Oxidative stress occurs when free radicals increase and exceed the levels of antioxidant mechanisms that can neutralize them. It causes tissue damage by causing protein, lipid and polysaccharide oxidation, DNA fragmentation, base modifications and breaks in the DNA chain [1,2]. Oxidative stress has been shown to cause increase in cytokine and chemokine levels in the previous experimental and clinical studies [[3], [4], [5], [6]]. Chemokines are members of the inflammatory cytokine family. They play role in leucocyte migration [7]. Their levels increase in inflammation. After stimulation of chemokines, secretion of leucocyte enzymes and induction of oxidative radicals were shown in in-vitro studies [7,8]. Moreover, oxidative impulse increases chemokine expression [[3], [4], [5], [6]] while antioxidants decrease them [6,9].

Newborns, especially preterm babies, have limited antioxidative capacity and they are more valuable against the oxidative stress [2]. Free radical injury has been shown as a cause in pathogenesis in bronchopulmonary dysplasia (BPD), intraventricular hemorrhage (IVH), periventricular leukomalacia (PVL), necrotizing enterocolitis (NEC), retinopathy of prematurity (ROP) [2,10]. This study hypothesizes that if oxidative stress begins during the antenatal period, it may contribute to a higher incidence of prematurity-related morbidities. Therefore, it was aimed to evaluate oxidative stress by measuring chemokine levels in cord blood and to investigate the correlation between these levels and acute and chronic prematurity-related morbidities such as respiratory distress syndrome (RDS), BPD, patent ductus arteriosus (PDA), IVH, PVL, NEC and ROP.