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Role of free Radicals

Inflammatory Diseases

Inflammation is characterized by a respiratory burst of activated neutrophils and macrophages, leading to the destruction of invading micro-organisms. This mechanism is a useful function protecting against attack, however the inflammatory response can also be detrimental as it is non-specific and may lead to the development of inflammatory diseases such as rheumatoid arthritis, inflammatory bowel disease, psoriasis, etc,. Reactive oxygen species (ROS) and free radicals are thought to act indirectly as cellular messengers and elicit an inflammatory response. Over production of these species may cause oxidative modification of biological molecules e.g. trypsin, collagen, LDL, DNA and lipids. ROS and free radicals also activate a series of enzyme systems, including protein kinases, protein phosphatases, transcription factors and heat shock proteins. ROS are also critical for gene expression which encode inflammatory proteins e.g. proteinases involved in tissue destruction such as collagenases and gelatinases. Nuclear factor-kß (NF-kß) has been implicated in AIDS, as HIV is NF-kß dependent. In the case of rheumatoid arthritis, rheumatoid factor binds IgG when it is exposed to free radicals. This binding stimulates the production of more free radicals, which then attack the cartilage matrix.

  1. 1. Oldenburg B. van Kats-Renaud H. Koningsberger JC. van Berge Henegouwen GP. van Asbeck B. Chemiluminescence in inflammatory bowel disease patients: a parameter of inflammatory activity. Clinica Chimica Acta. 310(2):151-6, 2001.

  2. Kunsch C. Medford RM. Oxidative stress as a regulator of gene expression in the vasculature. Circulation Research. 85(8):753-66, 1999.

  3. Hanselmann C. Mauch C. Werner S. Haemoxygenase-1: a novel player in cutaneous wound repair and psoriasis?. Biochemical Journal. 353(Pt 3):459-66, 2001.

  4. Anjalika. Gupta I. Gupta SK. Ganguly NK. Reactive oxygen intermediates and reactive nitrogen intermediates in copper intrauterine device users. Contraception. 59(1):67-70, 1999.

  5. Odeh M. New insights into the pathogenesis and treatment of rheumatoid arthritis. Clinical Immunology & Immunopathology. 83(2):103-16, 1997.

  6. Wiseman H. Halliwell B. Damage to DNA by reactive oxygen and nitrogen species: role in inflammatory disease and progression to cancer. Biochemical Journal. 313 ( Pt 1):17-29, 1996.

  7. Man WK. Ben-Hamida A. Spencer J. Helicobacter pylori, oxygen-derived free radicals and histamine in peptic ulcer and inflammatory disease. Inflammation Research. 44 Suppl 1:S104-5, 1995.

  8. Teahon K. Bjarnason I. Comparison of leukocyte excretion and blood loss in inflammatory disease of the bowel. Gut. 34(11):1535-8, 1993.

  9. Allan IM. Lunec J. Salmon M. Bacon PA. Reactive oxygen species selectively deplete normal T lymphocytes via a hydroxyl radical dependent mechanism. Scandinavian Journal of Immunology. 26(1):47-53, 1987.

  10. Hull DS. Green K. Thomas L. Alderman N. Hydrogen peroxide-mediated corneal endothelial damage. Induction by oxygen free radical. Investigative Ophthalmology & Visual Science. 25(11):1246-53, 1984.

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