Superoxide dismutase prevents lipid peroxidation in burned patients

Thomson, Philip D.; Till, Gerd O.; Woolliscroft, James O.; Smith, David J.; Prasad, J.K.

doi:10.1016/0305-4179(90)90066-6

Cited by 49 publications

(14 citation statements)

References 10 publications

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“…Conjugated dienes and the more stable MDA are often used as markers of lipid peroxidation. 14,20,[31][32][33] We confirmed herein that high-dose ascorbic acid reduces postburn serum MDA levels in burned patients. We did not measure cardiac output and cardiac contractility, and so cannot exclude the possibility of a direct cardiotonic action of ascorbic acid.…”

Section: Commentsupporting

confidence: 60%

Reduction of Resuscitation Fluid Volumes in Severely Burned Patients Using Ascorbic Acid Administration

Tanaka

Matsuda²,

Miyagantani³

et al. 2000

Arch Surg

402

318

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High-dose ascorbic acid (vitamin C) therapy (66 mg/kg per hour) attenuates postburn lipid peroxidation, resuscitation fluid volume requirements, and edema generation in severely burned patients. Study Design and Setting:A prospective, randomized study at a university trauma and critical care center in Japan.Subjects and Methods: Thirty-seven patients with burns over more than 30% of their total body surface area (TBSA) hospitalized within 2 hours after injury were randomly divided into ascorbic acid and control groups. Fluid resuscitation was performed using Ringer lactate solution to maintain stable hemodynamic measurements and adequate urine output (0.5-1.0 mL/kg per hour). In the ascorbic acid group (n = 19; mean burn size, 63% ± 26% TBSA; mean burn index, 57 ± 26; inhalation injury, 15/ 19), ascorbic acid was infused during the initial 24hour study period. In the control group (n = 18; mean burn size, 53% ± 17% TBSA; mean burn index, 47 ± 13; inhalation injury, 12/18), no ascorbic acid was infused. We compared hemodynamic and respiratory measurements, lipid peroxidation, and fluid balance for 96 hours after injury. Two-way analysis of variance and Tukey test were used to analyze the data.

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Section: Commentsupporting

confidence: 60%

Reduction of Resuscitation Fluid Volumes in Severely Burned Patients Using Ascorbic Acid Administration

Tanaka

Matsuda²,

Miyagantani³

et al. 2000

Arch Surg

402

318

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“…Isolated PMNs have enhanced production of superoxide anion and hydrogen peroxide from 5 h to 7 days after experimental burn injury [61][62][63]. During thermal injury, increased oxidative ability of PMNs appears to contribute to cell and organ injuries, which are prevented by agents that detoxify superoxide anion [64,65]. However, as is the case with endotoxemia models, instances of depressed oxidative status of PMNs are also reported [66,67].…”

Section: Burn Patientsmentioning

confidence: 99%

Neutrophil migration during endotoxemia

Wagner

Roth

1999

Journal of Leukocyte Biology

177

125

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Endotoxemia is marked by a global activation of inflammatory responses, which can lead to shock, multiple organ failure, and the suppression of immune and wound healing processes. Neutrophils (PMNs) play a central role in some of these responses by accumulating in tissues and releasing reactive oxygen species and proteases that injure host structures. This review focuses on altered PMN migratory responses that occur during endotoxemia and their consequences in the development of pulmonary infection. The inflammatory mediators that might be responsible for these altered responses are discussed. The oxidant potential of PMNs is increased after exposure to endotoxin both in vitro and during clinical and experimental endotoxemia. However, other functions such as chemotaxis and phagocytosis are often depressed in these same cells. Endotoxin exposure renders PMNs hyperadhesive to endothelium. The sum of these effects produces activated inflammatory cells that are incapable of leaving the vasculature. As such, the endotoxic PMN is more likely to promote tissue injury from within microvascular beds than to clear pathogens from extravascular sites. Moreover, the functional characteristics of endotoxic PMNs are similar to those observed during trauma, burn injury, sepsis, surgery, and other inflammatory conditions. Accordingly, several clinical conditions might have a common effector in the activated, yet migratorially dysfunctional, PMN. Direct effects of endotoxin on PMNs as well as effects of endogenous mediators released during endotoxemia are discussed. Understanding PMN behavior during endotoxemia may provide basic and critical insights that can be applied to a number of inflammatory scenarios. J. Leukoc. Biol. 66: 10-24; 1999.

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“…The release of MDA into injured tissue is secondary production after polyunsaturated fatty acid oxidation and a benchmark of the level of active oxygen production and lipid peroxidation in burned tissue. Thomson et al 33 reported that active oxygen is released during the early phase of burn injury, that consequent lipid metabolism is important and that SOD administration suppresses such lipid peroxidation.…”

Section: Discussionmentioning

confidence: 99%

Lecithinized Superoxide Dismutase Suppresses Free Radical Substrates During the Early Phase of Burn Care in Rats

Koizumi

Goto

Tanaka

et al. 2009

Journal of Burn Care & Research

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Severe hypovolemia is caused by an increase in blood vessel permeability in the early phase after an extensive burn; massive fluid volume replacement has been used for the treatment of this condition. The release of oxygen free radicals and chemical mediators, especially from skin tissue, induces the increase in blood vessel permeability. Free radical burst is associated with ischemia-related skin tissue injury. Although various antioxidant therapies have been used to inhibit the consequences of hypovolemia, an effective method has not been established. To elucidate the protective effects of lecithinized superoxide dismutase (PC-SOD) as an antioxidant agent. Each rat sustained a 30% total body surface area burn (n = 20) on the back by the Walker and Mason method were allocated into three groups: (1) no treatment group (n = 6), (2) a low dose of PC-SOD (0.67 mg/kg) group (n = 7), and (3) a high dose of PC-SOD (1.33 mg/kg) group (n = 7). The concentrations of malondialdehyde and SOD in the serum, skin tissue, and lung tissue were measured in each group 1 hour after burning. Both low and high doses of PC-SOD prevented malondialdehyde concentration associated with free radical burst after burning compared with the no treatment group (P < .05); serum (27.7 +/- 6.8, 10.8 +/- 2.7, and 12.1 +/- 2.8 nmol/L), skin tissue (2251.3 +/- 560.5, 802.7 +/- 228.8, and 790.1 +/- 188.3 nmol/wet.g), and lung (157.3 +/- 19.5, 109.1 +/- 23.9, and 81.9 +/- 20.3 nmol/wet.g). These data suggest that PC-SOD may be a protective agent against free radical-induced vasodilatation caused by severe, extensive burns.

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Superoxide dismutase prevents lipid peroxidation in burned patients

Cited by 49 publications

References 10 publications

Reduction of Resuscitation Fluid Volumes in Severely Burned Patients Using Ascorbic Acid Administration

Reduction of Resuscitation Fluid Volumes in Severely Burned Patients Using Ascorbic Acid Administration

Neutrophil migration during endotoxemia

Lecithinized Superoxide Dismutase Suppresses Free Radical Substrates During the Early Phase of Burn Care in Rats

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