Oxidative Stress in the Newborn

Oxidative stress (OS) occurs when there is an unbalance between free radicals (FR) production and antioxidant capacity. OS can be a risk factor for fetal programming, representing a key process linking adverse fetal growth, impaired fetal well-being or preterm birth, and later increased risks of diseases in adolescence and adulthood. Adverse outcome to the offspring can extend beyond the neonatal period and includes neurodevelopmental disorders (motor and cognitive problems , attention deficit hyperactivity, and psychotic disorders), asthma, insulin resistance, diabetes mellitus, hypertension, coronary heart disease, and stroke. Free radicals can alter gene expression or damage lipids, proteins, and DNA at a critical developmental point leading to a higher susceptibility to many disorders. The present special issue aims to stimulate the continuing efforts to understand the pathophysiology underlying OS damage in neonates. Furthermore we aimed to highlight new possible strategies to treat or prevent OS-mediated diseases and to evaluate neonatal outcomes. This issue includes papers on (i) recent developments in OS-mediated diseases in fetus and newborns in both human and animal models; (ii) advances in identification of prenatal and neonatal characteristics of the infant/fetus at increased risk of OS-mediated damage; (iii) mechanisms of OS-mediated tissue damage using model systems; (iv) recent advances in antioxidant and other protective strategies. Each manuscript was reviewed by at least 2 external reviewers and one guest editor. We received about 20 papers and only the present 8 papers were selected for the final draft. All the papers were selected on the basis of relevance and novelty for the reader. The review by Y. Ozsurekci and K. Aykac is an overview on the complex and wide world of oxidative stress pathophys-iology and its link to neonatal diseases. M. Chełchowska and colleagues examined the relationship between selected adipokines and markers of oxidative stress/antioxidant defense in the umbilical cord of neonates exposed and nonexposed in utero to tobacco smoke. Maternal smoking is considered as a source of oxidative stress, which has been implicated to disrupted adipokines expression in adipose tissue. To support this thesis, they found that cord serum visfatin, oxidized low density lipoproteins, and total oxidant capacity were significantly higher, while adi-ponectin and total antioxidant capacity were lower in smoking group than in nonsmoking group, demonstrating that maternal smoke enhances oxidative status and depletes antioxidant potential in otherwise " healthy " term newborns. The research group from Italy showed, in the paper authored by S. Perrone et al., …