Affiliations: Department of Pediatrics, Dr. Peset University
Hospital, Valencia, Spain | Department of Pediatrics, Obstetrics and Gynecology,
University of Valencia, Valencia, Spain
Note: [] Corresponding author: Sonia Aparici, Department of Pediatrics,
Dr. Peset University Hospital, Avenida Gaspar Aguilar 90, 46017 Valencia,
Spain. Tel.: +34 96 1622389; Fax: +34 96 3864815; E-mail: [email protected]
Abstract: Inflammation is one of the main causes of preterm birth, frequently
associated to intrauterine infection or chorioamnionitis. Oxidative stress is
involved in preterm birth. On the one hand, reactive oxygen species are
released by inflammatory cells against infection; on the other hand it is
responsible of placental tissue damage after chorioamnionitis. Because of
improvement in obstetric and perinatal care, survival rate in preterm births
has increased, leading to changes in pathology of several processes, such as
bronchopulmonary dysplasia. Bronchopulmonary dysplasia is a multifactorial
entity which is consequence of multiple mechanisms, including perinatal
inflammation and oxygen free radicals. Preterm newborn is very susceptible to
chronic lung damage because of both, low antioxidant capacity, and exposure to
high oxygen fractions during postnatal life. Modest lung oxidative stress
damage after exposure to fetal endotoxin in premature newborns has been shown.
Postnatal injury is needed to amplify the intrauterine inflammatory damage.
Cell death induction by reactive oxygen species has been suggested as mechanism
of lung damage. Several antioxidant therapies have been used in experimental
studies in order to reduce or prevent bronchopulmonary dysplasia. So far, care
is needed to standardize its use, because of its undesirable effects on
inflammatory defense and development.