Beginning Main ContentSite Navigation

Role of free Radicals

Lung Diseases

A range of lung conditions have been associated with oxidative stress including lung cancer, emphysema, and cystic fibrosis. The lungs are prone to oxidative damage as they are exposed to an oxygen rich environment and are continually exposed to environmental toxins. Prolonged exposure to oxygen and environmental toxins stimulate phagocytic cells in the lung to generate ROS and free radicals, which cause lipid per-oxidation. Oxidative attack on the respiratory tract lining causes cell injury and tissue damage, which in turn leads to further stimulation of phagocytes for the production of ROS . Some lung conditions, for example, cystic fibrosis, cause increased levels of free iron, decreased levels of glutathione and selenium and increased oxidative damage to DNA. The fluid contains low molecular weight antioxidants e.g. ascorbic acid, glutathione, uric acid, albumin, alpha-tocopherol, metal binding proteins, antioxidant enzymes and glycoconjugates, which can act as potent free radical scavengers. Treatment of lung disease patients with antioxidants may offer protection against the disease, including the idea of antioxidants in aerosol form for direct application to the respiratory tract lining. However, this form of administration may simply result in decreased antioxidant production by the phagocytes in the respiratory lining and may not serve to increase the antioxidant levels. It is currently unknown whether oral administration of vitamins has any beneficial effects for lung disease patients, as high levels of vitamins A and ß-carotene could be potentially harmful.

  1. Johnston CJ. Oberdorster G. Finkelstein JN. Recovery from oxidant-mediated lung injury: response of metallothionein, MIP-2, and MCP-1 to nitrogen dioxide, oxygen, and ozone exposures. Inhalation Toxicology. 13(8):689-702, 2001.

  2. Saugstad OD. Update on oxygen radical disease in neonatology. Current Opinion in Obstetrics & Gynecology. 13(2):147-53, 2001.

  3. Dorger M. Krombach F. Interaction of alveolar macrophages with inhaled mineral particulates. Journal of Aerosol Medicine-Deposition Clearance & Effects in the Lung. 13(4):369-80, 2000

  4. Nader-Djalal N. Knight PR 3rd. Thusu K. Davidson BA. Holm BA. Johnson KJ. Dandona P. Reactive oxygen species contribute to oxygen-related lung injury after acid aspiration. Anesthesia & Analgesia. 87(1):127-33, 1998 Jul.

  5. Sehgal A. Saili A. Gupta RP. Bajaj P. Free oxygen radicals and immune profile in newborns with lung diseases.Journal of Tropical Pediatrics. 46(6):335-7, 2000.

  6. Loitsch SM. von Mallinckrodt C. Kippenberger S. Steinhilber D. Wagner TO. Bargon J. Reactive oxygen intermediates are involved in IL-8 production induced by hyperosmotic stress in human bronchial epithelial cells.Biochemical & Biophysical Research Communications. 276(2):571-8, 2000.

  7. Traber MG. van der Vliet A. Reznick AZ. Cross CE. Tobacco-related diseases. Is there a role for antioxidant micronutrient supplementation?. Clinics in Chest Medicine. 21(1):173-87, x, 2000.

  8. Kishi M. Richard LF. Webster RO. Dahms TE. Role of neutrophils in xanthine/xanthine oxidase-induced oxidant injury in isolated rabbit lungs. Journal of Applied Physiology. 87(6):2319-25, 1999.

  9. Takahashi K. Yang GH. Osanai K. Toga H. Lung tissue injury caused by oxidant-antioxidant imbalance. Nippon Rinsho - Japanese Journal of Clinical Medicine. 57(9):1988-94, 1999.

  10. Kinnula VL. Oxidant and antioxidant mechanisms of lung disease caused by asbestos fibres. European Respiratory Journal. 14(3):706-16, 1999.

End of Main Content