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Effects of hyperoxia on phospholipid metabolism and on intracellular structure of cultured type II pneumocytes Kotaro Saito 1 1Department of Pediatrics, The University of Texas Health Science Center at Dallas pp.1079-1085
Published Date 1986/10/15
DOI https://doi.org/10.11477/mf.1404204943
  • Abstract
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Alveolar type II cells isolated from the lung of 6 days old rats fed in air (air-rat) and in 100% O2 (O2-rat) for 6 days after birth were used to observe the effects of oxygen of 95%-100% on phospholipid metabolism and intracellular structure for 24 hrs in culture. Total PC synthesis from choline in the cells of air-and O2-rat was decreased to 77.64% and 71.33% by 95% O2. After the culutre of the cells of O2-rat in 95% air and 95% O2, the incorporation of glycerol into phospho-lipid of the cells was reduced to 28.91% and 23.37%, respectively, and the release of total phospholipid was also reduced to 53.63% and 60. 29%. The ratio of PC in the cells of air-rat was decreased from 58.58% to 51.24%. In accordance with the alteration of PC syn-thesis in the cells by O2 treatment, the ratio of other phospholipids, such as PA, LPC, CL, was increased. The ratio of PC released from the cells of O2-rat was 26. 22% and 28. 52% in culture of air and O2, respe-ctively. The total protein concentration of dishes in culture was decreased to 78.88%-87.01% by O2 treat-ment. DNA concentration was also eliminated to 54.28 %-50.74% by O2 treatment. The intracellular strucutre was altered by O2 treatment, i.e. loss of tight junctions, change of micro villi, loss of density of glycogen gra-nules, vacuolation in cytoplasm, smoothed membraneof mitochondria, loss of density of intra-mitochondrial structure, especially the destruction of endoplasmic reticulum where PC of surfactant is synthesized. The free radicals produced from O2 may alter the surface activity of lung by disrupting phospholipid synthesis in type II pneumocytes and by impairing the cellular structure.


Copyright © 1986, Igaku-Shoin Ltd. All rights reserved.

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電子版ISSN 1882-1200 印刷版ISSN 0452-3458 医学書院

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