Malondialdehyde levels are used in this research as a determining factor of free radical
mediated cell injury in burn trauma.
1. Horton, Jureta W.
JOURNAL NAME- Toxicology VOL. 189 NO. 1-2 July 15th 2003 2003 PP. 75-88.
DOCUMENT TYPE- Article ISSN- 0300-483X
ADDRESS- Department of Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas,
TX, 75390-9160, USA
Burn trauma produces significant fluid sh
ifts that, in turn, reduce cardiac output and
tissue perfusion. Treatment approaches to major burn injury include administration of crystalloid solutions to
correct hypovolemia and to restore peripheral perfusion. While this aggressive postburn volume replacement
increases oxygen delivery to previously ischemic tissue, this restoration of oxygen delivery is thought to initiate
a series of deleterious events that exacerbate ischemia-related tissue injury. While persistent hypoperfusion after
burn trauma would produce cell death, volume resuscitation may exacerbate the tissue injury that occurred during
low flow state. It is clear that after burn trauma, tissue adenosine triphosphate (ATP) levels gradually fall, and
increased adenosine monophosphate (AMP) is converted to hypoxanthine, providing substrate for xanthine oxidase.
These complicated reactions produce hydrogen peroxide and superoxide, clearly recognized deleterious free radicals.
In addition to xanthine oxidase related free radical generation in burn trauma, adherent-activated neutrophils
produce additional free radicals. Enhanced free radical production is paralleled by impaired antioxidant
mechanisms; as indicated by burn-related decreases in superoxide dismutase, catalase, glutathione, alpha
tocopherol, and ascorbic acid levels. Burn related upregulation of inducible nitric oxide synthase (iNOS) may
produce peripheral vasodilatation, upregulate the transcription factor nuclear factor kappa B (NF-kappaB), and
promote transcription and translation of numerous inflammatory cytokines. NO may also interact with the superoxide
radical to yield peroxynitrite, a highly reactive mediator of tissue injury. Free radical mediated cell injury has
been supported by postburn increases in systemic and tissue levels of lipid peroxidation products such as
conjugated dienes, thiobarbituric acid reaction products, or malondialdehyde ( MDA ) levels Antioxidant therapy in
burn therapy (ascorbic acid, glutathione, N-acetyl-L-cysteine, or vitamins A, E, and C alone or in combination)
have been shown to reduce burn and burn/sepsis mediated mortality, to attenuate changes in cellular energetics, to
protect microvascular circulation, reduce tissue lipid peroxidation, improve cardiac output, and to reduce the
volume of required fluid resuscitation. Antioxidant vitamin therapy with fluid resuscitation has also been shown to
prevent burn related cardiac NF-kappaB nuclear migration, to inhibit cardiomyocyte secretion
, IL -1beta, and IL-6, and to improve cardiac contractile
function. These data collectively support the hypothesis that cellular oxidative stress is a critical step in
burn-mediated injury, and suggest that antioxidant strategies designed to either inhibit free radical
formation ( malondialdehyde ) or to scavage free radicals may provide organ protection in patients with burn
Return from Free Radical Reference 1 Malondialdehyde
to Free Radical Laboratory Validation 1.