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Role of oxidative stress as physiopathologic factor in the preterm infant
1Division of Neonatology, Careggi University, Hospital of Florence, Florence, Italy. cdani@unifi.it
Insights
Oxidative stress, caused by an imbalance in free radicals (ROS), significantly impacts preterm infants, contributing to severe illnesses. Current antioxidant therapies have proven ineffective in preventing these conditions.
Area of Science:
- Neonatal Medicine
- Biochemistry
- Pediatric Pathology
Background:
- Oxidative stress arises when reactive oxygen species (ROS) overwhelm antioxidant defenses.
- In preterm infants, antioxidant systems are underdeveloped and highly stressed, increasing vulnerability.
- Maternal pregnancy complications and preterm birth can expose the fetus to oxidative stress.
Purpose of the Study:
- To review the role of oxidative stress in severe neonatal diseases in preterm infants.
- To explore the correlation between oxidative stress and hyperbilirubinemia in this population.
- To evaluate the efficacy of antioxidant therapies in managing oxidative stress-related conditions.
Main Methods:
- Literature review of studies on oxidative stress in preterm neonates.
- Analysis of the pathophysiology linking ROS to neonatal diseases.
- Examination of clinical trial data for antioxidant interventions.
Main Results:
- Oxidative stress is implicated in bronchopulmonary dysplasia, retinopathy of prematurity, hypoxic-ischemic encephalopathy, and intraventricular hemorrhage.
- Preterm infants exhibit deficient antioxidant mechanisms, exacerbating ROS-related damage.
- Clinical trials using antioxidant agents to prevent these conditions have largely failed.
Conclusions:
- Oxidative stress plays a critical role in the pathogenesis of major neonatal morbidities in preterm infants.
- The immaturity of the antioxidant system in preterm neonates is a key factor.
- Novel therapeutic strategies are needed as current antioxidant treatments are ineffective.
Abstract:
Oxidative stress usually occurs when the production of damaging free radicals (ROS) and other oxidative molecules exceeds the capacity of the body's antioxidant defenses. This process is supposed to begin after the delivery, but it can even affect the fetus when maternal pregnancy diseases (i.e.: pre-eclampsia, eclampsia, maternal infections) occur and in the case of preterm delivery. Most living organisms have developed well integrated antioxidant defenses to prevent the potential negative role of the ROS, in order to scavenge them and to control their concentration. These mechanisms are deficient in preterm newborn. Many illnesses in preterm infants, including bronchopulmonary dysplasia (BPD), retinopathy of prematurity (ROP), brain injury such as hypoxic/ischemic encephalopathy, and intraventricular hemorrhage (IVH) are thought to be related to the action of ROS. This presumably occurs due to the fact that the antioxidant system of preterm infants is at the same time highly stressed and incompletely developed. Unfortunately, the clinical trials which tried to prevent oxidative stress using antioxidant agents failed their objective and therefore they cannot be considered as an effective therapy. The objective of this review is to clarify the role of oxidative stress in the development of the previous severe diseases in preterm infants, and its possible correlation with hyperbilirubemia.
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