607 - Postnatal Selenium Deficiency Blunts Alveolarization and Exacerbates the Effects of Hyperoxia Exposure in Newborn Mice

Poster Number: 607
Publication Number: 607.1146

Background: Selenium (Se) contributes to antioxidant responses through selenocysteine-containing glutathione peroxidases (Gpx). Extremely low birthweight (ELBW) infants are 17-times more likely to be Se deficient than term infants and are at greatest risk of developing bronchopulmonary dysplasia (BPD). The impact of postnatal Se status on lung development and hyperoxic responses is unknown.

Objective: The present studies tested the hypothesis that postnatal Se status modulates the effects of hyperoxia on lung development.

Design/Methods: Male and female C3H/HeN mice received Se-sufficient (SeS; 0.4 ppm Na2SeO3) or Se-deficient (SeD; < 0.01 ppm Na2SeO3) diets from weaning and were bred to create SeS and SeD litters. After birth, SeS pups remained with SeS dams or were nursed by SeD dams to create 2 groups (SeSp and SeDp). Pups were exposed to room air (RA) or hyperoxia (85% O2) from birth. Alveolar size and number were assessed in inflation-fixed lungs at 14d. Gpx activity was determined in 14d lung homogenates. Data (mean±SD) were analyzed by 2-way ANOVA followed by Tukey’s post-hoc (n=6-25; p< 0.001).

Results: In RA, Se deficiency (SeDp) independently decreased alveolar number (0.19±0.03 vs 0.27±0.03) and increased alveolar size (54.1±4.8 vs 43.8±3.7) vs SeSp. Se deficiency exacerbated the effect of hyperoxia on alveolar number (0.15±0.02 vs 0.18±0.02) and alveolar size (63.2±8.2 vs 54.6±4.5) vs SeSp. Alveolar number (0.19±0.03 vs 0.18±0.02) and alveolar size (54.6±4.5 vs 54.1±4.8) were not different between RA-exposed SeDp vs hyperoxia-exposed SeSp. Lung Gpx activity was significantly decreased in SeDp in RA (0.022±0.01 vs 0.15±0.05) and hyperoxia-exposed SeSp (0.008±0.02).

Conclusion(s): The impact of postnatal Se deficiency on alveolarization is equivalent to hyperoxia-exposure alone in Se sufficient pups. SeD exacerbates hyperoxic sensitivity and compromises GSH-dependent antioxidant defenses. Given the increased risk of Se deficiency in ELBW infants, strategies to optimize Se status may improve lung development and antioxidant responses.