Oxygen and Oxidative Stress in the Neonatal Period

Abstract

Aerobic metabolism in the mitochondria is highly efficient in providing energy for the living organisms. However, as byproducts, reactive oxygen species (ROS) are produced. Some of these chemical species are highly reactive-free radicals capable of causing functional and structural damage to cell components. To overcome free radical attack, cells have evolved both antioxidant defense and repairing systems. However, under certain circumstances the production of oxygen-free radicals overcomes antioxidant defense causing oxidative stress (OS) and damage. Newborn infants and especially preterm infants are endowed with an immature antioxidant defense and respiratory system and are therefore prone to OS. Too much oxygen may damage different organs (lung, brain, retina, and gastrointestinal tract), leading to severe acute and chronic conditions that will affect not only the survival but also the quality of life of these infants. Advances in our knowledge of oxygen metabolism, pathophysiology of oxygen-derived damage, and development of more efficient monitoring devices have drastically changed the scenario. We have learned that postnatal adaptation constitutes a slow adaptive process that needs more time than previously believed and that should be approached gently. Moreover, strict control of oxygen saturation as measured by pulse oximetry, while oxygen supplementation is needed, is also a relevant intervention contributing to reduce oxygen-derived deleterious consequences. Notwithstanding, the establishment of safe limits avoiding oxygen toxicity but not increasing the risk of mortality needs further studies. In this regard, the inclusion of new biomarkers may help clinicians to make better therapeutic decisions in the near future.