Role of Antioxidants in Neonatal Hypoxic–Ischemic Brain Injury: New Therapeutic Approaches
dc.contributor.author | Arteaga Cabeza, Olatz | |
dc.contributor.author | Álvarez Díaz, Antonia Ángeles | |
dc.contributor.author | Revuelta Aramberri, Miren | |
dc.contributor.author | Santaolalla Montoya, Francisco ![]() | |
dc.contributor.author | Urtasun Arricaberri, Andoni | |
dc.contributor.author | Hilario Rodríguez, Enrique | |
dc.date.accessioned | 2018-05-28T13:32:00Z | |
dc.date.available | 2018-05-28T13:32:00Z | |
dc.date.issued | 2017-02 | |
dc.identifier.citation | International Journal of Molecular Sciences 18(2) : (2017) // Article ID 265 | es_ES |
dc.identifier.issn | 1422-0067 | |
dc.identifier.uri | http://hdl.handle.net/10810/27137 | |
dc.description.abstract | Hypoxic-ischemic brain damage is an alarming health and economic problem in spite of the advances in neonatal care. It can cause mortality or detrimental neurological disorders such as cerebral palsy, motor impairment and cognitive deficits in neonates. When hypoxia-ischemia occurs, a multi-faceted cascade of events starts out, which can eventually cause cell death. Lower levels of oxygen due to reduced blood supply increase the production of reactive oxygen species, which leads to oxidative stress, a higher concentration of free cytosolic calcium and impaired mitochondrial function, triggering the activation of apoptotic pathways, DNA fragmentation and cell death. The high incidence of this type of lesion in newborns can be partly attributed to the fact that the developing brain is particularly vulnerable to oxidative stress. Since antioxidants can safely interact with free radicals and terminate that chain reaction before vital molecules are damaged, exogenous antioxidant therapy may have the potential to diminish cellular damage caused by hypoxia-ischemia. In this review, we focus on the neuroprotective effects of antioxidant treatments against perinatal hypoxic-ischemic brain injury, in the light of the most recent advances. | es_ES |
dc.language.iso | eng | es_ES |
dc.publisher | MDPI | es_ES |
dc.rights | info:eu-repo/semantics/openAccess | es_ES |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/es/ | * |
dc.subject | antioxidant | es_ES |
dc.subject | neuroprotection | es_ES |
dc.subject | hypoxia-ischemia | es_ES |
dc.subject | brain | es_ES |
dc.subject | newborn | es_ES |
dc.subject | focal cerebral-ischemia | es_ES |
dc.subject | alpha-linolenic acid | es_ES |
dc.subject | augments hypothermic neuroprotection | es_ES |
dc.subject | postresuscitation n-acetylcysteine | es_ES |
dc.subject | oxidative mitochondrial damage | es_ES |
dc.subject | central-nervous-system | es_ES |
dc.subject | fetal-rat brain | es_ES |
dc.subject | perinatal asphyxia | es_ES |
dc.subject | melatonin protects | es_ES |
dc.subject | newborn piglets | es_ES |
dc.title | Role of Antioxidants in Neonatal Hypoxic–Ischemic Brain Injury: New Therapeutic Approaches | es_ES |
dc.type | info:eu-repo/semantics/article | es_ES |
dc.rights.holder | © 2017 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/). | es_ES |
dc.rights.holder | Atribución 3.0 España | * |
dc.relation.publisherversion | http://www.mdpi.com/1422-0067/18/2/265 | es_ES |
dc.identifier.doi | 10.3390/ijms18020265 | |
dc.departamentoes | Biología celular e histología | es_ES |
dc.departamentoes | Dermatología, oftalmología y otorrinolaringología | es_ES |
dc.departamentoes | Neurociencias | es_ES |
dc.departamentoeu | Dermatologia, oftalmologia eta otorrinolaringologia | es_ES |
dc.departamentoeu | Neurozientziak | es_ES |
dc.departamentoeu | Zelulen biologia eta histologia | es_ES |
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Except where otherwise noted, this item's license is described as © 2017 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/).