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Maternal DHA Supplementation Attenuates Newborn Hyperoxia‐Induced Lung Developmental Deficits into Early Adulthood
Author(s) -
Rogers Lynette K,
Dingess Kelly,
Velten Markus,
Heyob Kathryn,
Valentine Christina J
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.990.17
Subject(s) - hyperoxia , bronchopulmonary dysplasia , medicine , lung , pulmonary compliance , retinopathy of prematurity , endocrinology , physiology , pregnancy , biology , gestational age , genetics
Newborn mice exposed to hyperoxia demonstrate decreased alveolarization similar to preterm infants with bronchopulmonary dysplasia. We tested the hypothesis that docosahexanoic acid (DHA) administration to pregnant and nursing dams would decrease inflammatory responses and improve lung function. Dams were fed purified control or DHA‐supplemented diets beginning at E16. After birth, the pups were exposed to >85%O 2 or room air (RA) for 14 days, then returned to standard diets and RA until 28 days. Lung development was assessed by morphometric analyses and pulmonary function. Protein levels of COX‐2 and sRAGE were analyzed by western blot. Mice receiving DHA and hyperoxia exposure during the newborn period demonstrated increased alveolarization (alveolar number, 103 vs 65; alveolar area, 1516 vs 2058 microns 2 ) and improved lung function (tissue elastance, 24.9 vs 32.0 ml/cmH 2 O; tissue compliance, 0.042 vs 0.035 ml/cmH 2 O) compared to control diet, hyperoxia exposed mice. Levels of COX‐2 and sRAGE were higher in pups exposed to hyperoxia but were attenuated by DHA supplementation. Neonatal hyperoxia exposure caused sustained lung deficits in adulthood that were lessened by DHA supplementation and may be mediated through RAGE or COX‐2 signaling pathways. We speculate that maternal DHA supplementation will be beneficial in preventing lung disease in premature infants. Supported by ATS unrestricted grant.