In the neonatal period, the clinical use of oxygen should be taken into consideration for its beneficial and toxicity effects. Oxygen toxicity is due to the development of reactive oxygen species (ROS) such as OH• that is one of the strongest oxidants in nature. Of note, generation of ROS is a normal occurrence in human and it is involved in a myriad of physiological reactions. Anyway an imbalance between production of oxidant species and antioxidant defenses, called oxidative stress, could affect various aspect of organisms’ physiology and it could determine pathological consequences to living beings. Neonatal oxidative stress is essentially due to decreased antioxidants, increased ROS, or both. Studies have demonstrated that antioxidant capacity is lower in preterm newborns than term babies. This well-known deficiency of antioxidant factors is only a piece of a cohort of factors, which can be involved in the neonatal oxidative stress and the increased production of ROS may be a main factor. Mechanisms of ROS generation are: mitochondrial respiratory chain, free iron and Fenton reaction, inflammation, hypoxia and/or ischemia, reperfusion, and hyperoxia. Oxidative stress following hyperoxia has been recognized to be responsible for lung, central nervous system, retina, red blood cell injuries, and possibly generalized tissue damage. When supplemental oxygen is needed for care, it would be prudent to avoid changes and fluctuations in SpO2. The definition of the safest level of oxygen saturations in the neonate remains an area of active research. Currently, on the basis of the published evidences, the most suitable approach would be to set alarm limits between 90 and 95%. It should allow to avoid SpO2 values associated with potential hypoxia and/or hyperoxia. Although the usefulness of antioxidant protection in the neonatal period is still under investigation, the risk of tissue damage due to oxidative stress in perinatal period should not be underestimated.
Fetal programming occurs when the normal pattern of fetal development is disrupted by an abnormal stimulus or an ?insult? during intrauterine life, which leads to adaptations by the fetus to allow its survival but could finally result in permanent structural and physiological changes with long-term consequences in adulthood. The availability of nutrients, hormones, and respiratory gases is the principal determinant of fetal growth and offspring's subsequent health. Fetal nutrient and oxygen availability depend on the rate of transfer across the ?placental barrier.? Nutritional status of the mother is also important: both maternal undernutrition and/or overnutrition during early gestation may increase the incidence of cardiovascular and metabolic disorders in the offspring in later life. Oxidative stress has been supposed to be the link between adverse intrauterine environment and later elevated risks of chronic diseases. It is an important initiating mechanism underlying the programming process due to suboptimal nutrition. Antioxidant vitamins, proteins, and trace elements can be compromised under condition of poor maternal nutrition leading to oxidant/antioxidant imbalance during pregnancy. On the other hand, maternal overnutrition is associated to chronic inflammatory states that increase free radicals' production. Developing dietary strategies to optimize maternal nutrition is necessary to supply the fetus with appropriate substrates and to avoid fetal redox status disruption.
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