**2. Introduction**

The human body possesses defense mechanisms against free radicals, consisting of 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 neonatal respiratory distress or birth asphyxia. Prematurity itself will be associated with deficient antioxidant mechanisms, which are primarily enzymatic, but also non-enzymatic. Antioxidant defenses, especially enzymatic ones, develop during the last trimester of pregnancy. Consequently, premature newborns will not have sufficient antioxidant defense. 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 [1, 9]. Reactive oxygen species (ROS) production occurs through various mechanisms, of which the most common are hyperoxia, reperfusion, and inflammation. The generated ROS will in turn influence antioxidant defense mechanisms, stimulating their synthesis, as an adaptation mechanism in response to the presence of increased ROS levels. In neonatology, a "free radical disease" is described, which includes a number of disorders:

#### *Antioxidants*

bronchopulmonary dysplasia, retinopathy of prematurity, necrotizing enterocolitis, and periventricular leukomalacia [1, 8, 17].

In the case of perinatal asphyxia, ROS will exert a considerable harmful effect on the brain because antioxidant levels are low and there is an increased oxygen consumption during transition from fetal life to neonatal life [14, 15, 25]. Randomized studies on relatively large numbers of term newborns with asphyxia have demonstrated the importance of resuscitation with atmospheric air in limiting injury and improving the survival rate [13, 26].
