Home > Journals > Minerva Pediatrica > Past Issues > Minerva Pediatrica 2004 August;56(4) > Minerva Pediatrica 2004 August;56(4):381-94





A Journal on Pediatrics, Neonatology, Adolescent Medicine,
Child and Adolescent Psychiatry

Indexed/Abstracted in: CAB, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,532




Minerva Pediatrica 2004 August;56(4):381-94

language: English, Italian

Role of oxidative stress as physiopathologic factor in the preterm infant

Dani C., Cecchi A., Bertini G.


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.

top of page

Publication History

Cite this article as

Corresponding author e-mail