Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Clin Pediatr. May 8, 2016; 5(2): 172-181
Published online May 8, 2016. doi: 10.5409/wjcp.v5.i2.172
Fetal programming and early identification of newborns at high risk of free radical-mediated diseases
Serafina Perrone, Antonino Santacroce, Anna Picardi, Giuseppe Buonocore
Serafina Perrone, Antonino Santacroce, Anna Picardi, Giuseppe Buonocore, Department of Molecular and Developmental Medicine, University of Siena, 53100 Siena, Italy
Author contributions: All authors equally contributed to this paper for conception, design of the study, literature review, analysis, drafting, critical revision, editing, and final approval of the final version.
Conflict-of-interest statement: The authors confirm that this article content has no conflicts of interest.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See:
Correspondence to: Serafina Perrone, MD, PhD, Department of Molecular and Developmental Medicine, University of Siena, Policlinico Santa Maria alle Scotte, Viale Bracci 36, 53100 Siena, Italy.
Telephone: +39-0577-586542 Fax: +39-0577-586182
Received: August 29, 2015
Peer-review started: September 6, 2015
First decision: October 8, 2015
Revised: January 25, 2016
Accepted: February 14, 2016
Article in press: February 16, 2016
Published online: May 8, 2016

Nowadays metabolic syndrome represents a real outbreak affecting society. Paradoxically, pediatricians must feel involved in fighting this condition because of the latest evidences of developmental origins of adult diseases. Fetal programming occurs when the normal fetal development is disrupted by an abnormal insult applied to a critical point in intrauterine life. Placenta assumes a pivotal role in programming the fetal experience in utero due to the adaptive changes in structure and function. Pregnancy complications such as diabetes, intrauterine growth restriction, pre-eclampsia, and hypoxia are associated with placental dysfunction and programming. Many experimental studies have been conducted to explain the phenotypic consequences of fetal-placental perturbations that predispose to the genesis of metabolic syndrome, obesity, diabetes, hyperinsulinemia, hypertension, and cardiovascular disease in adulthood. In recent years, elucidating the mechanisms involved in such kind of process has become the challenge of scientific research. Oxidative stress may be the general underlying mechanism that links altered placental function to fetal programming. Maternal diabetes, prenatal hypoxic/ischaemic events, inflammatory/infective insults are specific triggers for an acute increase in free radicals generation. Early identification of fetuses and newborns at high risk of oxidative damage may be crucial to decrease infant and adult morbidity.

Keywords: Fetal programming, Oxidative stress, High-risk newborn, Biomarkers, Perinatal medicine, Metabolic syndrome

Core tip: The adverse outcomes on the offspring born from altered gestation are already known. The consequences of these perturbations have been demonstrated even after many decades from birth. In this review we summarize gestational conditions associated to fetal programming and elucidate the mechanisms involved in such kind of occurrence. We also describe to what extent oxidative stress (OS) is involved in a very wide spectrum of genetic, metabolic, and cellular responses, through the gene expression regulation, and cell growth modulation. By virtue of these properties, OS has been nominated as the lowest common denominator of adult disease programming.