Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Copper,zinc superoxide dismutase (CuZnSOD), an antioxidant enzyme, is unique in requiring two essential metals for catalytic function. Yet, only one, copper, seems to regulate the expression of functional activity. Restricting dietary copper quickly impairs catalytic functioning of CuZnSOD in numerous tissues. Diets supplemented with copper or small amounts of CuCl2 administered intraperitoneally restore the enzyme activity in animals deprived of copper. Thus, CuZnSOD has been considered a good marker of copper status. A metal-free (apo) form of CuZnSOD could exist in tissues at all times, but especially when an animal is deprived of copper. Restoring CuZnSOD activity with copper permits elucidation of the pathway of copper incorporation into the enzyme. Ceruloplasmin and albumin transport copper to the enzyme in vitro. K562 cells, a human erythroleukemic cell line, can extract copper from ceruloplasmin and incorporate it into CuZnSOD. Ascorbic acid stimulates the transfer of 67Cu transfer from ceruloplasmin to the cells, and somewhat unexpectedly, appears to restrict the amount of transferred copper that becomes bound to the enzyme. Reactivation of CuZnSOD in healthy individuals has the potential of being a useful tool for assessing copper status. This approach has merit, but one must consider that the levels of apo-enzyme that prevail in tissue could be influenced by other metals.
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PMID:Copper as a cofactor and regulator of copper,zinc superoxide dismutase. 154 24

Periodontitis induction causes a drastic elevation of free-radical lipid peroxidation, of ceruloplasmin level, and a reduction of antioxidant enzyme activities. Blood analysis shows hypercoagulation, appearance of paracoagulation products, reduced fibrinolysis, enhanced proaggregation activity of the periodontium, elevated levels of circulating immune complexes; this may by regarded as adaptation failure manifesting by these reactions. Morphologic examinations show foci of destructive changes. Administration of periodontal cytomedin reduced the level of free-radical oxidation, enhanced the activity of antioxidant enzymes, normalized antiaggregation activity of the periodontium and hemostasis and fibrinolysis parameters, and reduced the level of circulating immune complexes. The inflammatory reaction disappears completely, that is seen from reduced ceruloplasmin level and clinically. Morphologic study shows disappearance of foci of destruction. Thus, cytomedin of periodontal tissues may be regarded as an effective agent for the therapy of experimental periodontitis.
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PMID:[The mechanism of the therapeutic effect of periodontal cytomedin on the course of experimental periodontitis]. 178 Sep 21

An examination of 100 patients with ulcer disease of the stomach duodenum and 20 practically healthy people has shown that the level of extracellular antioxidant enzyme defense (ceruloplasmin) is higher than those in practically healthy people. This dependence was most pronounced in the group of patients requiring surgical interventions. In the process of treatment the level of ceruloplasmin activity gradually decreased, without reaching normal values. The level of ceruloplasmin activity in patients with ulcer disease of the stomach and duodenum are thought to characterize the state of compensatory reactions in these patients.
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PMID:[Ceruloplasmin activity in blood serum in stomach and duodenal ulcers]. 196 96

The ethanol-preferring (EP) rats have a higher level of lipid peroxidation in the brain and blood serum than the water-preferring rats. At the same time it was found that EP rats have a decreased antioxidant enzyme activity in the brain tissue (catalase and superoxide dismutase) and blood serum (ceruloplasmin and superoxide dismutase). This antioxidant status can lead to a greater sensitivity of the EP rat brain to ethanol toxicity. The increased catalase activity in blood of EP rats reflects the elevated metabolic tolerance of this group of animals to ethanol.
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PMID:[The characteristics of the enzyme status of the antioxidant protection and the level of lipid peroxidation in the brain tissue and blood of rats with differing preferences for ethanol]. 225 54

Preexposure of male Lewis rats to Cd aerosols (1.6 mg Cd/m3, 3 hr/day, 5 days/week, for 4 weeks) has been found to produce a marked degree of tolerance to hyperoxia (greater than 96% O2). Cd-pretreated animals were still alive after 8 days of continuous exposure to oxygen. In contrast, hyperoxia was fatal to all air-preexposed animals within 54-62 hr. Lungs of Cd-pretreated animals were characterized by hyperplasia and/or hypertrophy of the type II alveolar cell compartment which may have enabled them to more rapidly repair oxidant damage resulting from hyperoxia. Cd pretreatment augmented enzymatic antioxidant enzyme activities, including total lung Se-dependent glutathione peroxidase, catalase, glutathione reductase, and Mn-superoxide dismutase, and caused elevations in pulmonary nonprotein thiols and metallothionein (MT). MT, a thiol-rich, low-molecular-weight protein, was 400-fold higher in Cd-pretreated animals and bound more than 80% of the total Cd in the lung. We have hypothesized that MT serves as an expendable yet renewable cellular target for free radical damage during oxygen exposure. A systemic acute-phase response, characterized by alterations in plasma Zn and Cu concentrations and increased ceruloplasmin oxidase activity, was initiated in Cd-pretreated animals by the fourth day of hyperoxia. This response was accompanied by improvement in pulmonary status and extensive pulmonary repair.
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PMID:Cross-tolerance to hyperoxia following cadmium aerosol pretreatment. 233 May 88

The antioxidant enzyme ceruloplasmin effect on the state of lipid and peroxide metabolism in rats with alimentary hypercholesterolemia was studied. Ceruloplasmin was found to inhibit the development of hyperlipoproteinemia, to decrease the level of free-radical oxidation of lipids and to increase the antioxidant demands of tissues. The observed effects could be explained by the antioxidant properties of ceruloplasmin.
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PMID:[Lipid free-radical oxidation in rats with alimentary hypercholesterolemia and its correction with ceruloplasmin]. 262 52

The administration of very low doses of bacterial endotoxin protects rats during exposure to hyperoxia and is associated with the induction of lung antioxidant enzyme activities. Copper-deficient rats have increased susceptibility to O2 toxicity, which may be related to their decreased lung superoxide dismutase activity (SOD) or decreased plasma ceruloplasmin concentrations. To determine whether endotoxin can protect against hyperoxia in this susceptible model, we exposed copper-deficient and control rats to a fractional inspiratory concentration of O2 greater than 0.95 for 96 h after pretreatment with 500 micrograms/kg of bacterial endotoxin or phosphate-buffered saline (PBS). Mortality in the copper-deficient and control rats given PBS and exposed to O2 for 96 h was 100%. Copper-deficient rats died significantly earlier during the exposure than controls. No mortality occurred in either group treated with endotoxin and hyperoxia despite the decreased activity of copper-dependent enzymes in the copper-deficient rats. Copper-deficient rats treated with endotoxin and exposed to hyperoxia did increase lung Cu-Zn-SOD activity, but activity remained below levels found in air-exposed controls. Mn-SOD activity was found to be induced above air-exposed controls in the copper-deficient rats treated with endotoxin and exposed to hyperoxia. Hyperoxic exposure resulted in a marked increase in plasma ceruloplasmin concentrations in the control rats, but no increases in ceruloplasmin occurred in the copper-deficient animals. Endotoxin protects copper-deficient rats from hyperoxia despite their decreased lung Cu-Zn-SOD activity, and decreased plasma ceruloplasmin.
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PMID:Effects of bacterial endotoxin on protecting copper-deficient rats from hyperoxia. 375 84

The antioxidant enzyme superoxide dismutase (SOD) found in the cytosol of eucaryotic cells and the plasma protein ceruloplasmin are copper containing proteins though to be important in providing protection from oxygen toxicity. To investigate the hypothesis that copper deficiency in the rat could result in decreased lung SOD activity and plasma ceruloplasmin concentration resulting in increased susceptibility to O2 lung damage, we performed a series of experiments exposing copper-deficient and control rats to normobaric and hyperbaric hyperoxia. Lung SOD activity in the copper-deficient rats was found to be 56% of control and ceruloplasmin content was 6% of control. The copper-deficient rats exhibited increased mortality and enhanced pulmonary toxicity as evidenced by increased pathologic damage and lung edema during the normobaric exposure to 85% O2. Copper-deficient animals also showed increased susceptibility to a hyperbaric exposure of 4 ata of 100% O2 with a decreased time of survival. The copper-deficient rat represents a new model for the study of oxidant injury.
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PMID:Enhanced pulmonary toxicity in copper-deficient rats exposed to hyperoxia. 672 91

There is a close relationship between inflammation and reactive oxygen species (ROS). Primary source of ROS are activated leucocytes. Antioxidant system protects organism against the deleterious effect of ROS. The aim of the present study was to follow the activity of antioxidant system in blood and colonic mucosa of 17 patients with idiopathic proctocolitis. All patients were treated with 5-aminosalicylic acid (Salofalk), 7 patients with a combination of prednison. The following biochemical parameters were ascertained: malondialdehyde (MDA) and ceruloplasmin in serum, glutathione (GSH) and activities of superoxide dismutase, catalase and glutathione peroxidase in erythrocytes and colonic mucosa. Before treatment there was found: an increase of MDA and all antioxidant enzyme activities, an a decrease of GSH. After 3 weeks of therapy in 59% of patients, initial clinical remission was observed without serious improvement of biochemical parameters. After 10 weeks of therapy the clinical course improved in all patients, a significant decrease of MDA and activities of all antioxidant enzymes as well as an increase of GSH were stated. The authors assume that IP was positively affected by 5-ASA, and in some patients by its combination with prednisom. The effect of 5-ASA is based on its known antiinflammatory impact and its functioning as a "scavanger" of free radicals (or ROS). (Tab. 1, Fig. 3, Ref. 23.)
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PMID:[Activity of the antioxidant system in patients with idiopathic proctocolitis and the effect of 5-aminosalicylic acid (Salofalk)]. 792 42

Erythrocyte and plasma antioxidant enzyme activities and antioxidants as well as concentrations of total sulfate and thiocyanate were estimated in a group of healthy subjects and three groups of smokers (cigarette smokers, mixed tobacco smokers, and miscellaneous tobacco smokers). Plasma vitamin E, uric acid, ascorbic acid, ceruloplasmin, and urinary total sulfate concentrations were decreased, whereas dehydroascorbate and urinary thiocyanate concentrations were elevated in the three groups of smokers in comparison to the corresponding levels of the control subjects. On the other hand, erythrocyte superoxide dismutase and catalase as well as plasma superoxide dismutase activities were elevated in subjects of the three groups of smokers compared with the corresponding activity in subjects of the control group. Plasma catalase activity is statistically unaffected by smoking, but blood glutathione peroxidase activities were decreased in the three groups of smokers in comparison with the corresponding levels of the control group. There were also statistically meaningful differences between mean values of the antioxidant concentrations and the activities of the antioxidant enzymes in most of the smokers groups.
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PMID:Blood antioxidant status and urine sulfate and thiocyanate levels in smokers. 902 72


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