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Abstract The neonatal period is a highly vulnerable time for an infant, who is completing many of the physiologic adjustments required for extrauterine existence. The high neonatal morbidity and mortality rates attest to the fragility of life during this period Very low-birthweight preterm infants are at risk of unique immaturity-related neonatal diseases. One common factor in the pathogenesis of such diseases, including bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), necrotizing enterocolitis (NEC), intraventricular hemorrhage (IVH), and periventricular leukomalacia (PVL), is free radical tissue aggression resulting from oxidative stress. In a broad sense, oxidative stress may be considered as an imbalance between pro- and antioxidant forces or between the amount of reactive oxygen species (ROS) and antioxidant defenses. The term oxygen radical disease of neonatology has been suggested to designate diseases whose pathogenesis includes tissue aggression from free radicals and ROS. The transition from an intrauterine hypoxic environment to an extrauterine normoxic environment leads to an acute increase in oxygenation, which induces the production of R0S. Moreover, 5% to 10% of newly born infants require active resuscitation with supplementary oxygen at birth, and the ideal oxygen concentration for neonatal resuscitation is uncertain, which is of major concern. This study was aimed to evaluate the extent of oxidative stress in some neonatal disorders and to evaluate the effect of treatment of these disorders on oxidative stress . Free radicals are considered the main product of oxidative stress and its level can be used as a direct parameter of oxidative stress extent. These free radicals are highly reactive and unstable intermediate products, it is difficult to measure them directly in vivo. 0xidative effects are assessed indirectly by determining total antioxidant capacity through measuring individual antioxidant enzymes or by determining the stable end products of oxidative stress on lipids, proteins, and DNA This study included 50 neonates consisted of 35 patients and 15 controls of matched age and sex. The patient group was subdivided into 3 groups 1- Preterm group included 20 preterm infants ( were born before completing 37 weeks of G.A.). 2- Neonatal hyperbiliribinemia group included 10 neonates with total and indirect bilirubin level are indicated for phototherapy 3- Perinatal asphyxia group included 5 neonates exposed to perinatal asphyxia which wass confirmed clinically Each of members of both main groups and subgroups are subjected to the following : History taking with Special Emphasis on: History of consanguinity, maternal history of previous pregnancy, labor or abortion, History of present pregnancy, labor and resuscitation, history of perinatal and/or postnatal events Thorough Clinical Examination and anthropometric measurements: Investigations: in the form of : 1- Routine Laboratory investigations as, Complete blood picture , Indirect and total billirubin, CRP and blood grouping. 2-Antioxidants profile Antioxidant enzymes : Glutathione peroxidase in haemolysate., Catalase in haemolysate., and Superoxide dismutase in haemolysate Oxidation reaction products: Isoprostane metabolite (F-8 isoprostane)in plasma , and Melanodialdehyde(MDA) in plasma. These clinical and laboratory procedures were performed twice 1-at the postnatal age of 2 days or at admission (in neonatal hyperbiliurubinemia group) 2- after recovery and just before discharge ( to detect the effect of treatment of different neonatal conditions on oxidant/antioxidant profile) . Then the results of these 2 steps were statistically analyzed and showed the following The capacity of antioxidant enzymes were reduced in preterm infants when compared to healthy full term infants. Oxygen therapy of preterm respiratory disorders( which constitute the main cause of admission in most preterm cases)caused a rise in products of oxidation reactions. Neonatal jaundice and phototherapy did not affect products of oxidation reactions. Perinatal asphyxia and its treatment caused a detectable depression in antioxidant enzyme levels and a significant rise in products of oxidation reactions from this study it can be concluded that : preterm capacity of dealing with oxidative stress is reduced in comparison with healthy full term, though most of these preterm infants are exposed to major oxidative stress because of intense oxygen therapy. Neonatal jaundice nor its phototherapy had caused any additional oxidative stress. Perinatal asphyxia is a major cause of oxidative stress in neonatal period, and resuscitation and treatment of such neonates had been a main source of oxidative stress. -207- Summary So it is recommended that, the main strategy of competing oxidative stress is its prevention Prevention of oxidative stress mainly depends on judicial use of oxygen in different neonatal situations monitored by infant oxygen saturation. |