Selenium: implications for outcomes in extremely preterm infants

Abstract

Extremely preterm infants are at high risk for morbidities including bronchopulmonary dysplasia, intraventricular hemorrhage, and retinopathy of prematurity likely related to their exposure to reactive oxygen and nitrogen species early in life. Selenium is a trace mineral contributes to the proper function of multiple systems including immunity, redox regulation, and inflammation via the "selenoenzymes" glutathione peroxidase, thioredoxin reductase, and selenoprotein P. Given that selenium accretion via the placenta occurs primarily during the third trimester, preterm neonates are born selenium deficient. While the role of selenium in animals and adults is better described, publications are lacking in the neonatal population regarding consequences of selenium deficiency or toxicity, accurate monitoring of levels, and proper enteral and parental dosages. This review highlights the role of selenium as it relates to the optimal function of antioxidant systems in extremely preterm infants in order to highlight the gaps in knowledge as it relates to the pathogenesis and prevention of morbidities in this population.