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A Potential Role for Oxygen Radicals in Mineral Dust-Induced Lung Injury: Lessons from Lung Injury from Hyperoxia

  • J. E. Repine
Part of the NATO ASI Series book series (volume 3)

Abstract

There is considerable interest currently in determining the contribution of toxic oxygen metabolites (commonly called “oxygen radicals”) to the development of lung injury. As requested, the purpose of this article will be twofold. First, we will briefly present a summary of our research about the potential contributions of O2 radicals to the development of lung injury from hyperoxia. Second, we will propose a number of possibilities for the involvement of O2 radicals in the pathogenesis of lung injuries from inhaled mineral dusts. The latter is wholly speculative and should be considered in the context of the other research presented in this book and elsewhere.

Keywords

Lung Injury Alveolar Macrophage Adult Respiratory Distress Syndrome Phorbol Myristate Acetate Mineral Dust 
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.

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References

  1. Harada RN, Vatter AE, Repine JE (1983) Oxygen radical scavengers protect alveolar macrophages from hyperoxia injury in vitro. Am Rev Respir Dis 128: 761–762PubMedGoogle Scholar
  2. McCord JM (1985) Free radicals and ischemia. Mechanisms of Disease. New Engl J Med 312: 159–163PubMedCrossRefGoogle Scholar
  3. Tate RM, Repine JE (1983) Neutrophils and the adult respiratory distress syndrome. Am Rev Respir Dis 128: 552–559PubMedGoogle Scholar
  4. Tate RM, Morris HG, Schroeder WR, Repine JE (1984) Oxygen metabolites stimulate thromboxane generation and cause vasoconstriction in isolated saline-perfused rabbit lungs. J Clin Invest 78: 608–613CrossRefGoogle Scholar
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Copyright information

© Springer-Verlag Berlin Heidelberg 1985

Authors and Affiliations

  • J. E. Repine
    • 1
  1. 1.Webb-Waring Lung InstituteUniversity of Colorado Medical CenterDenverUSA

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