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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 6-17 |
| Number of pages | 12 |
| Journal | Burns |
| Volume | 34 |
| Issue number | 1 |
| DOIs | |
| State | Published - Feb 2008 |
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Keywords
- Antioxidants
- Burn injury
- NAD(P)H oxidase
- Reactive nitrogen species
- Reactive oxygen species
ASJC Scopus subject areas
- Emergency Medicine
- Surgery
Cite this
Oxidative stress and anti-oxidative mobilization in burn injury. / Parihar, Arti; Parihar, Mordhwaj S.; Milner, Stephen; Bhat, Satyanarayan.
In: Burns, Vol. 34, No. 1, 02.2008, p. 6-17.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Oxidative stress and anti-oxidative mobilization in burn injury
AU - Parihar, Arti
AU - Parihar, Mordhwaj S.
AU - Milner, Stephen
AU - Bhat, Satyanarayan
PY - 2008/2
Y1 - 2008/2
N2 - 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.
AB - 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.
KW - Antioxidants
KW - Burn injury
KW - NAD(P)H oxidase
KW - Reactive nitrogen species
KW - Reactive oxygen species
UR - http://www.scopus.com/inward/record.url?scp=38049185351&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=38049185351&partnerID=8YFLogxK
U2 - 10.1016/j.burns.2007.04.009
DO - 10.1016/j.burns.2007.04.009
M3 - Article
C2 - 17905515
AN - SCOPUS:38049185351
VL - 34
SP - 6
EP - 17
JO - Burns
JF - Burns
SN - 0305-4179
IS - 1
ER -