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Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice
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, cha...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2020
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7569933/ https://www.ncbi.nlm.nih.gov/pubmed/32825609 http://dx.doi.org/10.3390/metabo10090340 |
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author | Peterson, Abigail L. Carr, Jennifer F. Ji, Xiangming Dennery, Phyllis A. Yao, Hongwei |
author_facet | Peterson, Abigail L. Carr, Jennifer F. Ji, Xiangming Dennery, Phyllis A. Yao, Hongwei |
author_sort | Peterson, Abigail L. |
collection | PubMed |
description | 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. |
format | Online Article Text |
id | pubmed-7569933 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2020 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-75699332020-10-29 Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice Peterson, Abigail L. Carr, Jennifer F. Ji, Xiangming Dennery, Phyllis A. Yao, Hongwei Metabolites Article 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. MDPI 2020-08-21 /pmc/articles/PMC7569933/ /pubmed/32825609 http://dx.doi.org/10.3390/metabo10090340 Text en © 2020 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Peterson, Abigail L. Carr, Jennifer F. Ji, Xiangming Dennery, Phyllis A. Yao, Hongwei Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title | Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title_full | Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title_fullStr | Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title_full_unstemmed | Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title_short | Hyperoxic Exposure Caused Lung Lipid Compositional Changes in Neonatal Mice |
title_sort | hyperoxic exposure caused lung lipid compositional changes in neonatal mice |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7569933/ https://www.ncbi.nlm.nih.gov/pubmed/32825609 http://dx.doi.org/10.3390/metabo10090340 |
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