Role of Antioxidants in Neonatal Hypoxic-Ischemic Brain Injury: New Therapeutic Approaches
| Autor: | Enrique Hilario, Miren Revuelta, Olatz Arteaga, Antonia Alvarez, Francisco Santaolalla, Andoni Urtasun |
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| Rok vydání: | 2016 |
| Předmět: |
Antioxidant
antioxidant medicine.medical_treatment fetal-rat brain Review hypoxia–ischemia Bioinformatics medicine.disease_cause Antioxidants 0302 clinical medicine newborn Spectroscopy chemistry.chemical_classification oxidative mitochondrial damage General Medicine Computer Science Applications alpha-linolenic acid hypoxia-ischemia focal cerebral-ischemia Hypoxia-Ischemia Brain newborn piglets neuroprotection medicine.symptom medicine.medical_specialty Programmed cell death brain postresuscitation n-acetylcysteine Brain damage Neuroprotection Catalysis Inorganic Chemistry Lesion 03 medical and health sciences 030225 pediatrics medicine Humans Physical and Theoretical Chemistry Molecular Biology perinatal asphyxia melatonin protects Reactive oxygen species business.industry Organic Chemistry Infant Newborn Surgery Oxidative Stress chemistry Apoptosis augments hypothermic neuroprotection central-nervous-system business 030217 neurology & neurosurgery Oxidative stress |
| Zdroj: | International Journal of Molecular Sciences Addi. Archivo Digital para la Docencia y la Investigación instname |
| ISSN: | 1422-0067 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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