Oxygen radicals in lung pathology

Free Radic Biol Med. 1990;9(5):381-400. doi: 10.1016/0891-5849(90)90015-b.


Pulmonary tissue can be damaged in different ways, for instance by xenobiotics (paraquat, butylated hydroxytoluene, bleomycin), during inflammation, ischemia reperfusion, or exposure to mineral dust or to normobaric pure oxygen levels. Reactive oxygen species are partly responsible for the observed pulmonary tissue damage. Several mechanisms leading to toxicity are described in this review. The reactive oxygen species induce bronchoconstriction, elevate mucus secretion, and cause microvascular leakage, which leads to edema formation. Reactive oxygen species even induce an autonomic imbalance between muscarinic receptor-mediated contraction and the beta-adrenergic-mediated relaxation of the pulmonary smooth muscle. Vitamin E and selenium have a regulatory role in this balance between these two receptor responses. The autonomic imbalance might be involved in the development of bronchial hyperresponsiveness, occurring in lung inflammation. Finally, several antioxidants are discussed which may be beneficial as therapeutics in several lung diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antioxidants / pharmacology
  • Asthma / etiology
  • Bleomycin / toxicity
  • Butylated Hydroxytoluene / toxicity
  • Free Radicals
  • Humans
  • Inflammation / metabolism
  • Lung / drug effects*
  • Lung / pathology
  • Lung Injury
  • Minerals / toxicity
  • Oxygen / metabolism
  • Oxygen / pharmacology*
  • Paraquat / toxicity


  • Antioxidants
  • Free Radicals
  • Minerals
  • Bleomycin
  • Butylated Hydroxytoluene
  • Paraquat
  • Oxygen