Extracellular superoxide dismutase, nitric oxide, and central nervous system O2 toxicity.

Oury, Tim D.; Ho, Ye-Shih; Piantadosi, Claude A.; Crapo, James D.

doi:10.1073/pnas.89.20.9715

Cited by 217 publications

(148 citation statements)

References 35 publications

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“…EcSOD is released from glial cells and a number of potential roles for this enzyme have been proposed, e.g. it is suggested to be involved in prolonging the lifespan of nitric oxide (Oury et al 1992), and decreasing the production of peroxynitrite (Huie and Padmaja 1993). However, to our knowledge, protection of released GSH has not been considered.…”

Section: Figmentioning

confidence: 93%

Preservation of extracellular glutathione by an astrocyte derived factor with properties comparable to extracellular superoxide dismutase

Stewart¹,

Stone²,

Gegg³

et al. 2002

Journal of Neurochemistry

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Cultured rat and human astrocytes and rat neurones were shown to release reduced glutathione (GSH). In addition, GSH oxidation was retarded by the concomitant release of a factor from the cells. One possibility is that this factor is extracellular superoxide dismutase (SOD). In support of this, the factor was found to bind heparin, have a molecular mass estimated to be between 50 and 100 kDa, and CuZn-type SOD protein and cyanide sensitive enzyme activity were demonstrated in the cell-conditioned medium. In addition, supplementation of native medium with exogenous CuZn-type SOD suppressed GSH oxidation. We propose that preservation of released GSH is essential to allow for maximal up-regulation of GSH metabolism in neurones. Furthermore, cytokine stimulation of astrocytes increased release of the extracellular SOD, and enhanced stability of GSH. This may be a protective strategy occurring in vivo under conditions of oxidative stress, and suggests that SOD mimetics may be of therapeutic use.

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Section: Figmentioning

confidence: 93%

Preservation of extracellular glutathione by an astrocyte derived factor with properties comparable to extracellular superoxide dismutase

Stewart¹,

Stone²,

Gegg³

et al. 2002

Journal of Neurochemistry

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“…The generation of SOD3 KO and SOD3 Tg mice were described previously, with their background WT mice being the C57BL/6J strain (38,39,50). All animal procedures described in this study were approved by the University Committee on Animal Research Committee of the University of Rochester.…”

Section: Methodsmentioning

confidence: 99%

Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Yao

Arunachalam

Hwang

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

172

166

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Extracellular superoxide dismutase (ECSOD or SOD3) is highly expressed in lungs and functions as a scavenger of O 2 • ─ . ECM fragmentation, which can be triggered by oxidative stress, participates in the pathogenesis of chronic obstructive pulmonary disease (COPD) through attracting inflammatory cells into the lungs. The level of SOD3 is significantly decreased in lungs of patients with COPD. However, the role of endogenous SOD3 in the development/progression of emphysema is unknown. We hypothesized that SOD3 protects against emphysema by attenuating oxidative fragmentation of ECM in mice. To test this hypothesis, SOD3-deficient, SOD3-transgenic, and WT C57BL/6J mice were exposed to cigarette smoke (CS) for 3 d (300 mg total particulate matter/m 3 ) to 6 mo (100 mg/m 3 total particulate matter) or by intratracheal elastase injection. Airspace enlargement, lung inflammation, lung mechanical properties, and exercise tolerance were determined at different time points during CS exposure or after elastase administration. CS exposure and elastase administration caused airspace enlargement as well as impaired lung function and exercise capacity in SOD3-null mice, which were improved in mice overexpressing SOD3 and by pharmacological SOD mimetic. These phenomena were associated with SOD3-mediated protection against oxidative fragmentation of ECM, such as heparin sulfate and elastin, thereby attenuating lung inflammatory response. In conclusion, SOD3 attenuates emphysema and reduces oxidative fragmentation of ECM in mouse lung. Thus, pharmacological augmentation of SOD3 in the lung may have a therapeutic potential in the intervention of COPD/emphysema.antioxidants | cigarette smoke | chronic obstructive pulmonary disease | oxidants | glutathione E xtracellular superoxide dismutase (ECSOD or SOD3) is one of the three SOD antioxidant enzyme isoforms, and is highly expressed in lungs and vessels (1, 2). It is located in the ECM, the junctions of airway epithelial cells, the surface of airway smooth muscle, and the lining of vessels of the lung. SOD3 functions as a superoxide anion scavenger, thereby attenuating oxidative stress, which may play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Acute loss of SOD3 in adult mice causes death, whereas low mortality rates are seen in SOD3-overexpressing animals exposed to hyperoxia, suggesting an essential role of SOD3 for survival (3,4). Accumulating evidence shows that SOD3 polymorphism is associated with a decline in lung function in rodents and humans, and susceptibility to COPD, which may be a result of alteration of its encoding protein structure, function, and level (5-14). However, it is unclear whether endogenous SOD3 participates in the development/ progression of the inflammatory response, leading to COPD/ emphysema.Cigarette smoke (CS) is the major etiological factor in the pathogenesis of COPD, which is characterized by chronic lung inflammation, parenchymal destruction (i.e., emphysema), and accelerated decline in lung function....

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“…EC-SOD is considered to serve for defence against superoxide, which can be produced by membranebound NADPH or secreted by inflammatory cells into the extracellular space (Oury, 1992). In spite of the relatively low EC-SOD concentration in whole brain, it may be important for ischemic event.…”

Section: Plasma Enzymatic Antioxidant Profile As the Predictor Of Funmentioning

confidence: 99%

Plasma Antioxidant Activity as a Marker for a Favourable Outcome in Acute Ischemic Stroke

Sapojnikova¹,

Asatiani²,

Kartvelishvili³

et al. 2012

Antioxidant Enzyme

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Extracellular superoxide dismutase, nitric oxide, and central nervous system O2 toxicity.

Cited by 217 publications

References 35 publications

Preservation of extracellular glutathione by an astrocyte derived factor with properties comparable to extracellular superoxide dismutase

Preservation of extracellular glutathione by an astrocyte derived factor with properties comparable to extracellular superoxide dismutase

Extracellular superoxide dismutase protects against pulmonary emphysema by attenuating oxidative fragmentation of ECM

Plasma Antioxidant Activity as a Marker for a Favourable Outcome in Acute Ischemic Stroke

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