The oxidative stress at newborns is augmented by different conditions like preterm birth, asphyxia, respiratory distress, and intraventricular hemorrhage. Preterm neonates associate a more pronounced oxidative stress than healthy term newborns. Several neonatal conditions like respiratory distress (RDS), asphyxia, intraventricular hemorrhage, bronchopulmonary dysplasia, retinopathy, and necrotizing enterocolitis will increase the oxidative stress. The harmful effects of free radicals are linked to their capacity to react with polyunsaturated fatty acids of cell membranes, proteins, and nucleic acids. Free radicals will produce protein alteration with function loss and lipid peroxidation.
Part of the book: Novel Prospects in Oxidative and Nitrosative Stress
Humans possess defense mechanisms against free radicals: enzymatic and non-enzymatic antioxidants. Antioxidant defense is deficient in newborns and can be enhanced by the action of reactive oxygen species, generated by perinatal diseases such as respiratory distress or asphyxia. Prematurity itself will be associated with deficient antioxidant mechanisms, which are primarily enzymatic, but also non-enzymatic. Under oxidative stress conditions, antioxidant defense is overcome and thus, low-molecular weight free iron is released, which is not bound to transferrin and will play a role in Fenton’s reaction, catalyzing lipid peroxidation. The generated ROS will in turn influence antioxidant defense mechanisms, stimulating their synthesis, as an adaptation mechanism of the body in response to the presence of increased ROS levels.
Part of the book: Antioxidants