Antioxidant Treatment in Experimental Thermal Injury

  • Gerd O. Till
  • Hans P. Friedl
  • Peter A. Ward
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 264)


There is increasing experimental evidence to suggest that oxygen-derived free radicals play an important role in the pathophysiology of thermal injury. Following thermal injury of skin, oxygen radicals have been linked to the appearance of lipid peroxidation products (1–3) and the pathogenesis of burn shock (4). Experimental studies have shown that edema formation in the skin of rats following a partialthickness burn is mainly mediated by oxidants derived from xanthine oxidase (5, 6). In addition, there is evidence that the development of intravascular hemolysis and acute lung injury secondary to thermal trauma can be linked to the generation of oxygen radicals from complement-activated blood neutrophils (7, 8). In these model systems of thermal injury, antioxidant interventions have demonstrated pronounced, protective effects supporting the concept that oxygen radicals are playing an important role in local as well as distant cell and tissue damage following thermal injury.


Acute Lung Injury Xanthine Oxidase Thermal Injury Lipid Peroxidation Product Edema Formation 
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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Gerd O. Till
    • 1
  • Hans P. Friedl
    • 1
  • Peter A. Ward
    • 1
  1. 1.Department of PathologyUniversity of Michigan Medical SchoolAnn ArborUSA

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