroxidation in the pathogenesis of inflammatory skin diseases. The aim of our study was to investigate the relationship between oxidative stress and inflammation in children affected by atopic dermatitis (AD), [...] Read more.
Background: previous studies reported the involvement of reactive oxygen species (ROS) and lipid peroxidation in the pathogenesis of inflammatory skin diseases. The aim of our study was to investigate the relationship between oxidative stress and inflammation in children affected by atopic dermatitis (AD), a chronic relapsing inflammatory skin disease. Methods: levels of lipid hydroperoxides, total antioxidant capacity, and activities of the enzymes myeloperoxidase (MPO), PON1, and PON2/3 were investigated in 56 atopic pediatric patients, and compared with 48 sex-/age-matched healthy controls. Results: significantly higher levels of lipid hydroperoxides and lower values of total antioxidant potential were observed in the serum of AD children compared to that of the controls. Significant lower PON1 activities, and a significant increase in levels of MPO were observed in serum of patients, with a higher serum MPO level/PON1 paraoxonase activity ratio in patients compared to that in the controls. Significantly lower lactonase activity of PON enzymes was observed in polymorphonuclear cells isolated from AD patients. Statistically negative correlation was established between the activity of intracellular PON2/3 activity and ROS levels. Conclusions: our data confirmed that AD is associated with higher oxidative damage and a decrease in antioxidant defense. Moreover, alterations of extracellular and intracellular PON activity can promote lipoprotein dysfunction in AD patients. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

Review

Jump to: Research

29 pages, 2704 KiB  
Review
Sustained Energy Deficit Following Perinatal Asphyxia: A Shift towards the Fructose-2,6-bisphosphatase (TIGAR)-Dependent Pentose Phosphate Pathway and Postnatal Development
by Carolyne Lespay-Rebolledo, Andrea Tapia-Bustos, Ronald Perez-Lobos, Valentina Vio, Emmanuel Casanova-Ortiz, Nancy Farfan-Troncoso, Marta Zamorano-Cataldo, Martina Redel-Villarroel, Fernando Ezquer, Maria Elena Quintanilla, Yedy Israel, Paola Morales and Mario Herrera-Marschitz
Antioxidants 2022, 11(1), 74; https://doi.org/10.3390/antiox11010074 - 29 Dec 2021
Cited by 2 | Viewed by 6436
Abstract
Labor and delivery entail a complex and sequential metabolic and physiologic cascade, culminating in most circumstances in successful childbirth, although delivery can be a risky episode if oxygen supply is interrupted, resulting in perinatal asphyxia (PA). PA causes an energy failure, leading to [...] Read more.
Labor and delivery entail a complex and sequential metabolic and physiologic cascade, culminating in most circumstances in successful childbirth, although delivery can be a risky episode if oxygen supply is interrupted, resulting in perinatal asphyxia (PA). PA causes an energy failure, leading to cell dysfunction and death if re-oxygenation is not promptly restored. PA is associated with long-term effects, challenging the ability of the brain to cope with stressors occurring along with life. We review here relevant targets responsible for metabolic cascades linked to neurodevelopmental impairments, that we have identified with a model of global PA in rats. Severe PA induces a sustained effect on redox homeostasis, increasing oxidative stress, decreasing metabolic and tissue antioxidant capacity in vulnerable brain regions, which remains weeks after the insult. Catalase activity is decreased in mesencephalon and hippocampus from PA-exposed (AS), compared to control neonates (CS), in parallel with increased cleaved caspase-3 levels, associated with decreased glutathione reductase and glutathione peroxidase activity, a shift towards the TIGAR-dependent pentose phosphate pathway, and delayed calpain-dependent cell death. The brain damage continues long after the re-oxygenation period, extending for weeks after PA, affecting neurons and glial cells, including myelination in grey and white matter. The resulting vulnerability was investigated with organotypic cultures built from AS and CS rat newborns, showing that substantia nigra TH-dopamine-positive cells from AS were more vulnerable to 1 mM of H2O2 than those from CS animals. Several therapeutic strategies are discussed, including hypothermia; N-acetylcysteine; memantine; nicotinamide, and intranasally administered mesenchymal stem cell secretomes, promising clinical translation. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

15 pages, 1420 KiB  
Review
Thiamine as a Possible Neuroprotective Strategy in Neonatal Hypoxic-Ischemic Encephalopathy
by Gian Pietro Sechi, Flaminia Bardanzellu, Maria Cristina Pintus, Maria Margherita Sechi, Maria Antonietta Marcialis and Vassilios Fanos
Antioxidants 2022, 11(1), 42; https://doi.org/10.3390/antiox11010042 - 25 Dec 2021
Cited by 8 | Viewed by 3858
Abstract
On the basis that similar biochemical and histological sequences of events occur in the brain during thiamine deficiency and hypoxia/ischemia related brain damage, we have planned this review to discuss the possible therapeutic role of thiamine and its derivatives in the management of [...] Read more.
On the basis that similar biochemical and histological sequences of events occur in the brain during thiamine deficiency and hypoxia/ischemia related brain damage, we have planned this review to discuss the possible therapeutic role of thiamine and its derivatives in the management of neonatal hypoxic-ischemic encephalopathy (HIE). Among the many benefits, thiamine per se as antioxidant, given intravenously (IV) at high doses, defined as dosage greater than 100 mg IV daily, should counteract the damaging effects of reactive oxygen and nitrogen species in the brain, including the reaction of peroxynitrite with the tyrosine residues of the major enzymes involved in intracellular glucose metabolism, which plays a key pathophysiological role in HIE in neonates. Accordingly, it is conceivable that, in neonatal HIE, the blockade of intracellular progressive oxidative stress and the rescue of mitochondrial function mediated by thiamine and its derivatives can lead to a definite neuroprotective effect. Because therapeutic hypothermia and thiamine may both act on the latent period of HIE damage, a synergistic effect of these therapeutic strategies is likely. Thiamine treatment may be especially important in mild HIE and in areas of the world where there is limited access to expensive hypothermia equipment. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

25 pages, 930 KiB  
Review
Free Radicals and Neonatal Brain Injury: From Underlying Pathophysiology to Antioxidant Treatment Perspectives
by Silvia Martini, Laura Castellini, Roberta Parladori, Vittoria Paoletti, Arianna Aceti and Luigi Corvaglia
Antioxidants 2021, 10(12), 2012; https://doi.org/10.3390/antiox10122012 - 18 Dec 2021
Cited by 12 | Viewed by 3724
Abstract
Free radicals play a role of paramount importance in the development of neonatal brain injury. Depending on the pathophysiological mechanisms underlying free radical overproduction and upon specific neonatal characteristics, such as the GA-dependent maturation of antioxidant defenses and of cerebrovascular autoregulation, different profiles [...] Read more.
Free radicals play a role of paramount importance in the development of neonatal brain injury. Depending on the pathophysiological mechanisms underlying free radical overproduction and upon specific neonatal characteristics, such as the GA-dependent maturation of antioxidant defenses and of cerebrovascular autoregulation, different profiles of injury have been identified. The growing evidence on the detrimental effects of free radicals on the brain tissue has led to discover not only potential biomarkers for oxidative damage, but also possible neuroprotective therapeutic approaches targeting oxidative stress. While a more extensive validation of free radical biomarkers is required before considering their use in routine neonatal practice, two important treatments endowed with antioxidant properties, such as therapeutic hypothermia and magnesium sulfate, have become part of the standard of care to reduce the risk of neonatal brain injury, and other promising therapeutic strategies are being tested in clinical trials. The implementation of currently available evidence is crucial to optimize neonatal neuroprotection and to develop individualized diagnostic and therapeutic approaches addressing oxidative brain injury, with the final aim of improving the neurological outcome of this population. Full article
(This article belongs to the Special Issue Oxidative Stress in Newborns and Children)
►▼ Show Figures

Figure 1

Show export options expand_more Show export options expand_less
Select all
Export citation of selected articles as:
 
Displaying articles 1-7
Back to TopTop