Extracellular superoxide dismutase in biology and medicine

Fattman, Cheryl L.; Schaefer, Lisa M.; Oury, Tim D.

doi:10.1016/s0891-5849(03)00275-2

Cited by 570 publications

(383 citation statements)

References 203 publications

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“…ROS including superoxide anion, hydrogen peroxide, and hydroxyl radical act as subcellular messengers in complex processes such as mitogenic signal transduction, gene expression, and regulation of cell proliferation when they are generated excessively or when enzymatic and non-enzymatic defense systems are impaired (Michiels et al 1994). Low levels of ROS are vital for proper cell functioning, while excessive in vivo generation of these products can adversely affect cell functioning (Fattman et al 2003;Gregorevic et al 2001). Attacks by ROS cause alterations in molecular structure and biological properties which may be detrimental to the cell when antioxidant mechanisms are compromised or ROS scavenging is ineffective (Fujita 2002).…”

Section: Introductionmentioning

confidence: 99%

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

2014

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The aim of this study was to examine the oxidative status in Egyptian patients suffering chronic fascioliasis. The relationship between serum malondialdehyde (MDA) levels, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPX) activities was investigated in relation to the level of liver enzymes; ALT and AST compared to healthy controls. Twenty patients versus ten controls were included in the study. Among cases the MDA, CAT, AST and ALT were higher than controls, while SOD and GPX higher values were present among controls. There was a highly significant difference between cases and controls as regard MDA, CAT, SOD, GPX, and AST, and a significant difference regarding ALT. The findings of increased serum lipid peroxidation and decreased antioxidant enzymes in erythrocytes of chronic fascioliasis patients indicated the presence of persistent inflammation and oxidative stress which confirms the underlying pathogenesis and reflected the stage of infection providing a baseline data for comparison between normal and infected patients guided by the level of liver enzymes in relation to oxidative status.

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Section: Introductionmentioning

confidence: 99%

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

2014

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“…Arterial tissue-bound EC-SOD is decreased in diabetic individuals, promoting increased susceptibility to superoxide-mediated damage via NO depletion and endothelial dysfunction [19]. Elevation of plasma EC-SOD in patients with type 2 diabetes is strongly correlated with an interaction between plasma HbA 1c and total Cu levels [1].…”

Section: Introductionmentioning

confidence: 99%

Copper(II)-selective chelation improves function and antioxidant defences in cardiovascular tissues of rats as a model of diabetes: comparisons between triethylenetetramine and three less copper-selective transition-metal-targeted treatments

Gong

Choong

et al. 2010

Diabetologia

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Aims/hypothesis Treatment with the Cu(II)-selective chelator triethylenetetramine (TETA) improves cardiovascular disease in human patients, and cardiac and vascular/renal disease in rats used as a model of diabetes. Here we tested two hypotheses: first, that TETA elicits greater improvement in organ function than less Cu-selective transition-metal-targeted treatments; second, that the therapeutic actions of TETA are consistent with mediation through suppression of oxidative stress.Methods Rats were made diabetic with streptozotocin (55 mg/kg, i. v.) and treated from 8 weeks after disease induction for the following 8 weeks with effective dosages of oral TETA, or one of three less Cu-selective transitionmetal-targeted treatments: D-penicillamine, deferiprone or Zn acetate. Treatment effects were measured in ex vivo cardiac and aortic tissues, plasma and urine. Results Diabetes damaged both cardiac and renal/vascular function by impairing the ability of cardiac output to respond physiologically to rising afterload, and by significantly elevatElectronic supplementary material The online version of this article

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“…7 This isozyme of the superoxide dismutase family is highly expressed in the lung and arteries and is bound to the extracellular matrix via its positively charged heparin/matrix-binding domain. [7][8][9][10] EC-SOD acts as both an anti-inflammatory and antifibrotic agent in a number of pulmonary diseases including bleomycin-and asbestos-induced pulmonary fibrosis, [11][12][13][14] hyperoxia, [15][16][17] lipopolysaccharide-induced inflammation, 18 and pulmonary infection. 19,20 One mechanism by which EC-SOD inhibits inflammation is directly binding to and inhibiting oxidative fragmentation of several components in the extracellular matrix including collagen, heparan sulfate, and hyaluronan after interstitial lung injury.…”

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confidence: 99%

Extracellular Superoxide Dismutase in Macrophages Augments Bacterial Killing by Promoting Phagocytosis

Manni

Tomai

Norris

et al. 2011

The American Journal of Pathology

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Extracellular superoxide dismutase (EC-SOD) is abundant in the lung and limits inflammation and injury in response to many pulmonary insults. To test the hypothesis that EC-SOD has an important role in bacterial infections, wild-type and EC-SOD knockout (KO) mice were infected with Escherichia coli to induce pneumonia. Although mice in the EC-SOD KO group demonstrated greater pulmonary inflammation than did wild-type mice, there was less clearance of bacteria from their lungs after infection. Macrophages and neutrophils express EC-SOD; however, its function and subcellular localization in these inflammatory cells is unclear. In the present study, immunogold electron microscopy revealed EC-SOD in membrane-bound vesicles of phagocytes. These findings suggest that inflammatory cell EC-SOD may have a role in antibacterial defense. To test this hypothesis, phagocytes from wild-type and EC-SOD KO mice were evaluated. Although macrophages lacking EC-SOD produced more reactive oxygen species than did cells expressing EC-SOD after stimulation, they demonstrated significantly impaired phagocytosis and killing of bacteria. Overall, this suggests that EC-SOD facilitates clearance of bacteria and limits inflammation in response to infection by promoting bacterial phagocytosis.

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Extracellular superoxide dismutase in biology and medicine

Cited by 570 publications

References 203 publications

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

Biochemical assessment of oxidative status versus liver enzymes in patients with chronic fascioliasis

Copper(II)-selective chelation improves function and antioxidant defences in cardiovascular tissues of rats as a model of diabetes: comparisons between triethylenetetramine and three less copper-selective transition-metal-targeted treatments

Extracellular Superoxide Dismutase in Macrophages Augments Bacterial Killing by Promoting Phagocytosis

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