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How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models
Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554981/ https://www.ncbi.nlm.nih.gov/pubmed/32967335 http://dx.doi.org/10.3390/antiox9090898 |
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author | Kletkiewicz, Hanna Klimiuk, Maciej Woźniak, Alina Mila-Kierzenkowska, Celestyna Dokladny, Karol Rogalska, Justyna |
author_facet | Kletkiewicz, Hanna Klimiuk, Maciej Woźniak, Alina Mila-Kierzenkowska, Celestyna Dokladny, Karol Rogalska, Justyna |
author_sort | Kletkiewicz, Hanna |
collection | PubMed |
description | Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial. Pharmacotherapy with deferoxamine (DFO) is commonly recognized as a beneficial regimen for H/I insult. DFO, via iron chelation, reduces oxidative stress. It also assures an optimal antioxidant protection minimizing depletion of the antioxidant enzymes as well as low molecular antioxidants. In the present review, some aspects of recently acquired insight into the therapeutic effects of hypothermia and DFO in promoting neuronal survival after H/I are discussed. |
format | Online Article Text |
id | pubmed-7554981 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75549812020-10-14 How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models Kletkiewicz, Hanna Klimiuk, Maciej Woźniak, Alina Mila-Kierzenkowska, Celestyna Dokladny, Karol Rogalska, Justyna Antioxidants (Basel) Review Oxygen free radicals have been implicated in brain damage after neonatal asphyxia. In the early phase of asphyxia/reoxygenation, changes in antioxidant enzyme activity play a pivotal role in switching on and off the cascade of events that can kill the neurons. Hypoxia/ischemia (H/I) forces the brain to activate endogenous mechanisms (e.g., antioxidant enzymes) to compensate for the lost or broken neural circuits. It is important to evaluate therapies to enhance the self-protective capacity of the brain. In animal models, decreased body temperature during neonatal asphyxia has been shown to increase cerebral antioxidant capacity. However, in preterm or severely asphyxiated newborns this therapy, rather than beneficial seems to be harmful. Thus, seeking new therapeutic approaches to prevent anoxia-induced complications is crucial. Pharmacotherapy with deferoxamine (DFO) is commonly recognized as a beneficial regimen for H/I insult. DFO, via iron chelation, reduces oxidative stress. It also assures an optimal antioxidant protection minimizing depletion of the antioxidant enzymes as well as low molecular antioxidants. In the present review, some aspects of recently acquired insight into the therapeutic effects of hypothermia and DFO in promoting neuronal survival after H/I are discussed. MDPI 2020-09-21 /pmc/articles/PMC7554981/ /pubmed/32967335 http://dx.doi.org/10.3390/antiox9090898 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Kletkiewicz, Hanna Klimiuk, Maciej Woźniak, Alina Mila-Kierzenkowska, Celestyna Dokladny, Karol Rogalska, Justyna How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title | How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title_full | How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title_fullStr | How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title_full_unstemmed | How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title_short | How to Improve the Antioxidant Defense in Asphyxiated Newborns—Lessons from Animal Models |
title_sort | how to improve the antioxidant defense in asphyxiated newborns—lessons from animal models |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7554981/ https://www.ncbi.nlm.nih.gov/pubmed/32967335 http://dx.doi.org/10.3390/antiox9090898 |
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