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.