The Free Radical Diseases of Newborn

Abstract

Abstract Free radicals (FRs) are unstable, short lived, and highly reactive molecules that are continuously generated by endogenous and exogenous mechanisms. The burden of FR generation is counteracted by the intracellular antioxidant systems, and the maintenance of oxidant/antioxidant balance is critical to normal cellular functions. The dangerous effects of FRs are linked to their property of being very unstable molecules and their ability to react with polyunsaturated fatty acids of cell membranes, proteins, polysaccharides, nucleic acids, causing functional alterations within the cell. In neonatal period, hypoxia, ischemia, ischemia-reperfusion, hyperoxia, inflammation, mitochondrial impairment, presence of nonprotein bound iron are responsible of excessive FRs production. Moreover, a less efficient antioxidant system is not able to counteract the harmful effects of FRs leading to FR-related cellular, tissue, and organ damages. In preterm babies, the severity of mechanisms responsible of FRs production, the stage at which the oxidative insult occurs, the degree of maturity of the organs have differential effects on the distinct cell populations of the body, with certain specific cell types being particularly vulnerable in perinatal period. We propose the hypothesis that oxidative stress (OS) is the common pathogenic factor involved in the onset and develop of intraventricular hemorrhage, periventricular leukomalacia, retinopathy of prematurity, bronchopulmonary dysplasia, and necrotizing enterocolitis. This suggests that developing effective antioxidant strategies for preterm infants requires a detailed understanding of oxidative stress reactions and cell responses in perinatal period.