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Neonatal Med > Volume 20(2); 2013 > Article
Neonatal Medicine 2013;20(2):199-206.
DOI: https://doi.org/10.5385/nm.2013.20.2.199    Published online June 26, 2013.
Effect of Short-term Exposure of Different Concentrations of Hyperoxia on Fetal Alveolar Type II Cell Death.
Hyeon Soo Lee
1Department of Pediatrics, Kangwon National University Hospital, Kangwon National University School of Medicine, Chuncheon, Korea. premee@kangwon.ac.kr
2Institute of Medical Sciences, Kangwon National University School of Medicine, Chuncheon, Korea.
Abstract
PURPOSE
Lung injury imposed by hyperoxia is the most important cause of bronchopulmonary dysplasia (BPD) in premature lungs, and hyperoxia has the chief biological effect of inducing cell death. The objective of this study was to investigate the response of cell death in fetal alveolar type II cells (FATIICs) exposed to different concentrations of hyperoxia for 36 h.
METHODS
FATIICs were isolated on embryonic day 19 and exposed to 65%- or 85%-oxygen for 36 h. Cells in room air were used as controls. FACScan was performed in hyperoxic and control samples at 0/6/12/24/36 h, and the patterns of cell death were compared at each time point using flow-cytometry.
RESULTS
Cell necrosis as measured by selective propidium iodide staining increased significantly from 12 h of 65%-hyperoxia and 6 h of 85%-hyperoxia, respectively. Cell necrosis increased 1.6-fold, 3.0-fold and 4.6-fold after 12 h, 24 h, and 36 h, respectively during 65%-hyperoxia and increased by 2.4-fold, 3.1-fold, 6.3-fold, and 8.8-fold after 6 h, 12 h, 24 h, and 36 h, respectively during 85%-hyperoxia compared to controls. Apoptotic cells as measured by selective Annexin-V staining peaked at 1.3% at 24 h of 65%-hyperoxia and peaked at 1.2% at 6 h of 85%-hyperoxia, respectively and then decreased rapidly.
CONCLUSION
This study shows that exposure to sublethal and lethal hyperoxia increases necrosis of FATIICs remarkably from the early stage of hyperoxia. These findings support the idea that short-term exposure to oxygen from birth may contribute to the evolution of "new" BPD in preterm lungs.
Key Words: Cell necrosis, Hyperoxia, Fetal alveolar type II cells
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