Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.15.1.1 (superoxide dismutase)
 58,858 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the role of oxygen radicals in the development of myocardial injury during ischemia, production of lipid peroxides mediated by oxygen radicals was determined in in vivo dogs subjected to regional ischemia and reperfusion. Myocardial injury was assessed by derangement in energy and carbohydrate metabolism caused by ischemia and reperfusion. The production of lipid peroxides mediated by oxygen radicals considerably increased not only during reperfusion after ischemia but also during ischemia. Removal of oxygen radicals by administration of radical scavengers [recombinant human superoxide dismutase + catalase or N-(2-mercaptopropionyl)glycine] completely prevented the increase in production of lipid peroxides during ischemia. However, the radical scavengers did not attenuate the myocardial energy and carbohydrate metabolic derangements caused by ischemia and reperfusion after ischemia. These results suggest that significant amounts of oxygen radicals are generated during ischemia as well as during reperfusion and that the oxygen radicals and subsequent lipid peroxidation are not major factors in development of myocardial injury during either ischemia or reperfusion after ischemia.
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PMID:Role of oxygen radicals in canine myocardial metabolic derangement during regional ischemia. 153 15

Preconditioning the heart with 5 min of ischemia renders the heart very resistant to infarction from subsequent ischemia by an unknown mechanism. We investigated whether the protective effect of preconditioning might be related to an increase in rabbit heart antioxidant defenses. The antioxidant activities of catalase, glutathione peroxidase, Mn superoxide dismutase, Cu,Zn superoxide dismutase, glucose-6-phosphate dehydrogenase, glutathione reductase, and total glutathione were measured in ischemic and normal regions from both control and preconditioned rabbit hearts. All hearts experienced 30 min regional ischemia and 5 min reperfusion. None of the antioxidant enzymes changed in activity when comparing nonischemic and postischemic zones in either nonpreconditioned or preconditioned hearts. Total glutathione, however, was reduced in reperfused zones and showed better preservation in preconditioned hearts. To determine whether this preservation resulted from a higher value at the onset of reperfusion or slower washout during reperfusion, we analyzed a second group of nonreperfused hearts after 30 min ischemia. The hearts had normal glutathione content in both ischemic and nonischemic zones of either preconditioned or control hearts. The most likely explanation is that preconditioned hearts experienced less washout of glutathione simply because they were less injured. We therefore conclude that enhancement of antioxidant defenses is not the mechanism of preconditioning.
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PMID:Protection from reperfusion injury by preconditioning hearts does not involve increased antioxidant defenses. 153 19

In this study, by using highly purified rat liver peroxisomes, we provide evidence from analytical cell fractionation, Western blot, and immunocytochemical analysis that Cu-Zn superoxide dismutase is present in animal peroxisomes. Treatment with ciprofibrate, a peroxisome proliferator, increased the peroxisomal superoxide dismutase activity by 3-fold with no effect on mitochondrial activity but a marked decrease in cytosolic superoxide dismutase activity, further supporting that besides cytosolic and mitochondrial localization, Cu-Zn superoxide dismutase is present in peroxisomes also. Demonstration of superoxide dismutase in peroxisomes suggests a new role for this organelle in pathophysiological conditions, such as ischemia-reperfusion injury.
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PMID:Demonstration of Cu-Zn superoxide dismutase in rat liver peroxisomes. Biochemical and immunochemical evidence. 155 95

Oxygen free radicals are implicated to cause tissue injury during ischemia and reperfusion and may play a central role in the no-reflow phenomena. Modulation of these substances has been suggested as a means of decreasing the amount of tissue loss due to ischemia and subsequent reperfusion. Pretreatment of tissues with a variety of agents has been reported to minimize the production of oxygen radicals and augment tissue survival after an ischemic insult. Ischemic clinical situations, however, usually present unexpectedly and thus pretreatment is not feasible. Our study evaluated the activity and effect of free radical scavengers delivered systemically during the ischemic interval to an ischemia/reperfusion rat intestinal model. Superoxide dismutase and dimethylthiourea were given systemically after occlusion and reperfusion to simulate a clinical sequence of a failing flap, that is, the vascular compromise, the diagnosis, and the successful resolution of the vascular embarrassment. Measurements of malonyldialdehyde (MDA), the end product of lipoperoxidation of cell walls, were compared with controls. Tissue histology was assessed and correlated with the use of these agents. A third group of rats was systemically alkalinized to attempt to shift the Bohr curve and decrease free oxygen substrate in the ischemic tissues on reperfusion. Rats treated with superoxide dismutase and dimethylthiourea showed significant reductions of MDA compared with nontreated rats (p less than 0.05), indicating attenuation of reperfusion lipoperoxidation. Systemic alkalinization of the rats did not significantly change the levels of MDA. Tissue histology showed severe injury in all ischemic groups regardless of the level of MDA.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Attenuation of reperfusion-induced lipoperoxidation by systemic use of oxygen radical scavengers after pedicle occlusion. 156 20

An experimental model of optic nerve ischemia was designed in the rabbit to determine early biochemical alterations, i.e.--changes of high energy phosphate metabolites (ATP and phosphocreatine)--in occlusive and peri-occlusive areas. Vascular occlusion provoked a rapid fall of ATP and phosphocreatine in the optic nerve. Free radicals scavengers, superoxide dismutase plus catalase or dimethylthiourea were able to counteract the drop of phosphate metabolites in the peri-occlusive area. These results show that hypoxia leads to oxygen-derived free radical generation which can be responsible for cell damage and emphasize the role of free radicals in the pathogenesis of ocular diseases related to vascular dysfunction.
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PMID:Alterations of energetic metabolite levels by free radicals during optic nerve ischemia. 158 50

Endothelial dysfunction, as evidenced by decreased stimulated release of endothelium-derived relaxing factor (EDRF), occurs after reperfusion of the ischemic myocardium. To better understand this endothelial dysfunction, isolated cat hearts were perfused under constant flow by the Langendorff procedure with Krebs-Henseleit solution devoid of blood cells. Following global ischemia (90 minutes) and reperfusion (20 minutes), coronary vasorelaxation to the endothelium-dependent vasodilator acetylcholine (ACh) was 70 +/- 3% of initial values (p less than 0.01) compared with 90 +/- 4% in nonischemic control perfused hearts. No decrement occurred in response to the endothelium-independent vasodilator nitroglycerin (NTG). Coronary artery rings isolated from the ischemic left circumflex coronary artery showed a similar degree of endothelial dysfunction to ACh, with normal relaxation in response to NaNO2. Autologous cat neutrophils (100 million cells), activated with 100 nmol/L f-met-leu-phe infused into the heart directly before and throughout reperfusion, resulted in a further decrement in ACh-induced vasodilation, to 55 +/- 5% of initial response, with no effect on NTG-induced vasodilation. Similar results were obtained with coronary artery rings isolated from perfused cat hearts and exposed to neutrophils. This neutrophil-enhanced endothelial dysfunction was inhibited by human superoxide dismutase as well as by an antibody to the adherence glycoprotein complex CD-18 (i.e., MAbR 15.7). Therefore endothelial dysfunction occurs initially upon reperfusion of the previously ischemic heart and is aggravated by superoxide radicals produced by activated neutrophils.
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PMID:Activated neutrophils aggravate endothelial dysfunction after reperfusion of the ischemic feline myocardium. 824 14

The effectiveness of high-potassium cardioplegic solution in the neonatal heart remains controversial. Our previous study indicated that the protection afforded by a cardioplegic solution was inadequate in the neonatal heart. On the hypothesis that oxyradicals were responsible for the ineffectiveness of cardioplegic solution in neonatal heart, the effects of a cardioplegic solution (a modified St. Thomas' Hospital cardioplegic solution) with recombinant human superoxide dismutase on the isolated perfused neonatal guinea pig hearts (within 2 days after delivery, body weight of 60 to 120 g) were studied in comparison with those on the adult hearts (6 to 8 weeks after delivery, body weight of 300 to 500 g). After arrest induced by modified St. Thomas' Hospital cardioplegic solution, hearts were subjected to 120 min of ischemia at 20 degrees C, during which time the cardioplegic solution was injected every 30 minutes. Then the heart was reperfused for 60 minutes at 37 degrees C. Under this condition, the left ventricular developed pressure recovered to 84.4% +/- 4.0% of the preischemic value in the adult heart, whereas the recovery was only 68.1% +/- 3.1% in the neonatal heart. Thiobarbituric acid-reactive substance level, a parameter of lipid peroxidation by oxyradicals, significantly increased during ischemic arrest both in the adult and neonatal heart. However, the increase was much greater in the neonatal heart than in the adult. Cardioplegia with recombinant human superoxide dismutase (300 and 1,000 U/mL) significantly inhibited this accumulation of thiobarbituric acid-reactive substance in the neonatal heart; at 1,000 U/mL, the myocardial function of the reperfused neonatal heart recovered to the level of the adult heart.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial protection of neonatal heart by cardioplegic solution with recombinant human superoxide dismutase. 161 Feb 23

The effects of recombinant human superoxide dismutase (r-hSOD) on ischemic neuronal injury were examined. Cerebral ischemia was produced in Mongolian gerbils by occluding bilateral common carotid arteries for 5 min. Preischemic treatment with r-hSOD clearly reduced hippocampal neuronal damages while postischemic treatment did not. This result suggests that oxygen free radicals play an important role in selective vulnerability to ischemia and r-hSOD has a potential clinical usefulness against cerebral ischemia.
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PMID:Recombinant human superoxide dismutase can attenuate ischemic neuronal damage in gerbils. 162 16

In the present study, we quantified the biochemical [thiobarbituric acid (TBA) reactants, superoxide dismutase (SOD) and vitamin E] and histologic changes in the small intestinal tissue after ischemia and/or reperfusion. Sixty-seven Wistar rats were divided into 7 groups; N group: control, A-I group: 30 min. ischemia, A-II group: 120 min. ischemia, B-I group: Declamp after 30 min. ischemia, B-II group: 30 min. reperfusion after 30 min. ischemia, B-III group: 30 min. reperfusion after 120 min. ischemia, E group: vitamin E administration 30 min. reperfusion after 30 min. ischemia. The levels of TBA reactants were significantly different between A-II and B-II, B-II and E (all p less than 0.01). For SOD, there were significant differences between N and B-I (p less than 0.01), N and E (p less than 0.05). For vitamin E, there were significant differences between A-I and B-I, A-I and B-I, B-II and E (all p less than 0.01). Histologic changes showed that the grade of tissue injury was more severe in B-I and B-II than in A-I, and was less in E than in B-II. It is suggested that vitamin E protected cells from injury due to oxygen free radicals.
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PMID:[Experimental studies on the effects of alpha-tocopherol in small intestinal ischemia and reperfusion injury]. 163 Apr 35

To determine the contribution of oxygen-derived free radicals to the changes in microvascular structure and function which follow reperfusion of ischemic myocardium, isolated perfused rat hearts were subjected to 15 or 45 min of global ischemia followed by 5 min of oxygenated reperfusion. Hearts were then fixed by perfusion with glutaraldehyde and perfused with nuclear track photographic emulsion to identify competent capillaries in scanning and transmission electron micrographs. Reperfusion after 15 min caused a significant reduction in the density of competent capillaries in the subendocardial third of the left ventricle, but this reduction was lessened but not eliminated by the addition of 0.61 mmole/liter desferrioxamine, but not by 60,000 U/liter superoxide dismutase plus 60,000 U/liter catalase, to the perfusate. After 45 min of ischemia both interventions prevented the myocyte swelling, endothelial cell changes, bleb formation, and reduction in microvascular lumina characteristic of unprotected reperfusion, but only desferrioxamine significantly improved microvascular competence. This suggests that the hydroxyl radical rather than superoxide and/or hydrogen peroxide has a pathogenic role, although desferrioxamine may have other effects as nonspecific chelator. Postischemic reductions in capillary function also occur in reversibly injured myocardium in the absence of structural abnormality. Preventing postischemic microvascular incompetence has the potential to minimize ischemic cell injury and to enhance repair following myocardial infarction, but it also may increase the risk of hemorrhage from venules.
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PMID:Anti-oxidant therapy improves microvascular ultrastructure and perfusion in postischemic myocardium. 163 71


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