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)

Oxygen free radicals (OFRs) generated during reperfusion are putative mediators of postischemic renal dysfunction. To address this issue, the renal response to ischemia and reperfusion was compared to the response to OFR generation without ischemia. Isolated rat kidneys were perfused at 37 degrees C and 90-100 mm Hg with an asanguinous modified Krebs' buffer. Kidneys were subjected to 30 min of ischemia followed by reperfusion or to OFRs generated by combining 25 mumole hypoxanthine with 1 unit xanthine oxidase. Both insults caused a 50% increase in vascular resistance. This was accompanied by a 30% reduction in perfusate flow rate and an 80% reduction in glomerular filtration and urine flow rates. The OFR scavengers, superoxide dismutase (SOD, 250 units/ml) and catalase (CAT, 500 units/ml), prevented these alterations after OFR generation but not after 30 min of ischemia and reperfusion. SOD and CAT also afforded no protection against the less severe dysfunction observed after 10 or 20 min of ischemia and reperfusion. OFRs do not appear to be prominent mediators of postischemic renal dysfunction; other factors, probably associated with ischemia must be primarily responsible.
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PMID:Postischemic renal dysfunction: the limited role of xanthine oxidase-generated oxygen free radicals. 226 85

The effects of glucagon, heparin, urokinase, thromboxane synthetase inhibitor (OKY-046), and the free radical scavengers, superoxide dismutase and catalase (SOD + CAT), on the viability of ischemic intestine were evaluated based on various parameters measured. The mucosal blood flow, the fluorescence pattern, and the histopathological findings in a rabbit model with 3.5 hr total vascular occlusion of a short small intestine indicated that glucagon improved the ischemic intestine. Glucagon increased, tremendously, the mucosal blood flow by 112% in the ischemic intestine compared with that of 25% in the nonischemic intestine. This indicated that vascular spasm, not reperfusion injury or thrombosis, played the initial role in the progression of transmural bowel necrosis. In addition, the outcome in the viability of the ischemic intestine was not detected by the fluorescence technique but was able to be detected through the mitochondrial morphology under the electron microscope.
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PMID:Does glucagon improve the viability of ischemic intestine? 226 88

Twigs-dry leaves smoke condensate (TDS) was investigated for its DNA damaging activity in human peripheral lymphocytes, by using a sensitive method, fluorescence analysis of DNA unwinding (FADU). An aqueous turmeric component (Aq.T) was studied as a protective agent. TDS at one to 100 folds dilution induced 55% DNA damage at 20 min, while 12-O-tetradecanoylphorbol-13-acetate (TPA) at 10 ng/ml induced only 25% damage. Aq.T at 300 ng/microliter afforded 90% protection to DNA against TDS and 65% against TPA. The mechanism of Aq.T protection was investigated by using (i) inhibitors of arachidonate cascade, viz., indomethacin (28 microM), NDGA (10 microM), DBAP (36 microM), (ii) antioxidant enzymes viz., CAT (0.2 U/microliter), SOD (0.6 U/microliter), (iii) antioxidants--BHA, curcumin (40 microM), mixed gangliosides (20 nM) and protease inhibitor TLCK (100 microM). These compounds offered the following extents of protection to DNA against TDS: indomethacin--40%, NDGA--83%, DBAP--70%, SOD--38%, CAT--40%, BHA--38%, curcumin--60%, mixed gangliosides--88%, TLCK--85%. Against TPA as clastogenic agent, the extents of protection were: indomethacin--73%, NDGA--32%, DBAP--72%, SOD--60%, CAT, BHA-negligible, curcumin--23%, mixed gangliosides--60%, TLCK--59%. These results indicate that (i) TDS and TPA induce DNA damage possibly by different mechanisms, (ii) Aq.T is a more effective protectant against TDS whereas it is on par with other inhibitors against TPA.
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PMID:Fuel smoke condensate induced DNA damage in human lymphocytes and protection by turmeric (Curcuma longa). 236 50

Superoxide dismutase and catalase enzymatically scavenge superoxide and hydrogen peroxide, respectively. Conjugation of polyethylene glycol to superoxide dismutase (PEG-SOD) or catalase (PEG-CAT) prolongs the circulatory half-life of the native enzymes and enhances their intracellular access. We studied the protective effect of these free radical scavengers on ischemic brain injury using a rat model of focal cerebral ischemia, which is suitable for therapeutic trials. Intravenous administration of PEG-SOD (10,000 U/kg) and PEG-CAT (10,000 U/kg) before ischemia reduced the infarct volume (treatment, 139 +/- 9 mm3, means +/- SE, N = 38; placebo, 182 +/- 8 mm3, n = 37, P less than 0.002). This finding supports the concept that superoxide and hydrogen peroxide contribute to brain injury following focal cerebral ischemia.
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PMID:Polyethylene glycol-conjugated superoxide dismutase and catalase reduce ischemic brain injury. 249 71

When exposed continuously to hyperoxia (100% O2, 760 Torr barometric pressure), rats pretreated with polyethylene glycol (PEG)-attached superoxide dismutase and catalase (PEG-SOD + PEG-CAT) lived longer (79.1 + 7.6 h) than rats pretreated with saline (60.7 +/- 2.1 h) or PEG-inactivated-SOD + PEG-inactivated-CAT (62.3 +/- 1.6 h). Rats pretreated with PEG-SOD + PEG-CAT also had less hyperoxia-induced acute oxidative edematous lung injury, as assessed by increases in lung oxidized glutathione (GSSG) contents, pleural effusions, and lung lavage albumin concentrations than saline-pretreated rats. Rats pretreated with the long-lived conjugates PEG-inactivated-SOD + PEG-inactivated-CAT or PEG-albumin also had decreased acute oxidative edematous lung injury compared with rats pretreated with PEG, SOD + CAT + PEG, SOD + CAT, or saline. In vitro studies suggested that PEG itself may have contributed to protection by scavenging hydroxyl radical (.OH) but not superoxide (O2-.) or H2O2. Compared with more effective endogenous (via preexposure to hypoxia) or exogenous (via liposomes) means for increasing lung antioxidant enzymes, PEG enzymes are less protective against lung injury from continuous hyperoxia.
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PMID:Polyethylene glycol-attached antioxidant enzymes decrease pulmonary oxygen toxicity in rats. 254 Jan 39

The changes in endogenous superoxide dismutase (ESOD) during myocardial ischemia and reperfusion and the efficacy of oxygen free radical scavengers in myocardial protection were investigated in an isolated heart model connected with the recirculating nonpulsatile perfusion circuit. Subjected to a 2-hour period of global ischemia (27 C), the heart was reperfused with 37 C oxygen diluted auto-blood for 60 minutes. Superoxide dismutase plus catalase was added into the cardioplegic solution and reperfusates. ESOD activity was measured by pyrogallol method. The results of the experiment showed that ESOD activity after ischemia and reperfusion was decreased and the addition of oxygen free radical scavengers (SOD and CAT) to the cardioplegic solution and the reperfusates greatly reduced the leakage of myocardial enzymes, coronary vascular resistance, and the ultrastructural damages of the myocardium. These results suggest that the use of SOD and CAT may inhibit myocardial reperfusion injury by scavenging oxygen-derived free radicals.
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PMID:Prevention of myocardial reperfusion injury with free radical scavengers. An experimental study. 256 Sep 53

In the feline intestine studies have implicated superoxide (O.-) and other oxygen derived free radicals as initiators of injury as measured by increased capillary permeability during the reperfusion period. Biochemical mechanisms of this free radical generation include: xanthine oxidase dependent O.- production, hydrogen peroxide (H2O2) formation by superoxide dismutase (SOD), hydroxyl radical (OH-) production via the Haber-Weiss reaction, and lipid radical formation from membrane peroxidation. Pathological consequences of these events include inflammatory neutrophil infiltration, damage to the collagen and mucosal basement membrane, increased capillary permeability, edema, cell degeneration and necrosis. Animal models of neonatal necrotizing enterocolitis (NNEC) indicate that intestinal injury occurs after the etiologic factors (hypothermia, hypoxia) are removed. In order to determine the role of active oxygen species in the pathogenesis of NNEC, weanling hamsters and neonatal piglets were cold stressed and activities of pro/antioxidant enzymes were determined, and histopathologic and ultrastructural studies were performed. Cold stressed weanling hamsters showed a 55.7% (P less than 0.05) decrease in xanthine dehydrogenase/xanthine oxidase activity ratio. Light microscopy revealed scattered colonic mucosal erosions and submucosal edema in 50% of cold stressed animals. Transmission electron microscopy demonstrated degeneration of colonic mucosal epithelial cells, enlarged intracellular spaces, cytoplasmic vacuolization, and nuclear membrane swelling. The colonic serosa was also edematous and infiltrated with bacteria. Large intestinal tissue from cold stressed neonatal piglets showed a significant increase (P less than 0.05) in Mn and Cu, Zn, SOD, CAT, GSH-Red, total GSH, and Glc6-PD at 0 and 12 hrs. post stress.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Intestinal post-ischemic reperfusion injury: studies with neonatal necrotizing enterocolitis. 259 24

To obtain a profile of erythrocyte antioxidant defense potential during late fetal development, we studied selected antioxidant parameters in blood samples from 65 neonates with birth wt between 520 and 4210 g and from 12 healthy adults. Erythrocyte superoxide dismutase activity did not change significantly with maturation and no significant differences were observed among preterm infants grouped in increasing birth wt categories, term neonates, and adults. Erythrocyte catalase and glutathione peroxidase, as well as plasma vitamin E levels, showed highly significant positive correlations (p less than 0.001) with increasing fetal wt and gestational age; by term, CAT activity reached a level similar to the adult control group, but glutathione peroxidase activity, as well as plasma vitamin E levels, were markedly lower in all the preterm and in the term groups than in adults (p less than 0.01). Erythrocyte glutathione S-transferase activity showed a negative correlation with increasing gestational age (p less than 0.01) and the adult values were considerably lower than any of the neonatal levels (p less than 0.001). The role of glutathione S-transferase in erythrocyte metabolism remains obscure. Maturational changes in the activity of the red cell enzymes that were studied and in the plasma vitamin E level were apparent from about 31-36 wk of gestation, suggesting that the stimulation for these changes may have commenced from about 28-31 wk.
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PMID:Developmental patterns of antioxidant defense mechanisms in human erythrocytes. 279 51

These experiments evaluated the leukocyte as a potential source of oxygen free radical (OFR) generation during reperfusion injury in post-ischemic skeletal muscle. The infrarenal aorta of heparinized Sprague-Dawley rats was clamped for 90 min, declamped, and reperfused for 60 min. Hindlimb muscle resting transmembrane potential difference (Em) and high-energy phosphate content were determined at base line, during ischemia, and on reperfusion. Four groups were studied: a control group, a second group receiving superoxide dismutase and catalase (SOD + CAT) on declamping, a third group receiving dimethylmyleran (DMM) 7 days before the experiment to obtain a selective leukopenia (white blood cells = 1,210 +/- 144/mm3, neutrophils = 1.2%), and a fourth group pretreated with allopurinol (ALLO). During the ischemic period, resting Em was significantly depolarized (-78.6 +/- 0.5 mV from -90.3 +/- 0.3; P less than 0.05) in the control group, whereas creatine phosphate (CP) was depleted and ATP maintained. Data collected during the ischemic phase of the three other groups were similar to the control group (P = NS). On reperfusion, persistent depolarization of resting Em was observed despite restoration of muscle CP content in the control and ALLO groups (-75.4 and -77.0 mV, respectively). In contrast, significant repolarization of resting Em was noted after reperfusion in the SOD + CAT and DMM groups (-86.5 and -88.6 mV, respectively). These data implicate leukocyte-generated OFR as mediators of reperfusion-associated cellular membrane injury in postischemic skeletal muscle.
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PMID:Role of leukocytes in reperfusion injury of skeletal muscle after partial ischemia. 280 69

We hypothesized that superoxide anion (O2-.) and hydrogen peroxide (H2O2) might be important mediators of endotoxin-induced acute respiratory failure (ARF) in pigs. As specific scavengers of O2-. and H2O2, we infused polyethylene glycol-superoxide dismutase (PEG-SOD; 2,000 IU/kg) and PEG-catalase (CAT; 15,000 IU/kg), respectively. Escherichia coli endotoxin (055-B5) was infused intravenously into anesthetized 10- to 14-wk-old pigs at 5 micrograms/kg the 1st h, followed by 2 micrograms.kg-1.h-1 for 3.5 h. During phase 1 (i.e., 0-2 h) and 2 (i.e., 2-4.5 h), endotoxin decreased cardiac index (CI) and lung dynamic compliance, and increased mean pulmonary arterial pressure (Ppa), pulmonary vascular resistance (PVR), total peripheral resistance (TPR), alveolar-arterial O2 gradient, and hematocrit. Endotoxemia also caused granulocytopenia and increased the postmortem bronchoalveolar lavage fluid (BALF) albumin concentration and wet-to-dry ratio of bloodless lung. During endotoxemia, PEG-SOD failed to significantly alter any measured or calculated parameter. On the other hand, PEG-CAT attenuated the early (i.e., 0-1 h) endotoxin-induced decrease in CI and increases in Ppa, PVR, and TPR, but failed to modify these parameters during phase 2. PEG-CAT also attenuated the endotoxin-induced granulocytopenia and the increased BALF albumin concentration. In the presence of inactivated PEG-CAT, these protective effects were reversed. We conclude that O2-. does not directly contribute to endotoxin-induced lung injury and that H2O2 (or a subsequent metabolite) contributes to the early endotoxin-induced hemodynamic changes, granulocytopenia, and increased permeability of the alveolar-capillary membrane.
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PMID:Effect of polyethylene glycol-superoxide dismutase and catalase on endotoxemia in pigs. 282 78


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