%0 Journal Article
%T Protective Role of Melatonin in Neonatal Diseases
%A Eloisa Gitto
%A Lucia Marseglia
%A Sara Manti
%A Gabriella D¡¯Angelo
%A Ignazio Barberi
%A Carmelo Salpietro
%A Russel J. Reiter
%J Oxidative Medicine and Cellular Longevity
%D 2013
%I Hindawi Publishing Corporation
%R 10.1155/2013/980374
%X Oxidative stress contributes to the severity of several newborn conditions to the extent that Saugstad coined the phrase ¡°oxygen radical diseases of neonatology.¡± In order to counteract free radicals damage many strategies to augment antioxidant status in ill-term and preterm infants have been proposed and several medications have been experimented with mixed results. Several studies have tested the efficacy of melatonin to counteract oxidative damage in diseases of newborns such as chronic lung disease, perinatal brain injury, necrotizing enterocolitis, and retinopathy of prematurity, giving promising results. The peculiar perinatal susceptibility to oxidative stress indicates that prophylactic use of antioxidants as melatonin could help to prevent or at least reduce oxidative stress related diseases in newborns. However, more studies are needed to confirm these beneficial effects. 1. Introduction Oxygen- and nitrogen-derived metabolites, collectively termed reactive oxygen species (ROS) and reactive nitrogen species (RNS), are persistently produced in aerobic organisms. When generated in excess, ROS/RNS mutilate molecules and are important mediators of cell and tissue damage [1, 2]. The resulting damage, which is unavoidable, is referred to as oxidative stress caused by free radicals. Free radicals are highly unstable and, normally, their formation is controlled by several beneficial compounds known as antioxidants; these protective molecules are part of the antioxidative defence system. There is a critical balance between free radical generation and antioxidant defences. Free radicals production is the endpoint of a cascade of several biochemical events such as hypoxia, hyperoxia, ischemia, and inflammation. A direct relation has been demonstrated between the degree of hypoxia and the severity of oxidative stress due to free radicals production during hypoxia in fetal life [3]. Free radical reactions lead to the oxidation of lipids, proteins, and polysaccharides and to DNA damage (fragmentation, base modifications, and strand breaks); as a consequence, radicals have a wide range of biologically toxic effects. Oxidative stress can be defined as an imbalance between the amount of ROS and the intracellular and extracellular antioxidant protection systems. Newborns, especially if born prematurely, are very susceptible to free radical oxidative damage, for many several reasons [4]. In fact (a) infants at birth are naturally exposed to the hyperoxic challenge due to the transition from the hypoxic intrauterine environment to extrauterine life, and this gap
%U http://www.hindawi.com/journals/omcl/2013/980374/