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:1.16.3.1 (ceruloplasmin)
5,074 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxygen free radicals are probably involved in the pathogenesis of rheumatoid arthritis (RA). The enzymes involved in protection against oxygen free radicals and H2O2 (superoxide dismutase, catalase, and glutathione peroxidase) were measured. Superoxide dismutase was not increased, glutathione peroxidase was slightly and catalase was strongly elevated in RA synovial fluid (SF) compared with control SF. Although these enzymes are present in SF, the activities are insufficient to protect against oxygen free radicals and H2O2. In contrast to transferrin, ferritin was increased in RA synovial fluid. Ceruloplasmin was also elevated. When rat liver microsomes were used as a target for oxygen free radicals, serum and SF were both protective. Gel filtration experiments showed that the fraction pattern in which there was maximal protective potential against lipid peroxidation corresponded closely to the level of ceruloplasmin. After removal of ceruloplasmin from serum or SF, about 70% of the protective capacity disappeared. It is concluded that ceruloplasmin is an important protector against oxygen free radicals.
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PMID:Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid. 674 61

1. On exposure of synovial fluid to superoxide and hydrogen peroxide, generated enzymically or by activated polymorphonuclear leucocytes, hyaluronic acid is depolymerized and the fluid loses its lubricating properties. The ability of synovial fluid from rheumatoid patients to scavenge superoxide and hydrogen peroxide was therefore examined. 2. Synovial fluid from a range of rheumatoid patients contained no superoxide dismutase activity, insufficient caeruloplasmin to scavenge any superoxide radical and little, if any, catalase activity. 3. Total ascorbate (reduced ascorbate + dehydroascorbate) concentrations in the plasma and synovial fluid of rheumatoid patients were similar in each case. The values are at the low end of the normal range. 4. These results are discussed in relation to the role of oxygen radicals in inflammatory joint disease.
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PMID:Protection against superoxide and hydrogen peroxide in synovial fluid from rheumatoid patients. 728 98

Human ceruloplasmin was found to have a neutralizing effect against the toxohormone activities of the basic protein isolated from Ehrlich carcinoma cells; this basic protein decreases the levels of serum iron and liver catalase activity upon intraperitoneal injection into mice and shows direct cytotoxicity toward normal mouse lymphocytes and macrophages. Furthermore, it was also shown that ceruloplasmin has antitumor activity against sarcoma-180 cells implanted in ICR mice.
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PMID:Antitumor and toxohormone-neutralizing activities of human ceruloplasmin. 731 96

The biotic doses of trace elements (iron, copper, and manganese) contained by hemostimulin exert a favourable effect on working capacity of athletes, hemopoiesis, catalase and ceruloplasmin activity as well as on transferrin saturation with iron.
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PMID:[Effect of biotic doses of manganese and hemostimulin on the physical work capacity of athletes 13 to 16 years old]. 740 44

In two experiments with a total of 56 piglets the influence of intravenous injections of ceruloplasmin (CP) on the 2nd and 4th day of their lives on criteria of the Cu- and Fe-metabolism was investigated. Due to the injections, the CP-activities and the Cu-concentration in the plasma increased, as a rule, more than in the untreated control animals. This effect was more distinct and longer recognisable after the injections on the 2nd day of life. Effects on the Fe-metabolism registered in a increased Fe-concentration in the plasma. Hemoglobin content, number of erythrocytes as well as the activities of blood catalase were in no case influenced by the injections.
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PMID:[The influence of ceruloplasmin injections on the Cu- and Fe-metabolism of piglets]. 745 63

Recent studies have demonstrated that preincubation of SK-Mel-28 melanoma cells with ferric ammonium citrate (FAC) resulted in marked stimulation of 59Fe uptake from 59Fe-125I-transferrin (Tf), but only at Tf concentrations above that required for saturation of the Tf receptor (Richardson and Baker (1992) J. Biol. Chem. 267, 13972-13979). The mechanism responsible for this stimulation was unknown and is the subject of the present report. Preincubation of cells with FAC (25 micrograms/ml), followed by a 2 h incubation with 59Fe-125I-Tf (0.1 mg/ml; 1.25 microM), resulted in temperature-dependent 59Fe uptake to approx. 200% of the control value. Furthermore, the effect was not specific for melanoma cells and was also observed in other normal and neoplastic cells. Preincubation of melanoma cells with FAC also stimulated 59Fe uptake from 59Fe-citrate, but to a far greater extent than that observed with 59Fe-125I-Tf (viz., > 20-fold that seen for the control). Interestingly, neither receptor-mediated endocytosis nor the postulated diferric Tf reductase were involved in the FAC-activated Fe uptake process from Tf. However, the addition of free radical scavengers to FAC such as catalase, superoxide dismutase, ceruloplasmin, Hepes, mannitol and high concentrations of BSA or ascorbate, markedly depressed FAC-activated 59Fe uptake from 59Fe-125I-Tf and 59Fe-citrate. These agents when added to control cells had no effect on 59Fe uptake. The addition of superoxide generating agents and hydrogen peroxide to minimum essential medium (MEM) containing FAC but not to MEM alone, also stimulated 59Fe uptake. These data suggest that the initial activation of the FAC-stimulated Fe uptake system was caused by the production of hydroxyl radicals via the Fe-catalysed Haber-Weiss reaction. We propose that this Fe uptake process represents an important cellular defense mechanism against oxidant stress generated in the presence of low-molecular-weight Fe complexes.
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PMID:Identification of a mechanism of iron uptake by cells which is stimulated by hydroxyl radicals generated via the iron-catalysed Haber-Weiss reaction. 748 42

The aim of the paper was to compare the erythrocyte serum and hepatic chomogenate antioxidative factors in order to assess their involvement in the detoxification events. The catalase and superoxiddismutase levels, important factors of the cellular defence, were sensitivity modulated in an acute experiment on Wistar rats. Carbofuran was administered in a non-lethal dose (7 mg/b.w.) single or in the presence of certain antioxidative agents (Vitamin E, Caffeine, Aspirin) EDTA and Cysteine for their role in protecting membranes against oxidative damage. The erythrocyte parameters (SOD, Catalase) were well related to seric factors, especially ceruloplasmin level, with varied magnitudes. GGT a marker of hepatotoxicity and G1-DH, a mitochondrial marker, were in a good correlation with erythrocyte factors. The changes seem to modulate a transmembranary disturbance process, as in hepatocyte pictures.
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PMID:Interference of some enzymatic modulators in the hepatic aggression induced by xenobiotics. 754 89

We are constantly exposed, throughout life, to a wide variety of extrinsic and intrinsic agents which have the potential to damage cellular biomolecules, including DNA. Imperfections in cellular defence systems which protect against the fixation of DNA damage can lead to an accumulation of mutations which on their own, or in combination with other age-related changes, may contribute to ageing and the development of age-related pathologies. We have previously reported an increase in frequency of mutation with age in human lymphocytes taken from healthy males in the age groups, 35-39, 50-54 and 65-69 years. In this article we report on the findings of a recent study which was designed to assess whether the age-related increase in frequency of mutation was due to a decreased efficacy of the defence systems against ROS-induced DNA damage, namely antioxidant status and DNA repair processes, in the same study subjects. In vivo antioxidant status was assessed in each of the study subjects by measuring blood levels of; superoxide dismutase (SOD; EC 1.15.1.1), glutathione peroxidase (GPx; EC 1.11.1.9), catalase (EC 1.11.1.6), caeruloplasmin (CPL), uric acid and bilirubin. We did not find any statistically significant differences in the mean levels of these antioxidants between the three different age groups. To investigate the efficacy of DNA repair processes against ROS-induced DNA damage, an ELISA was used to quantitate DNA damage (as % single-stranded DNA; %SS-DNA) at various times following treatment of peripheral blood lymphocytes with hydrogen peroxide (H2O2). The results of this part of the study showed that in untreated lymphocytes, basal levels of %SS-DNA were significantly higher in individuals from the 65-69 years age group compared to the 35-39 years age group (p = 0.039, 0.0013; at 5% level of significance). No significant differences were found in H2O2 susceptibility with age immediately following treatment (p = 0.71, 1.00; at 5% level of significance) but a consistent and significant increase was observed in %SS-DNA remaining 90 min post-treatment in lymphocytes from subjects in the 65-69 years age group, compared to %SS-DNA present in lymphocytes from the 35-39 years age group (p = 0.013, 0.024; at 5% level of significance). The results of this study suggest that the age-related increase in frequency of mutations is not contributed to by alterations of in vivo antioxidant status with age but is by a decreased efficacy of the repair of ROS-induced DNA damage with age. The biological implications of somatic mutations in the ageing process are discussed.
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PMID:An investigation of antioxidant status, DNA repair capacity and mutation as a function of age in humans. 756 67

Groups of six female rats were treated with low-dose oral contraceptive (0.667 mg progestin [norethisterone acetate] and 0.02 mg oestrogen [ethinyloestradiol]/kg body-weight), or its components, separately, at the same doses, for 6 weeks. Changes in liver and kidney levels of lipid peroxides (as indicated by malondialdehyde production), free fatty acids, superoxide dismutase, and catalase liver glutathione and serum ceruloplasmin compared with the untreated control group were studied. Combined oral contraceptive treatment produced a significant increase in the activity of catalase in the kidneys (P < 0.05). The levels of lipid peroxides, free fatty acids and glutathione in the liver, and of serum ceruloplasmin increased significantly with oestrogen treatment (P < 0.05). Lipid peroxides (in the liver only), and serum ceruloplasmin decreased significantly when progestin was administered (P < 0.05). The activities of superoxide dismutase and catalase decreased significantly in the oestrogen group (except for catalase in the kidney) but increased in the progestin group (P < 0.05). The results indicate that the components of the low-dose oral contraceptive may alter liver and kidney metabolism.
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PMID:Effects of low-dose oral contraceptive oestrogen and progestin on lipid peroxidation in rats. 758 70

Six- and 24-month-old rats were fed a copper deficient diet for 10 weeks; the copper content of the diet was one fourteenth that of a control diet. After the 10-week feeding period, the copper contents of the cerebrums, livers, lungs, and serum were decreased by 20-17, 49-47, 48-37, and 84-83%, respectively, while those of hearts and muscles were unchanged or only slightly decreased. There was no difference in the decreases in copper content of tissues between young and old rats. Copper deficiency decreased the activity level of ceruloplasmin in the serum of young and old rats by 95%, and the copper/zinc superoxide dismutase (CuZn-SOD) activity levels of cerebrums, lungs, and livers of young rats by 16, 36, and 34%, respectively, but did not change the CuZn-SOD activity levels of tissues of old rats. Although copper deficiency affected catalase activity, vitamin E concentration, and reduced glutathione concentration in several tissues, no consistent trends were observed. On the basis of the survival time of rats exposed to more than 96% oxygen, it is suggested that a decrease in CuZn-SOD activity due to copper deficiency increases oxygen susceptibility.
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PMID:Effect of copper deficiency on the activity levels of ceruloplasmin and superoxide dismutase in tissues of young and old rats. 759 50


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