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Abstract
A severe burn is associated with release of inflammatory mediators which ultimately
cause local and distant pathophysiological effects. Mediators including Reactive Oxygen
Species (ROS) and Reactive Nitrogen Species (RNS) are increased in affected tissue,
which are implicated in pathophysiological events observed in burn patients. The purpose
of this article is to understand the role of oxidative stress in burns, in order to
develop therapeutic strategies. All peer-reviewed, original and review articles published
in the English language literature relevant to the topic of oxidative stress in burns
in animals and human subjects were selected for this review and the possible roles
of ROS and RNS in the pathophysiology of burns are discussed. Both increased xanthine
oxidase and neutrophil activation appear to be the oxidant sources in burns. Free
radicals have been found to have beneficial effects on antimicrobial action and wound
healing. However following a burn, there is an enormous production of ROS which is
harmful and implicated in inflammation, systemic inflammatory response syndrome, immunosuppression,
infection and sepsis, tissue damage and multiple organ failure. Thus clinical response
to burn is dependent on the balance between production of free radicals and its detoxification.
Supplementation of antioxidants in human and animal models has proven benefit in decreasing
distant organ failure suggesting a cause and effect relationship. We conclude that
oxidative damage is one of the mechanisms responsible for the local and distant pathophysiological
events observed after burn, and therefore anti-oxidant therapy might be beneficial
in minimizing injury in burned patients.