Abstract
Premature infants are exposed to increased generation of reactive oxygen species, and on the other hand, they have a deficient antioxidant defense system. Oxidative insult is a salient part of lung injury that begins as acute inflammatory injury in respiratory distress disease and then evolves into chronic and structural scarring leading to bronchopulmonary dysplasia. Oxidative stress is also involved in the pathogenesis of pulmonary hypertension in newborns through the modulation of the vascular tone and the response to pulmonary vasodilators, with consequent decrease in the density of the pulmonary vessels and thickening of the pulmonary arteriolar walls. Oxidative stress has been recognized as both a trigger and an endpoint for several events, including inflammation, hypoxia, hyperoxia, drugs, transfusions, and mechanical ventilation, with impairment of pulmonary function and prolonged lung damage. Redoxomics is the most fascinating new measure to address lung damage due to oxidative stress. The new challenge is to use omics data to discover a set of biomarkers useful in diagnosis, prognosis, and formulating optimal and individualized neonatal care. The aim of this review was to examine the most recent evidence on the relationship between oxidative stress and lung diseases in preterm newborns. What is currently known regarding oxidative stress-related lung injury pathogenesis and the available preventive and therapeutic strategies are also discussed.
Highlights
Pulmonary development begins early in intrauterine life and continues in the first years of life according to a sequence of events that can be summarized in five phases: embryonic, pseudoglandular, canalicular, saccular, and alveolar stages [1]
Animal studies showed that intratracheal administration of antioxidants and recombinant human SOD decreased reactive oxygen species (ROS), increased endothelial NO synthase (eNOS) expression, and improved nitric oxide (NO)-mediated vasodilation in neonatal lamb models of pulmonary hypertension of the newborn (PPHN) exposed to 100% O2 for 24 h [76,77]
The effect of recombinant human SOD (rhSOD) in reducing oxidative stress and restoring coupling of eNOS is recognized, the evidence is limited to animal models of PPHN, as its use has never been studied in humans
Summary
Pulmonary development begins early in intrauterine life and continues in the first years of life according to a sequence of events that can be summarized in five phases: embryonic, pseudoglandular, canalicular, saccular, and alveolar stages [1]. The factors that play a key role in the impairment of the pulmonary maturation process can be classified into intrauterine and postnatal causes [2]. Intrauterine factors include maternal disease, inadequate placental function, and exposure to antenatal steroids. There is growing evidence linking early exposure to oxidative stress (OS) with an altered lung development process making the lung more susceptible to a number of diseases typical of premature babies such as respiratory distress syndrome, bronchopulmonary dysplasia (BPD) and persistent pulmonary hypertension. What is currently known regarding oxidative stress-related lung diseases pathogenesis and the available preventive and therapeutic strategies are discussed
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