Superoxide dismutase with prolonged in vivo half-life inhibits intravascular hemolysis and renal injury in burned rats

Saitoh, Daizoh; Kadota, Toshio; Senoh, A.; Takahara, Takashi; Okada, Yoshiaki; Mimura, Kazuo; Yamashita, Hitoshi; Ohno, Hideki; Inoue, Masayasu

doi:10.1016/0735-6757(93)90167-a

Cited by 17 publications

(4 citation statements)

References 19 publications

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“…Their findings showed that SOD binds to styrene maleic acid and reduces the mortality, hemolysis, and the increase of vessel permeability during the early phase after burn injury. [40][41][42] The free radical scavenger, vitamin C, can also curtail the resuscitative volume required to treat up to 25% hypovolemia. 44 -46 Our data also imply that PC-SOD mitigates the amount of volume replacement required to resuscitate rats with imposed hypovolemia.…”

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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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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“…[22] In experimental studies, it has been found that allopurinol, superoxide dismutase, deferoxamine, GSH, NAS, sildenafil and other PDE inhibitors and antioxidants, such as Vit-C reduce oxidative stress and tissue damage. [23][24][25] In clinical studies performed in patients with septic shock, antioxidant and PDE inhibitor therapy has been shown to reduce lipid peroxidation, maintain cardiac hemodynamic stability, and reduce the number of days spent with a ventilator and in the intensive care unit. [26,27] However, antioxidant and PDE inhibitor therapy did not have any effects on mortality in these studies.…”

Section: Discussionmentioning

confidence: 99%

The effects of specıfıc and non-specıfıc phosphodıesterase ınhıbıtors and n-acetylcysteıne on oxıdatıve stress and remote organ ınjury ın two hıt trauma model

Özer

Topal

Şen

2019

Ulus Travma Acil Cerrahi Derg

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BACKGROUND: Sepsis is a systemic inflammatory response to infection and is one of the leading causes of morbidity and mortality. The second hit after trauma causes increased inflammatory response and multiple organ failure (MOF). The infection which develops after burn injury is a suitable model for a two-hit trauma study. Sepsis causes the release of biochemical mediators, such as Free Oxygen Radicals (FORs), which may lead to lipid peroxidation, which may play a key role in multiple organ failure. In this study, we aimed to investigate the effects of phosphodiesterase (PDE) inhibitors (sildenafil, milrinone, pentoxifylline) and N-acetylcysteine (NAS) on oxidative stress and organ damage in two-hit models. METHODS: In this experimental study, peritonitis was created by cecal ligation and puncture (CLP) method in 40 rats, 72 hours after creating a 30% scalding injury. Rats were divided into five groups of eight rats each as follows: Group I: No treatment; Group II: 10/mg/ kg/day dosage of intraperitoneal (i.p) sildenafil treatment was applied for 72 hours after CLP; Group III: 1/mg/kg/day dosage of i.p milrinone treatment was applied for 72 hours after CLP; Group IV: 150/mg/kg/day dosage of i.p NAS treatment was applied for 72 hours after CLP; Group V: 50/mg/kg/day dosage of i.p pentoxifylline treatment was applied for 72 hours after CLP. All rats were sacrificed on the seventh day of this study. Malondialdehyde (MDA), Glutathione Peroxidase (GPx), Superoxide Dismutase (SOD), catalase, Tumor Necrotic Factor-alpha (TNF-α) levels, and tissue (lung, kidney) and serum samples were taken for histopathological study. RESULTS: When compared to the control group, the tissue damage score was found to be lower in all treatment groups. Sildenafil, milrinone and NAS groups had higher kidney GPx levels compared to the control group. Milrinone and pentoxifylline were higher in the lung tissue compared to the SOD control group. TNFα levels were lower in pentoxifylline and milrinone groups compared to the control group. CONCLUSION: This experimental study has shown that PDE inhibitors and NAS have a decreasing effect on oxidative stress and distant organ damage in the two-hit model. Further clinical and experimental studies are needed on this subject.

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“…Numerous studies in experimental animals and humans have reported reduced antioxidant status related to thermal injury [65]. A rat model of extensive burn was utilized to provide initial evidence about the importance of free radicals in burn-induced AKI [66]. Since most free radicals have extremely short half-lives, luminol-mediated chemiluminescent reactions have been used as a proxy for ROS levels in the kidney [67].…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

Burmeister

Gómez

Dubick

2017

Biochimica et Biophysica Acta (BBA) - Molecular Basis of Diseas

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Trauma-induced acute kidney injury (AKI), such as after hemorrhagic shock (HS) or burn, remains a significant problem in the intensive care unit and is associated with increased mortality. The pathophysiology that drives AKI post-trauma is multi-factorial, and includes both inflammatory and metabolic alterations. Identifying the systemic profile that contributes to AKI is crucial not only for early diagnosis, but also for identifying treatments that improve kidney function and maintaining long-term patient health. In an effort to elucidate this molecular pathophysiology researchers have utilized a variety of animal models including chemically-induced (i.e., cisplatin), blocking renal perfusion (i.e., arterial clamping) and inducing burn or HS. As the latter burn and HS models are unequivocally applicable to studying AKI in the context of traumatic injury, this review will summarize the inflammatory and metabolic insights associated with AKI gained with these animal models. Moreover, novel therapeutic strategies brought forth with these models will be discussed.

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Superoxide dismutase with prolonged in vivo half-life inhibits intravascular hemolysis and renal injury in burned rats

Cited by 17 publications

References 19 publications

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

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

The effects of specıfıc and non-specıfıc phosphodıesterase ınhıbıtors and n-acetylcysteıne on oxıdatıve stress and remote organ ınjury ın two hıt trauma model

Molecular mechanisms of trauma-induced acute kidney injury: Inflammatory and metabolic insights from animal models

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