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Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice.

Abigail L Peterson1, Jennifer F Carr1, Xiangming Ji2

  • 1Department of Molecular Biology, Cell Biology & Biochemistry, Division of Biology and Medicine, Brown University, Providence, RI 02912, USA.

Metabolites
|August 23, 2020
PubMed
Summary

Neonatal hyperoxia alters lung lipid profiles during early development, impacting lipid metabolism and potentially contributing to bronchopulmonary dysplasia. These changes were most prominent in the early stages of lung development.

Keywords:
bronchopulmonary dysplasialipidomicslung alveolarizationmetabolomicsoxidative stress

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Area of Science:

  • Biochemistry
  • Developmental Biology
  • Pulmonary Medicine

Background:

  • Supplemental oxygen therapy in premature infants can hinder lung development, leading to bronchopulmonary dysplasia (BPD).
  • Neonatal hyperoxia is a known mediator of BPD in rodent models.
  • The impact of neonatal hyperoxia on lung lipid profiles during critical developmental stages remains unclear.

Purpose of the Study:

  • To investigate the effects of neonatal hyperoxia on the developing mouse lung lipidome.
  • To identify specific lipid species and categories altered by hyperoxia during alveologenesis.

Main Methods:

  • Newborn mice were exposed to hyperoxia for 3 days, followed by recovery in normoxia until postnatal days 7 and 14.
  • Lung lipidomics was performed using liquid chromatography-mass spectrometry, detecting 2263 lipid species across 5 categories and 18 subclasses.
  • Metabolomic analysis assessed changes in key metabolic intermediates and antioxidants.

Main Results:

  • Hyperoxia significantly altered the lung lipidome at postnatal day 7, increasing glycerophospholipids, sphingolipids, and glycerolipids.
  • Metabolomic analysis revealed increased NADPH, acetyl CoA, citrate, and oxidized glutathione, with decreased carnitine, acyl carnitine, and catalase under hyperoxia.
  • By postnatal day 14, hyperoxia reduced docosahexaenoic acid and arachidonic acid levels, with most other observed changes resolving.
  • Normoxic lung development showed an increase in certain glycerophospholipid and glycerolipid species between postnatal days 7 and 14.

Conclusions:

  • Neonatal hyperoxia induces significant, stage-specific alterations in the lung lipidome during alveolarization.
  • These lipidomic changes, particularly the reduction in essential fatty acids and altered metabolic intermediates, may contribute to the pathogenesis of BPD, including alveolar simplification and vascular dysregulation.