Antioxidant Defense and Oxidant Load in Pediatric Health and Disease

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

Deadline for manuscript submissions: closed (31 December 2018) | Viewed by 7068

Special Issue Editors


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Guest Editor
Department of Pediatrics-Neonatology, CHU Sainte-Justine, Université de Montréal, Montréal, Canada
Interests: neonatal-peinatal medicine; oxidative stress; nutrition; parenteral nutrition; bronchopulmonary dysplasia

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Guest Editor
Department of Pediatrics-Neonatology and Nutrition, CHU Sainte-Justine, Université de Montréal, Montréal, QC H3T 1C5, Canada
Interests: oxidative stress; parenteral nutrition; bronchopulmonary dysplasia; epigenetic; perinatality
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Special Issue Information

Dear Colleagues,

The balance between oxidant load and antioxidant defenses is at the heart of health state, at all ages, especially in paediatrics. Starting from newborn infants and their transition, from the relatively hypoxic uterine environment to the relatively hyperoxic extrauterine environment until adolescence, with increased exposure to various qualities of nutrition, obesity, pollutants and smoking; infants and children are at high risk for unbalanced oxidant-antioxidant status. This unbalanced oxidant–antioxidants status is a cornerstone in many pediatric pathologies, including oxidative stress-related diseases in preterm infants (bronchopulmonary dysplasia, retinopathy of prematurity, etc.), and, later in life, type 1 diabetes, asthma, cystic fibrosis, juvenile idiopathic arthritis, and pediatric non-alcoholic liver disease

This Special Issue will welcome original research and reviews of literature concerning the oxidant load and antioxidant defenses in pediatric health and diseases, including the following topics:

  • Oxidant load and antioxidant defenses, including present strategies and future directions.
  • Unbalanced oxidant-antioxidant related diseases pathogenesis and the most recent advances in prevention and treatment in peditarics.
  • Environmental factors affecting the oxidant-antioxidant balance including air pollution, smoking, nutrition and physical activity.

Dr. Ibrahim Mohamed
Dr. Jean-Claude Lavoie
Guest Editors

Manuscript Submission Information

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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

  • Oxidant load
  • Antioxidant defenses
  • Unbalanced oxidant-antioxidant related diseases
  • Nutrition and oxidant-antioxidant status
  • Physical activity and oxidant-antioxidant balance
  • Pediatrics

Published Papers (1 paper)

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Research

12 pages, 5442 KiB  
Article
Mechanisms of LPS-Induced Acute Kidney Injury in Neonatal and Adult Rats
by Egor Y. Plotnikov, Anna A. Brezgunova, Irina B. Pevzner, Ljubava D. Zorova, Vasily N. Manskikh, Vasily A. Popkov, Denis N. Silachev and Dmitry B. Zorov
Antioxidants 2018, 7(8), 105; https://0-doi-org.brum.beds.ac.uk/10.3390/antiox7080105 - 08 Aug 2018
Cited by 36 | Viewed by 6611
Abstract
Neonatal sepsis is one of the major causes of mortality and morbidity in newborns, greatly associated with severe acute kidney injury (AKI) and failure. Handling of newborns with kidney damage can be significantly different compared to adults, and it is necessary to consider [...] Read more.
Neonatal sepsis is one of the major causes of mortality and morbidity in newborns, greatly associated with severe acute kidney injury (AKI) and failure. Handling of newborns with kidney damage can be significantly different compared to adults, and it is necessary to consider the individuality of an organism’s response to systemic inflammation. In this study, we used lipopolysaccharide (LPS)-mediated acute kidney injury model to study mechanisms of kidney cells damage in neonatal and adult rats. We found LPS-associated oxidative stress was more severe in adults compared to neonates, as judged by levels of carbonylated proteins and products of lipids peroxidation. In both models, LPS-mediated septic simulation caused apoptosis of kidney cells, albeit to a different degree. Elevated levels of proliferating cell nuclear antigen (PCNA) in the kidney dropped after LPS administration in neonates but increased in adults. Renal fibrosis, as estimated by smooth muscle actin levels, was significantly higher in adult kidneys, whereas these changes were less profound in LPS-treated neonatal kidneys. We concluded that in LPS-mediated AKI model, renal cells of neonatal rats were more tolerant to oxidative stress and suffered less from long-term pathological consequences, such as fibrosis. In addition, we assume that by some features LPS administration simulates the conditions of accelerated aging. Full article
(This article belongs to the Special Issue Antioxidant Defense and Oxidant Load in Pediatric Health and Disease)
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