Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.
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PMID:Oxygen radicals in cerebral ischemia. 133 9

Transient cerebral ischemia demonstrates an increase in activated oxygen species in the brain that could lead to eventual neuronal cell death. Neuronal cells respond to oxygen free radicals through the restructuring of the cytoskeleton and membranes, mobilization of calcium and gene expression which play a role in cell injury. Ten min of bilateral carotid artery occlusion resulted in a decrease in calcium/calmodulin dependent protein kinase II (CaM kinase II) phosphorylation and activity detected in the brain immediately following ischemia and was partially restored within 24 h of reperfusion. Pretreatment of animals with an anesthetic dose of pentobarbital (40 mg/kg) resulted in partial protection of inactivation of CaM kinase II following ischemia. CaM kinase II activity was maintained following pretreatment of animals with alpha-phenyl N-tert-butyl nitrone (PBN), which traps oxygen free radicals. Infusion of superoxide dismutase or catalase prior to ischemia, blocked CaM kinase II inactivation. Blockage of calcium uptake with bepridil resulted in a marked protection of CaM kinase II inactivation. In addition, trifluoperazine, a calmodulin antagonist also diminished the inhibition of CaM kinase II phosphorylation in our model. These results suggest that ischemia and reperfusion injury results in the generation of activated oxygen and the mobilization of calcium which inactivate CaM kinase II. These results indicate that changes associated with protein kinase activity in the brain following an ischemic insult may have profound effects upon neurodegeneration and neuronal survival.
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PMID:Role of calcium in inactivation of calcium/calmodulin dependent protein kinase II after cerebral ischemia. 133 39

After the middle cerebral artery of rats was occluded, changes in the content of 14 free amino acids and the activity of antioxidant enzymes in the ischemic striatum were assessed with respect to the duration of ischemia. Glu and Asp levels were significantly reduced by 60 min of ischemia, GABA was increased by 30 and 60 min and Ala was increased by 5, 15, and 30 min. During ischemia, the levels of striatal Gln, Asn, Ser, Tau, Gly and Pro were found to be normal. In comparison with the sham-operated rats, the changes in the content of Thr, His, Arg and Tyr were inconclusive, since the effect of operative stress could not be ruled out on such occasion. Concomitantly, the Zn-Cu superoxide dismutase and glutathione peroxidase activity were significantly reduced by 30 min of ischemia. It revealed that the reduced capacity to scavenge the oxygen free radicals occurred during the early stage of cerebral ischemia. The above changes of Glu, Gln, GABA and Pro level might be considered as the final outcome of the decrease of glutamate synthesis, the acceleration of its conversion to GABA, and the extracellular leakage of glutamate. According to our data, the oxygen free radicals might be involved in the evolution of primary neuronal damage at the ischemic striatum.
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PMID:[Mechanism of neuronal damage caused by cerebral ischemia]. 133 25

We investigated whether reversible oxidative stress induced by the administration of the superoxide dismutase inhibitor, diethyldithiocarbamate, could induce tolerance to subsequent cerebral ischemia in gerbil hippocampal neurons. Mature male gerbils received intraperitoneal injections of diethyldithiocarbamate (1.0 g/kg), which led to reduced superoxide dismutase activity and increases in thiobarbituric acid-reactive substance in the brain. Cerebral ischemia was produced by occluding the bilateral common carotid arteries for 5 min, either 2 or 4 days after diethyldithiocarbamate injection. One week after ischemia, samples from each brain were stained with hematoxylin-eosin to evaluate ischemic neuronal damage in the hippocampal CA1 sector. Diethyldithiocarbamate treatment 4 days before ischemia had significant protective effects against cerebral ischemia, while diethyldithiocarbamate 2-day pretreatment and vehicle treatment failed to show neuroprotection. Biochemical examinations showed a clear induction of heat shock protein 72 and a significant increase in manganese-containing superoxide dismutase in the hippocampus in animals treated with diethyldithiocarbamate 4 days prior to ischemia. These results suggested that the oxidative stress caused by diethyldithiocarbamate could induced tolerance to ischemia in the gerbil brain, and that the increase in the biosynthesis of manganese-containing superoxide dismutase and heat shock protein 72 could provide a biochemical explanation of the tolerance induced under these conditions.
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PMID:Influence of oxidative stress on induced tolerance to ischemia in gerbil hippocampal neurons. 133 59

Hydroxyl radical formation, secondary to superoxide radical generation, has been advocated as the actual mechanism of oxygen radical-mediated damage in biological systems. The present study was designed to compare the efficacy of administration of the hydroxyl radical scavenger mannitol vs. that of the superoxide radical scavenger superoxide dismutase (SOD) in reducing myocardial reperfusion injury, and to test whether combined treatment with both agents would confer better tissue protection compared with either intervention alone. Rabbit hearts perfused within a 31P nuclear magnetic resonance (31P-NMR) spectrometer were subjected to 30 minutes of total global ischemia at 37 degrees C. At reflow, 12 hearts in each group received either (a) a bolus of standard perfusion buffer, followed by 45 minutes of reperfusion (controls); (b) the superoxide radical scavenger recombinant human SOD (h-SOD, as a 60,000 U bolus followed by a 100 U/ml infusion for 15 minutes); (c) the hydroxyl radical scavenger mannitol (50 mM bolus followed by 15 minutes of 50 mM infusion; or (d) a combination of both agents. All treated hearts were switched to standard buffer for the remaining 30 minutes of reperfusion. Treatment with h-SOD alone was associated with a significant improvement in the recovery of cardiac contractility and coronary flow, as well as of ATP content, compared to control hearts. In contrast, mannitol treatment resulted in a small, nonsignificant improvement in these parameters. The addition of mannitol to h-SOD did not result in further significant improvement of contractility and ATP recovery compared to h-SOD alone. These data demonstrate that under our experimental conditions significant protection against reperfusion injury can be achieved by the administration of h-SOD alone, without the need for additional hydroxyl radical scavenger therapy with mannitol. These results do not exclude that significant tissue protection may be achieved by different doses of mannitol or by other agents. However, they suggest that under definite experimental conditions prevention of hydroxyl radical formation, rather than attempts to minimize hydroxyl radical toxicity, might be a more efficient method to prevent oxygen radical-mediated reperfusion injury in isolated hearts.
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PMID:Effects of the superoxide radical scavenger superoxide dismutase, and of the hydroxyl radical scavenger mannitol, on reperfusion injury in isolated rabbit hearts. 133 78

Using luminol- and lucigenin-enhanced chemiluminescence (Lm-CL and Lg-CL), we monitored oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver. Both enhanced chemiluminescence levels decreased during 30 min of ischemia and increased markedly at the onset of reperfusion. When the liver was subjected to another 30 min of ischemia, reperfusion caused a progressive increase in both types of enhanced chemiluminescence. Administration of superoxide dismutase (SOD) into the perfusate strongly attenuated Lm-CL, but had a limited effect on Lg-CL. Catalase (CAT) and allupurionol (ALP) failed to attenuate both types of enhanced chemiluminescence. Thus the predominant oxygen radicals in the liver during reperfusion is superoxide and the lack of effect of ALP on oxygen radical generation indicates that hypoxanthine-xanthine oxidase reaction is unlikely to be a primary source of oxygen radicals. The different response to SOD in Lm-CL and Lg-CL is considered to be based on the diffusion space of luminol and lucigenin in the tissue. The relationship between oxygen radical levels and tissue damage, and the site of oxygen radical detection are discussed.
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PMID:Oxygen radical generation during ischemia-reperfusion in the isolated perfused rat liver monitored by enhanced chemiluminescence. 133 37

In order to investigate the role of endothelin-1 during ischemia-reperfusion injury, 80 adult male Wistar rats were subjected to three hours of ischemia and one hour of reperfusion. Animals were evenly divided into eight groups. The rats in group 1 served as the normal control group, while the rats in group 2 received an intravenous infusion of endothelin-1 in a dosage of 0.5 ng/kg/min, group 3 in a dosage of 5 ng/kg/min, and group 4 in a dosage of 50 ng/kg/min. The rats in group 5 were infused with angiotensin II (10 ng/kg/min). The rats in group 6 received an intravenous infusion of 10,000 units of superoxide dismutase and 10,000 units of catalase. Group 7 rats were infused with endothelin-1 (50 ng/kg/min), superoxide dismutase (10,000 units), and catalase (10,000 units). Group 8 rats received an infusion of angiotensin II (10 ng/kg/min), superoxide dismutase (10,000 units) and catalase (10,000 units). The infusions were given during the reperfusion period. After one hour of reperfusion, the gastrocnemius and soleus muscles of the experimental animals were excised and assayed for ischemia-reperfusion injury by measuring triphenyltetrazolium chloride (TTC) reduction. The results showed that the limb activity of the ischemic extremity was 40.33 +/- 2.75% in group 1, 41.62 +/- 4.08% in group 2, 14.42 +/- 3.14% in group 3, 4.43 +/- 1.05% in group 4, 23.81 +/- 3.51% in group 5, 57.23 +/- 4.52% in group 6, 31.79 42- 3.63% in group 7, and 27.39 +/- 3.95% in group 8. Endothelin-1 reduced the limb activity in a dose-dependent manner.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of endothelin-1 during ischemia-reperfusion injury. 136 41

Oxygen-derived free radicals and leukocytes have been implicated in the pathogenesis of ischemia-reperfusion injury. This study aimed at determining, by using biochemical and histochemical techniques, whether an accumulation of neutrophils occurs in the ischemic reperfused rat liver and whether superoxide free radicals play a role in mediating this neutrophil accumulation. Hepatic ischemia was induced by occluding blood supply to the left and median lobes, and reperfusion was reinstituted by releasing the occlusion. Myeloperoxidase activity of the liver was measured with a tetramethylbenzidine-H2O2 assay after removal of glutathione (by dialysis) and in the presence of 3-aminotriazole (catalase inhibitor). A modification of Graham and Karnovsky's method was used to stain neutrophils in liver frozen sections, and the number of neutrophils was counted. Results showed that ischemia-reperfusion of the liver produced a 4.4-fold increase in myeloperoxidase activity (from 0.073 +/- 0.009 to 0.320 +/- 0.017 units/mg liver, means +/- SE), which was proportional to the number of neutrophils (3.1-fold increase from 18 +/- 7 to 57 +/- 4 cells/mm2) in the liver tissue. Pretreatment with long-acting superoxide dismutase significantly attenuated the elevated myeloperoxidase activity and the number of neutrophils. These results indicate that reperfusion after a period of ischemia induces an accumulation of neutrophils in the liver, and superoxide anion free radicals are important mediators in the mechanism of this neutrophil accumulation.
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PMID:Neutrophil accumulation in ischemic reperfused rat liver: evidence for a role for superoxide free radicals. 137 65

We have demonstrated that tumor necrosis factor-alpha (TNF-alpha) pretreatment protected the rat heart from ischemia-reperfusion injury. This effect was monitored by assaying for lactate dehydrogenase (LDH), an enzyme whose release correlates with loss of cell membrane integrity. Intact hearts removed from rats pretreated with TNF-released significantly lower amounts of LDH compared to control hearts after 20 min. of total global ischemia followed by reperfusion. Hearts from TNF-alpha-pretreated animals contained higher levels of manganous superoxide dismutase (MnSOD) mRNA than hearts from untreated rats. Because oxygen free radicals have been implicated as a major cause of reperfusion damage and the function of MnSOD is to detoxify superoxide anions in the mitochondria, a possible protective mechanism for TNF-alpha may be to induce expression of MnSOD in the heart and thus confer resistance to oxygen free radicals generated during reperfusion.
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PMID:Tumor necrosis factor-alpha pretreatment is protective in a rat model of myocardial ischemia-reperfusion injury. 137 34

The effects of decreasing blood viscosity by normovolemic hemodilution with dextran-40 or normal saline (NS) on myocardial lipid peroxides, superoxide dismutase, infarct size and left ventricular function during acute myocardial ischemia/reperfusion were studied in rabbits. It was found that normovolemic hemodilution with dextran-40 could decrease the content of ischemic myocardial malondialdehyde and preserve ischemic myocardial superoxide dismutase activity after 1 h of coronary occlusion followed by 1 h of reperfusion. However, after administration of NS only a tendency in this aspect exhibited without statistical significance. Besides, hemodilution with dextran-40 reduced infarct size and improved left ventricular systolic function after 1 h of ischemia followed by 23 h of reperfusion. These results suggest that normovolemic hemodilution with dextran-40 may have anti-injury effect on acute myocardial ischemia/reperfusion to a certain degree.
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PMID:The effects of normovolemic hemodilution with dextran-40 on acute myocardial ischemia/reperfusion injury in rabbits. 137 54


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