Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009443 (cold)
 92,137 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copper-zinc-superoxide dismutase (CuZn-SOD), a cytosolic antioxidant enzyme that is specific for scavenging superoxide radicals, is involved in neuroprotective mechanisms in brain injury following trauma and cerebral ischemia. Liposome-entrapped CuZn-SOD exhibit beneficial effects in vivo on cold-induced vasogenic edema and on blood-brain barrier disruption. The increased levels of edema and infarction following a focal cerebral ischemia also are decreased by the pretreatment of liposome-entrapped CuZn-SOD. The protective role of SOD on brain injury was further extended and confirmed in studies using transgenic mice overexpressing human CuZn-SOD. Our studies so far suggest that increased cerebral levels of SOD, either by means of external pharmacological application or by genetic manipulations, ameliorate brain edema and infarction induced by trauma and focal cerebral ischemia.
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PMID:Antioxidant-dependent amelioration of brain injury: role of CuZn-superoxide dismutase. 131 99

The efficacy of recombinant human extracellular-superoxide dismutase type C (EC-SOD C) on myocardial reperfusion injury was explored in hypothermically arrested rat hearts, as was its site of action. Forty isolated working rat hearts were subjected to 30 min of global ischemia followed by 30 min of reperfusion. The hearts were arrested by the administration of 10 mL of cold perfusate at the onset of ischemia. At the same time, they were randomly assigned to one of five groups; A: cold perfusate only; B: cold perfusate + EC-SOD C 10.4 mg/L (30,000 U/L); C: cold perfusate+bovine CuZn-SOD 7.5 mg/L (30,000 U/L); D: cold perfusate + EC-SOD C 10.4 mg/L + heparin 50,000U/L; E: cold perfusate + heparin 50,000 U/L. Heparin was given to prevent binding of EC-SOD C to endothelial cell surfaces. Left ventricular function was studied before ischemia and at the end of reperfusion. Percent recovery of maximal left ventricular dP/dt after reperfusion was more pronounced in group B (109 +/- 24%; p less than .05) than in groups A (42 +/- 40%), C (47 +/- 36%), D (44 +/- 33%) and E (58 +/- 25%). Likewise, percent recovery of the double product (heart rate x systolic left ventricular pressure) was better in group B (104 +/- 18%; p less than .05) than in the other groups (A: 47 +/- 37%, C: 49 +/- 36%, D: 50 +/- 35%, E: 69 +/- 31%). Compared to the preischemic level, creatine kinase increased significantly in the coronary effluent after reperfusion in groups A, C, D, and E, but not in group B. The results suggest that EC-SOD C, which attaches to the endothelial cell surfaces, might be particularly effective as protection against myocardial reperfusion injury when given together with cardioplegic solution.
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PMID:Effects of recombinant human extracellular-superoxide dismutase type C on myocardial reperfusion injury in isolated cold-arrested rat hearts. 151 40

1. The activity of antioxidant defense enzymes (SOD, CAT, GSH-Px and GST) was analysed during the autumn and winter in the ground squirrel adapted to 30 degrees C and subsequently exposed to cold for 6 and 24 hr. 2. The liver CAT activity as well as the IBAT CAT and GSH-Px activities differed between animals adapted to 30 degrees C, studied in autumn, and those studied in winter. 3. MnSOD activity in the liver was increased in autumn but decreased in winter after 6 hr cold exposure reaching the control level 24 hr later. Cold exposure induced a decrease in CAT activity (except after 24 hr cold exposure in winter) and an increase in GSH-Px activity. Lower GST activity was found after 24 hr exposure to cold in winter. 4. The IBAT SOD activity decreased under the influence of cold during both seasons with a tendency to return to the control level only in winter. Cold exposure produced a decrease in GST in both seasons and CAT activity in autumn. GSH-Px activity was increased in winter only. 5. The results indicate a seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel. Seasonal influence was evidenced in animals exposed to cold as well.
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PMID:Seasonal dependence of the activity of antioxidant defence enzymes in the ground squirrel (Citellus citellus): the effect of cold. 161 72

Rapid, polyamine-induced degradation of mammalian ornithine decarboxylase (L-ornithine carboxy-lyase, EC 4.1.1.17) (ODC) is though to be controlled by the availability of a small, ODC-binding protein termed antizyme. In this study we have investigated the ability of antizyme to bind ODC protein in various altered physiological states. In particular, cold, NaCl, spermidine and deprivation of coenzyme and substrate enhance enzyme-antizyme complex formation and are all found to promote ODC homodimer dissociation. Conversely, conditions that maintain the active ODC homodimer state prevent antizyme binding and inactivation of ODC. Further, covalent modification of ODC near its active site by difluoromethylornithine or phosphate also increases its sensitivity to antizyme. These results suggest that the initial signal in ODC degradation may actually be a subtle conformational change in the enzyme that enables antizyme to bind to the enzyme and may subsequently facilitate its degradation.
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PMID:Conformational changes in ornithine decarboxylase enable recognition by antizyme. 210 55

Oxygen reactive species are normally formed in cells and play an essential part of the bactericidal activity of phagocytic cells. The damaging effect of these oxygen reactive species is prevented by the endogenous scavengers SOD, glutathione peroxidase, catalase, circulating transferrin, ascorbic acid, and membrane-bound alpha-tocopherol. However, when excess amounts of oxygen radicals and hydrogen peroxide are formed, as in reperfusion injury or trauma, the endogenous scavengers are insufficient to react with these active molecules. Lipid peroxidation is an important part of the formation of oxygen reactive species. Lipid peroxidation, especially peroxidation of LDL, may have a significant role in atherosclerosis. Thus dietary manipulation of PG and TX formation through either feeding cold water fish oils or plant oils containing high amounts of polyunsaturated fatty acids may be a two-edged sword. Also, the dietary manipulation of arachidonic acid through increasing its precursor linoleate may cause a decrease in the immune response as seen in animal experiments. The marine oils may be regarded as a natural aspirin in that formation of PGs of the bisenoic series will be replaced by the PGs of the trienoic series. This results in the formation of TXA3, which is biologically inactive, and PGI3, which is biologically active like PGI2. This may have no physiologic consequences but it is used to illustrate a possible mechanism for the postulated beneficial cardiovascular effects of these oils. The issues and the mechanisms are controversial and frequently highly speculative. The subject is a boon for the lipid biochemist and nutritionist.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Free radicals, arachidonic acid metabolites, and nutrition. 212 35

We evaluated the potential role of SOD, an oxygen free radical scavenger, as a probe to cover the trigger period of injury and the prolonged period of development of edema in vasogenic brain edema. Vasogenic brain edema was produced in 34 cats by a standardized cortical freezing lesion. Brain edema and the disruption in the BBB were assessed by SG measurement and spread of Evans blue by planimetry. Detection of superoxide radicals was studied by topical application of NBT within the cranial window. Animals were separated into two groups: (a) controls; and (b) two SOD-treated groups--A was pretreated with 10,000 U/kg PEG-SOD intraperitoneally and sacrificed at 24 and 48 hr after lesions, and B received both a bolus injection of free SOD (4 mg/kg) and then 1 mg/kg/min for 20 min after the lesion and was sacrificed 6 hr later. Our preliminary data indicate that superoxide radicals were detected in the brain after cold-induced injury, but free and PEG-SOD had no beneficial effect on vasogenic brain edema produced by cold-induced injury. It is concluded that intracellular uptake of SOD might be necessary for an effect in the treatment of cold-induced brain edema.
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PMID:Effect of superoxide dismutase in cats with cold-induced edema. 216 63

The copper chelator N,N'-diethyldithiocarbamate (DDC), is often used to inactivate intracellular copper-zinc superoxide dismutase in erythrocytes. However, in studies with red cells we found that the compound also reacted with oxyhemoglobin to produce oxygen radicals in addition to generating lipid peroxidation products, oxidized N,N'-diethyldithiocarbamate, methemoglobin, and sulfhemoglobin. Moreover, intracellular glutathione was depleted and vital cellular enzymes were susceptible to inactivation. We, and others, have confirmed these findings in nonerythrocytic cell lines. Thus, cells exposed to DDC are severely damaged before studies on the effects of added putative superoxide producing compounds can be performed with them. In this report, we have systematically investigated other copper chelators for their ability to inactivate intracellular copper-zinc superoxide dismutase without producing the deleterious effects mentioned above. Catechol, triethylenetetramine, and tetraethylenepentamine were found to be such agents when erythrocytes were dialyzed in the cold against dilute solutions of these chelators. In addition, with a myeloid leukemic cell line (HL-60), triethylenetetramine inhibited SOD without causing significant GSH oxidation. Examination of the affinity constants of chelators active against purified copper-zinc superoxide dismutase indicated that an affinity binding constant (log K1) between 12.6 and 13.8 was required for the chelator to successfully remove copper from the enzyme.
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PMID:Inactivation of intracellular copper-zinc superoxide dismutase by copper chelating agents without glutathione depletion and methemoglobin formation. 254 68

The critical injury of cold preservation is to the hepatic microcirculation. Oxygen free radical injury and cell swelling have been proposed to be causes of allograft failure, and new solutions such as Marshall's isotonic citrate and University of Wisconsin (UW) solutions were designed to prevent cell swelling and free radical injury. Experiments were done to determine whether Marshall's solution and UW solution protect the microcirculation, and whether they do so by preventing cell swelling or free radical-induced injury. To determine if the new solutions reduce sinusoidal lining cell injury, rat livers were examined after preservation at 4 degrees C in NaCl 0.9% and CaCl2 2 mM for 4 hr and 8 hr, in Collins' solution for 8 hr, and in both UW and isotonic citrate solutions for 8 hr and 16 hr. Next, the role of cell swelling in preservation injury was studied by storing livers in hypotonic solutions that accelerate liver weight gain, and in a choline chloride-based preservation solution. Finally, to evaluate the role of active oxygen species, SOD, catalase, and allopurinol were added to preservation solutions. The effect of allopurinol alone was also studied. In a related study, sucrose was substituted for the free radical scavenger, mannitol, in isotonic citrate solution. All livers were studied by light microscopy after perfusion-fixation. Storage in UW and isotonic citrate solutions resulted in clear improvement in the morphology of the sinusoidal lining. Increasing the rate of liver weight gain by the use of hypotonic solutions did not accelerate the endothelial injury. Choline chloride-based solution prevented weight gain during preservation, but unlike UW or isocitrate solutions it did not retard the microcirculatory injury. After preservation in the presence of SOD and catalase, or allopurinol, no improvement in the defined morphological features of the endothelial injury was noted when compared with respective controls; nor was the benefit of isotonic citrate solution lessened by the removal of the free radical scavenger mannitol. We conclude that microvascular injury produced by cold injury is due neither to free radical-mediated injury nor to cell swelling. As both UW and isotonic citrate solutions provide significant protection to the microcirculation, they must do so by a yet-undetermined mechanism.
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PMID:Evidence that cold preservation-induced microcirculatory injury in liver allografts is not mediated by oxygen-free radicals or cell swelling in the rat. 266 3

Kidney preservation under mild hypothermic conditions (24 degrees C) was performed to preserve organs for a long time, to determine the viability of damaged organs, and to evaluate the viability of organs that have previously been stored in cold solution. Rabbit kidneys were perfused via the renal arteries. The perfusate was composed of glucose, allopurinol, PEG-SOD, adenosine, dexamethasone, insulin, HES and FC-43. This solution was an attempt to simulate the electrolyte constitution of extracellular fluid (pH 7.40 delta pH). The functions of all groups of kidneys were evaluated by measuring urine output, urine pH and urine electrolytes. The suitable perfusion pressure was 80 mmHg. The kidneys without a warm ischemic period were well stored and functioned for over 12 hours under 24 degrees C perfusion. In the warm ischemic groups, the viability and histological structure of the kidneys were well maintained and conditioned for 12 hours at up to 35 min of warm ischemia. The kidneys which were stored in 4 degrees C UW-solution for 24 hours had a good urination using mild hypothermic perfusion for 12 hours. This suggest that mild hypothermic perfusion will become a useful method for preserving the condition of organs and for determining and evaluating the viability of organs that have previously been stored in cold solution.
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PMID:[Experimental studies on functional preservation, conditioning and evaluation of the viability of rabbit kidneys utilizing mild hypothermic perfusion]. 805 26

The alpha-amylase from Pyrococcus furiosus, a hyperthermophilic archaebacterium, has been purified to homogeneity. The enzyme is a homodimer with a subunit molecular mass of 66 kDa. The isoelectric point is 4.3. The enzyme displays optimal activity, with substantial thermal stability, at 100 degrees C, with the onset of activity at approximately 40 degrees C. Unlike mesophilic alpha-amylases there is no dependence on Ca2+ for activity or thermostability. The enzyme displays a broad range of substrate specificity, with the capacity to hydrolyze carbohydrates as simple as maltotriose. No subtrate binding occurs below the temperature threshold of activity, and a decrease in Km accompanies an increase in temperature. Except for a decrease in Asp and an increase in Glu, the amino acid composition does not confirm previously defined trends in thermal adaption. Fourth derivative UV spectroscopy and intrinsic fluorescence measurements detected no temperature-dependent structural reorganization. Hydrogen exchange results indicate that the molecule is rigid, with only a slight increase in conformational flexibility at elevated temperature. Scanning microcalorimetry detected no considerable change in the heat capacity function, at the pH of optimal activity, within the temperature range in which activity is induced. The heat absorption peak due to denaturation, under these conditions, occurred within the temperature range of 90-120 degrees C. When the pH was increased, a change in the shape of the heat absorption peak was observed, which when analyzed thermodynamically shows that the process of heat denaturation is complex, and includes at least three stages, indicating that the protein structure consists of three domains. At temperatures below 90 degrees C no excess heat absorption or change in the CD spectra were observed which could be associated with the cooperative conformational transition of the protein. According to the thermodynamic characteristics of the heat denaturation, the cold denaturation of this protein can be expected only at -3 degrees C. Therefore, the observed inactivation of this enzyme is not caused by the cooperative change of its tertiary structure. It can be associated only with the gradual changes of protein domain interaction.
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PMID:The purification and characterization of an extremely thermostable alpha-amylase from the hyperthermophilic archaebacterium Pyrococcus furiosus. 822 89


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