Selenium is an essential trace element incorporated into selenoproteins via the amino acid selenocysteine (the 21st amino acid), encoded by UGA codon (normally a stop codon) with a special SECIS element in the 3'-UTR. Glutathione peroxidase (GPx1, GPx4) and thioredoxin reductase are selenoproteins. In severe selenium deficiency (Keshan disease — endemic in parts of China), myocardial involvement is characteristic. Selenium supplementation is also important in preventing which specific oxidative complication in premature neonates?

• A Retinopathy of prematurity (ROP) caused by oxidative damage to the developing retinal vasculature
• B Intraventricular hemorrhage caused by free radical damage to periventricular capillaries
• C Necrotizing enterocolitis (NEC) caused by oxidative damage to intestinal mucosal epithelium
• D Bronchopulmonary dysplasia (BPD) caused by oxidative damage from high FiO2 ventilation in GPx-deficient lungs ✓

Explanation

Premature neonates have low selenium stores (selenium is transferred to the fetus mainly in the third trimester) and immature antioxidant defenses. Selenium-dependent glutathione peroxidase (GPx1) in the lungs provides critical protection against hyperoxia-induced reactive oxygen species generated during high-FiO2 ventilatory support. Selenium supplementation in premature neonates has been studied for preventing bronchopulmonary dysplasia (chronic lung disease of prematurity), where oxidative injury from supplemental oxygen contributes to alveolar damage and fibrosis. GPx4 (phospholipid hydroperoxide GPx) also protects membrane lipids from peroxidation. While selenium's role is less dramatically established than vitamin E in ROP, the GPx-lung protection axis is the most biochemically supported rationale for selenium supplementation in premature neonates.

Reference: Harper's Illustrated Biochemistry, 32nd ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.