The Impact of Antioxidant Deficiency in Newborns

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Natural and Synthetic Antioxidants".

Deadline for manuscript submissions: closed (20 December 2022) | Viewed by 3279

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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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Dear Colleagues,

Redox homeostasis is a key regulator of several metabolisms. Thus, an imbalance between antioxidant and oxidant molecules has the potential to compromise health. The sources of antioxidants are both endogenous (e.g., enzymes and glutathione) and exogenous (e.g., diet). Similarly, oxidant molecules come from both endogenous metabolism and from the environment.

After birth, newborns are particularly sensitive to oxidative stress due to the fragility of their antioxidant defenses. The extent of this vulnerability depends, among other things, on their gestational age at birth, their sex and their environment. The fact of coming into the world and breathing the surrounding air, which is richer in oxygen than uterine environment, has been reported by several scientists as an oxidative stress with biological impacts. Therapeutic care can also generate oxidative stress—think of oxygen supplementation or parenteral nutrition, which is inherently contaminated with peroxides and aldehydes. To counter the impact of exposure to these oxidants, newborns must have functional antioxidant defenses. A low reserve of essential nutrients to support the antioxidant defenses could explain their great vulnerability to oxidative stress. The quality of the mother’s diet, especially during the last trimester of gestation, as well as the quality of breast milk or formula are crucial.

Imbalance between oxidant and antioxidant molecules compromises the health of the newborn, both at the time of this stress and throughout life. Neonatal oxidative stress has been linked to several diseases affecting different organs (lung, liver, intestine, brain, eye, etc.), compromising their development. In the long term, these infants are susceptible to developing cardiovascular disease, type II diabetes, asthma, chronic obstructive pulmonary disease, etc. The long-term impact of the imbalance between oxidants and antioxidants in early life may be caused by a neonatal change in organ development and/or permanent epigenetic modifications. Recently, the level of DNA methylation was strongly correlated with the redox value measured in the liver of a newborn animal model.

Exposure to a high level of oxidants is toxic, while a low level of oxidants is necessary to induce endogenous antioxidant defenses; too much exposure to oxidants can induce oxidative stress, while too high an intake of antioxidants could induce reductive stress. This Special Issue of Antioxidants seeks to publish works exploring the impacts of a neonatal deficit in molecules supporting the antioxidant defenses of the newborn, as well as the impacts of antioxidant therapy in this population.

Dr. Jean-Claude Lavoie
Guest Editor

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Keywords

  • antioxidant deficiency
  • antioxidant therapy
  • epigenetic
  • early life
  • newborn
  • nutrition
  • oxidative stress
  • redox biology
  • reductive stress
  • transcription factor

Published Papers (2 papers)

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Research

13 pages, 2428 KiB  
Article
Dose–Response Effects of Glutathione Supplement in Parenteral Nutrition on Pulmonary Oxidative Stress and Alveolarization in Newborn Guinea Pig
by Jean-Claude Lavoie, Ibrahim Mohamed and Vitor Teixeira
Antioxidants 2022, 11(10), 1956; https://doi.org/10.3390/antiox11101956 - 30 Sep 2022
Cited by 2 | Viewed by 1283
Abstract
In premature infants, glutathione deficiency impairs the capacity to detoxify the peroxides resulting from O2 metabolism and those contaminating the parenteral nutrition (PN) leading to increased oxidative stress, which is a major contributor to bronchopulmonary dysplasia (BPD) development. In animals, the supplementation [...] Read more.
In premature infants, glutathione deficiency impairs the capacity to detoxify the peroxides resulting from O2 metabolism and those contaminating the parenteral nutrition (PN) leading to increased oxidative stress, which is a major contributor to bronchopulmonary dysplasia (BPD) development. In animals, the supplementation of PN with glutathione prevented the induction of pulmonary oxidative stress and hypoalveolarization (characteristic of BPD). Hypothesis: the dose of glutathione that corrects the plasma glutathione deficiency is sufficient to prevent oxidative stress and preserve pulmonary integrity. Three-day-old guinea pigs received a PN, supplemented or not with GSSG (up to 1300 µg/kg/d), the stable form of glutathione in PN. Animals with no handling other than being orally fed constituted the control group. After 4 days, lungs were removed to determine the GSH, GSSG, redox potential and the alveolarization index. Total plasma glutathione was quantified. The effective dose to improve pulmonary GSH and prevent the loss of alveoli was 330 µg/kg/d. A 750 µg/kg/d dose corrected the low-plasma glutathione, high-pulmonary GSSG and oxidized redox potential. Therefore, the results suggest that, in a clinical setting, the dose that improves low-plasma glutathione could be effective in preventing BPD development. Full article
(This article belongs to the Special Issue The Impact of Antioxidant Deficiency in Newborns)
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19 pages, 7523 KiB  
Article
Supplementation of Dimethylglycine Sodium Salt in Sow Milk Reverses Skeletal Muscle Redox Status Imbalance and Mitochondrial Dysfunction of Intrauterine Growth Restriction Newborns
by Kaiwen Bai, Luyi Jiang, Qiming Li, Jingfei Zhang, Lili Zhang and Tian Wang
Antioxidants 2022, 11(8), 1550; https://doi.org/10.3390/antiox11081550 - 10 Aug 2022
Cited by 1 | Viewed by 1534
Abstract
The current study sought to understand the mechanism underlying skeletal muscle dysfunction brought on by intrauterine growth restriction (IUGR) and to explore the treatment benefits of applying dimethylglycine sodium salt (DMG-Na) in sow milk to newborns during the suckling period. Each of the [...] Read more.
The current study sought to understand the mechanism underlying skeletal muscle dysfunction brought on by intrauterine growth restriction (IUGR) and to explore the treatment benefits of applying dimethylglycine sodium salt (DMG-Na) in sow milk to newborns during the suckling period. Each of the 10 sows delivered one newborn with a normal birth weight (NBW) and one with an IUGR. Additionally, two NBW and two IUGR newborns were collected per litter of another 10 sows. The 20 NBW newborns were divided between the N (sow milk) and ND (sow milk + 0.1% DMG-Na) groups, while 20 IUGR newborns were divided between the I (sow milk) and ID (sow milk + 0.1% DMG-Na) groups. The skeletal muscle histomorphology, redox status, and levels of gene and protein expression were worse (p < 0.05) in the I group than in the N group. In addition, supplementation with DMG-Na (ND and ID groups) improved (p < 0.05) those parameters compared to the unsupplemented groups (N and I groups). Inhibited nuclear factor erythroid 2-related factor 2 (Nrf2)/sirtuin 1 (SIRT1)/peroxisome proliferator-activated receptorγcoactivator-1α (PGC-1α) activity resulted in decreased redox status, skeletal muscle structural damage, skeletal muscle mitochondrial function impairment, and decreased performance in IUGR newborns. Supplementation of DMG-Na in sow milk activated the Nrf2/SIRT1/PGC-1α in IUGR newborns, thereby improving their skeletal muscle performance. Full article
(This article belongs to the Special Issue The Impact of Antioxidant Deficiency in Newborns)
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