Free radical disorders of preterm infants

• Published in: British medical bulletin 1993-07, Vol.49 (3), p.668-678
• Main Author: Kelly, F J
• Format: Article
• Language: English
• Subjects: Bronchopulmonary Dysplasia - etiology; Cerebral Hemorrhage - etiology; Cerebral Ventricles; Endothelium - metabolism; Free Radicals - metabolism; Humans; Infant, Newborn; Infant, Premature; Lung - metabolism; Oxygen - metabolism; Reactive Oxygen Species - metabolism; Retinopathy of Prematurity - etiology
• ISSN: 0007-1420; 1471-8391
• DOI: 10.1093/oxfordjournals.bmb.a072639

In recent years increasing experimental and clinical data have provided compelling evidence for the involvement of oxygen free radicals in the 3 main disorders of prematurity—chronic lung disease, retinopathy of prematurity and intraventricular haemorrhage. Infants born prior to 30 weeks gestation or weighing less than 1500 g at birth appear to be most at risk. They are very underdeveloped and as a consequence of the immaturity of their lungs often require intense respiratory support, including the provision of supplemental oxygen. The theoretical basis for free radical involvement in these disorders is that oxygen centred radicals and related reactive oxygen metabolites are formed too rapidly to be detoxified by the antioxidant defence mechanisms in specific tissues. In the case of chronic lung disease, the evidence currently favours excess oxygen (hyperoxia) as the cause of the greater oxygen free radical production, whereas in retinopathy of prematurity and intraventricular haemorrhage, it is proposed that low oxygen tensions (hypoxia) followed by periods of reoxygenation is the more likely stimulus for excess radical formation.