Advertisement

Lung Energy Metabolism Following Twenty-Four Hours Exposure to One Hundred Percent Oxygen

  • D. J. P. Bassett
  • E. Bowen-Kelly
  • S. S. Reichenbaugh
Part of the Basic Life Sciences book series (BLSC, volume 49)

Abstract

The interstitial edema and endothelial cell damage observed in rat lungs following 48 hours of exposure to 100% oxygen is believed to result from oxygen-derived free-radical damage of cellular membranes, enzyme proteins, and possibly components of the extracellular matrix. Earlier physiological alterations of endothelial function have been demonstrated by depressed serotonin uptake in isolated perfused rat lungs following 18 to 24 hours of oxygen exposure,1 at a time when tissue adenine nucleotide levels have been found not to be affected.2 In vitro experiments using homogenates and isolated subcellular tissue fractions have demonstrated that key enzyme systems involved in energy generation are susceptible to oxygen inactivation. These include the dehydrogenases of glyceraldehyde-3-phosphate, pyruvate, succinate, and oxoglutarate.3–5 The purpose of the present investigation was to use an intact organ preparation to determine whether lung glycolytic and mitochondrial enzyme systems are impaired during the first 24 hours of oxygen exposure when pathological alterations are not observed.

Keywords

14C02 Production Oxygen Exposure Pyruvate Metabolism Phenazine Methosulfate Pyruvate Production 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    E. R. Block and A. B. Fisher, Depression of serotonin clearance by rat lungs during oxygen exposure, J. Appl. Physiol. 42:33 (1977).PubMedGoogle Scholar
  2. 2.
    A. B. Fisher, Energy status of the rat lung after exposure to elevated pO2, J. Appl. Physiol. 45:56 (1978).PubMedGoogle Scholar
  3. 3.
    N. Haugaard, Cellular mechanisms of oxygen toxicity, Ann. Rev. Physiol. 48:311 (1968).Google Scholar
  4. 4.
    W. D. Currie, P. C. Pratt, and A. P. Sanders, Hyperoxia and lung metabolism, Chest 66:19S (1974).Google Scholar
  5. 5.
    D. Jamieson and H. A. S. van den Brenk, Pulmonary damage due to high pressure oxygen breathing. 2. Changes in dehydrogenase activity of rat lung, Austral. J. Exp. Biol. 40:51 (1962).CrossRefGoogle Scholar
  6. 6.
    D. J. P. Bassett and A. B. Fisher, Stimulation of rat lung metabolism with 2,4-dinitrophenol and phenazine methosulfate, Am. J. Physiol. 231:898 (1976).PubMedGoogle Scholar
  7. 7.
    D. J. P. Bassett and A. B. Fisher, Pentose cycle activity of the isolated perfused rat lung, Am. J. Physiol. 231:1527 (1976).PubMedGoogle Scholar
  8. 8.
    D. J. P. Bassett and E. Bowen-Kelly, Pyruvate metabolism of perfused rat lungs after exposure to 100% oxygen, J. Appl. Physiol. 60:1605 (1986).PubMedGoogle Scholar
  9. 9.
    R. G. Spragg, D. B. Hinshaw, P. A. Hyslop, I. U. Schraufstatter, and C. G. Cochrane, Alterations in adenosine triphosphate and energy charge in cultured endothelial and P388D1 cells after oxidant injury, J. Clin. Invest. 76:1471 (1985).PubMedCrossRefGoogle Scholar
  10. 10.
    I. U. Schraufstatter, D. B. Hinshaw, P. A. Hyslop, R. G. Spragg, and C. G. Cochrane, Glutathione cycle activity and pyridine nucleotide levels in oxidant-induced injury of cells, J. Clin. Invest. 76:1131 (1985).PubMedCrossRefGoogle Scholar

Copyright information

© Plenum Press, New York 1988

Authors and Affiliations

  • D. J. P. Bassett
    • 1
  • E. Bowen-Kelly
    • 1
  • S. S. Reichenbaugh
    • 1
  1. 1.The Johns Hopkins University School of Hygiene and Public HealthBaltimoreUSA

Personalised recommendations