Free Radicals and Brain Damage in the Newborn
Autor: | Giuseppe Buonocore, Serafina Perrone, Rodolfo Bracci |
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Rok vydání: | 2001 |
Předmět: |
medicine.medical_specialty
Antioxidant Free Radicals Iron medicine.medical_treatment Brain damage Nitric Oxide medicine.disease_cause Superoxide dismutase Internal medicine medicine Humans Free-radical theory of aging chemistry.chemical_classification Brain Diseases biology business.industry Glutathione peroxidase Free radical injury Infant Newborn Newborn medicine.disease Mitochondria Oxidative Stress Endocrinology chemistry Reperfusion Injury Hypoxia-Ischemia Brain Pediatrics Perinatology and Child Health Immunology biology.protein Calcium medicine.symptom Energy Metabolism business Reperfusion injury Infant Premature Oxidative stress Developmental Biology Polyunsaturated fatty acid |
Zdroj: | Neonatology. 79:180-186 |
ISSN: | 1661-7819 1661-7800 |
Popis: | Newborns and particularly preterm infants are at high risk of oxidative stress and they are very susceptible to free radical oxidative damage. Indeed, there is evidence of an imbalance between antioxidant- and oxidant-generating systems which causes oxidative damage. The brain may be especially at risk of free radical-mediated injury because neuronal membranes are rich in polyunsaturated fatty acids and because the human newborn has a relative deficiency of brain superoxide dismutase and glutathione peroxidase. The brain of the term fetus is at higher risk of oxidative stress than that of the preterm fetus, as a consequence of its higher concentration of polyunsaturated fatty acids and the maturity of the N-methyl-D-aspartate receptor system at term. There seems to be a maturation-dependent window of vulnerability to free radical attack during oligodendrocyte development. Early in its differentiation, the oligodendrocyte may be vulnerable because of active acquisition of iron for differentiation at a time of relative delay in the development of certain key antioxidant defenses in the brain. Excess free iron and deficient iron-binding and -metabolizing capacity are additional features favoring oxidant stress in premature infants. Free radicals may be generated by different mechanisms, such as ischemia-reperfusion, neutrophil and macrophage activation, Fenton chemistry, endothelial cell xanthine oxidase, free fatty acid and prostaglandin metabolism and hypoxia. Reactive oxidant production by these different mechanisms contributes in a piecewise manner to the pathogenesis of perinatal brain injury. |
Databáze: | OpenAIRE |
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