Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice.

Abigail L Peterson,Hongwei Yao,Phyllis A Dennery,Xiangming Ji,Jennifer F Carr

doi:10.3390/metabo10090340

Abigail L Peterson, Hongwei Yao + Show 3 more

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https://doi.org/10.3390/metabo10090340

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Abstract

Treatments with supplemental oxygen in premature infants can impair lung development, leading to bronchopulmonary dysplasia (BPD). Although a stage-specific alteration of lung lipidome occurs during postnatal lung development, whether neonatal hyperoxia, a known mediator of BPD in rodent models, changes lipid profiles in mouse lungs is still to be elucidated. To answer this question, newborn mice were exposed to hyperoxia for 3 days and allowed to recover in normoxia until postnatal day (pnd) 7 and pnd14, time-points spanning the peak stage of alveologenesis. A total of 2263 lung lipid species were detected by liquid chromatography–mass spectrometry, covering 5 lipid categories and 18 lipid subclasses. The most commonly identified lipid species were glycerophospholipids, followed by sphingolipids and glycerolipids. In normoxic conditions, certain glycerophospholipid and glycerolipid species augmented at pnd14 compared to pnd7. At pnd7, hyperoxia generally increased glycerophospholipid, sphingolipid, and glycerolipid species. Hyperoxia increased NADPH, acetyl CoA, and citrate acid but reduced carnitine and acyl carnitine. Hyperoxia increased oxidized glutathione but reduced catalase. These changes were not apparent at pnd14. Hyperoxia reduced docosahexaenoic acid and arachidonic acid at pnd14 but not at pnd7. Altogether, the lung lipidome changes throughout alveolarization. Neonatal hyperoxia alters the lung lipidome, which may contribute to alveolar simplification and dysregulated vascular development.

Highlights

1 in 10 babies are born prematurely each year in the US
Mechanical ventilation and supplemental oxygen are commonly employed to sustain life in these premature infants. These therapies can impair lung development, which leads to continued dependency on supplemental oxygen beyond 36 weeks corrected gestational age, referred to as bronchopulmonary dysplasia (BPD) [1]
The pathology of BPD is characterized by alveolar simplification and dysregulated vascular development [1]

Summary

Introduction

1 in 10 babies are born prematurely each year in the US. Mechanical ventilation and supplemental oxygen are commonly employed to sustain life in these premature infants. These therapies can impair lung development, which leads to continued dependency on supplemental oxygen beyond 36 weeks corrected gestational age, referred to as bronchopulmonary dysplasia (BPD) [1]. The pathology of BPD is characterized by alveolar simplification and dysregulated vascular development [1]. The mechanisms underlying alveolar simplification and dysregulated vascular development in BPD are not fully understood. Mouse lungs at birth are structurally similar to human neonates born at 30 to 34 weeks of gestation, when the lung is in the saccular phase of development

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