Affiliations: Department of Pediatrics, Dr. Peset University
Hospital, Valencia, Spain | Department of Pediatrics, Obstetrics and Gynecology,
University of Valencia, Valencia, Spain
Note: [] Corresponding author: Pilar Codoñer-Franch, 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: Pregnancy, delivery and neonatal age are critical developmental
stages that are particularly prone to the formation of excess reactive oxygen
species (ROS). Oxidative stress is manifested at the maternal-fetal interface
from early pregnancy onwards. During the first trimester, the conceptus
develops in a low-oxygen environment that favors organogenesis in the embryo,
and may protect against teratogenesis mediated by ROS. The establishment of
fetoplacental circulation at the end of the first trimester is associated with
a three-fold increase in the oxygen concentration within the placenta. ROS
generation is stimulated at higher rates than it was previously and can lead to
oxidative stress. This physiological placental oxidative stress occurs in every
normal pregnancy. It constitutes an essential part of placental remodeling.
Healthy pregnant women overcome oxidative stress by upregulating the
antioxidation machinery. However, the increase in antioxidants could be
insufficient to offset the increase in lipid peroxidation. Given these
findings, the balance favors increased oxidative stress during pregnancy. Labor
and childbirth may be associated with periods of both hypoxia and oxidative
stress for the newborn while neonatal plasma is relatively deficient in
antioxidants.