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)

Recently it has been shown that ceruloplasmin presents a protective action against reperfusion-induced arrhythmias in the isolated perfused rat heart, an effect that is lost when the protein is denaturated by heat. The present study was carried out to see whether ceruloplasmin can alter electrophysiological properties such as ventricular effective refractory periods, conduction time, and action potential duration calculated at 50, 75, and 90% levels of repolarization (APD50, APD75, APD90). To check the specificity of the electrophysiological effects of ceruloplasmin, we have also compared them with those of heat-denatured ceruloplasmin, superoxide dismutase, catalase, deferoxamine, and albumin. In isolated rat hearts, ceruloplasmin (0.25-3 microM) (n = 8 for each concentration) was shown to increase the effective refractory period in a concentration-dependent manner by 26 to 89%. Conduction time was not significantly altered. Heat-denatured ceruloplasmin (0.50-3 microM) (n = 8 for each concentration) increased the effective refractory period by 33 to 70% and did not affect the conduction time. In contrast, superoxide dismutase (1-4 microM), catalase (1-2 microM), deferoxamine (500 microM-1 mM), and albumin (1-4 microM) (n = 8 for each substance and for each concentration) had no significant effect on effective refractory period and conduction time at any dose, suggesting that the ceruloplasmin effect might be specific. In rat ventricular preparations, ceruloplasmin (1 microM) also induced a constant prolongation of APD50 (52%), APD75 (64%), and APD90 (41%) after 15 min of infusion (n = 6). The prolongation of effective refractory period and of action potential duration, by native and heat-denatured ceruloplasmin, suggests that this substance has specific class III effects, although this cannot entirely account for its antifibrillatory action at reperfusion in isolated rat hearts.
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PMID:Class III antiarrhythmic effects of ceruloplasmin on rat heart. 890 75

Glutathione is activated to a mutagen by gamma-glutamyl transpeptidase. Other thiols, such as cysteine, penicillamine, cysteine ethylester, and cysteinylglycine, are direct mutagens in the Ames Salmonella mutagenicity test. Thiol mutagenesis is oxidative in nature and involves H2O2 and possibly hydroxyl radicals. Transition metals are crucial for thiol autoxidation. The role of copper and ceruloplasmin (CP) in thiol-dependent mutagenesis was studied in Salmonella typhimurium strain TA102. Cu and CP at low concentrations enhanced thiol-dependent mutagenesis in the presence, but not in the absence, of added Fe. The degree of enhancement depended on the type of thiol. At high Cu or CP concentrations, thiol mutagenesis was inhibited. Cu also decreased the mutagenicity of H2O2. Cu- and CP-enhanced mutagenesis were inhibited by radical scavengers, catalase, and peroxidase but not by superoxide dismutase. The effects of Cu and CP on thiol-dependent mutagenesis were similar to their effects on thiol-driven lipid peroxidation. The results indicate that the role of Cu and CP in the enhancement of thiol mutagenesis is the facilitation of the transfer of electrons from a thiol to iron, rather than in catalysis of the Fenton reaction.
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PMID:Role of copper and ceruloplasmin in oxidative mutagenesis induced by the glutathione-gamma-glutamyl transpeptidase system and by other thiols. 902 Mar 9

Oxidative damage (lipid peroxidation, LPO) induced in a completely defined system containing glutathione (GSH), purified gamma-glutamyl transpeptidase (GGT), and EDTA- and ADP-chelated ferric iron was enhanced by catalytic amounts of cupric ions and by ceruloplasmin (CP). The enhancement depended on GSH concentration, GGT activity, the presence of iron, and the chelation of copper by o-phenanthroline. High concentrations of CP inhibited LPO. Cu- and CP-enhanced, GSH-GGT-driven LPO was inhibited by the chain-breaking radical scavengers butylated hydroxyanisol, alpha-tocopherol, and Trolox C (a synthetic analog of alpha-tocopherol) but not by the hydroxyl scavenger mannitol. Ascorbic acid increased LPO in the presence of Cu or CP. Cu-enhanced LPO was partially sensitive to superoxide dismutase but not to catalase or horseradish peroxidase. The results indicate that Cu and CP enhance thiol-driven LPO and promote thiol-dependent mutagenesis by a very similar, if not the same, mechanism and are in agreement with the idea that this enhancement is due to redox reactions of chelated Cu and Fe, rather than to the reactivity of Cu in the Fenton reaction.
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PMID:Promotion of glutathione-gamma-glutamyl transpeptidase-dependent lipid peroxidation by copper and ceruloplasmin: the requirement for iron and the effects of antioxidants and antioxidant enzymes. 902 Mar 10

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

The spontaneous autoxidation of the neurotoxin 6-hydroxydopamine proceeds by a free radical chain reaction involving the superoxide anion radical and produces the corresponding chromogen 6-hydroxydopamine quinone and hydrogen peroxide. The rate of this reaction is increased in the presence of ceruloplasmin and peroxidase, and reduced by superoxide dismutase, catalase, and DT-diaphorase. We report some explanations of why these proteins may increase or reduce the rate of autoxidation of 6-hydroxydopamine.
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PMID:Modulation of 6-hydroxydopamine oxidation by various proteins. 917 10

The accumulation of damage to cellular biomolecules, including DNA, over time may play a significant role in the aetiology of the ageing process. We have previously quantified DNA damage and mutation within cultured lymphocytes from healthy human male subjects in three different age groups (35-39, 50-54 and 65-69 years). The results of that study showed an age-related increase in DNA damage and mutations in lymphocytes. In addition, an age-related decrease in the capacity of the lymphocytes to repair H2O2-induced DNA damage was found. In this article, we report the findings of an extension to the earlier study. Thirty-one generally healthy male and female subjects between the ages of 75 and 80 years were recruited. Using a number of bioassays, we were able to determine; basal levels of DNA damage (for 18 subjects) and mutant frequency at the hypoxanthine phosphoribosyltransferase (hprt) gene locus (for 16 subjects) within cultured lymphocytes. In addition, in vivo antioxidant status (for all study subjects) and the capacity of lymphocytes to repair H2O2-induced DNA damage (for 18 subjects) were also assessed. The results obtained showed: that the mean basal level of DNA damage in lymphocytes from subjects in the 75- to 80-year age group (12.6 +/- 4.7%) was similar to that of the 35- to 39-year age group (13.3 +/- 3.3%), p = 0.42 (Mann-Whitney); there was no significant difference between log mean mutant frequency at the hprt gene locus in lymphocytes from the 75- to 80-year age group (0.31 +/- 0.33) compared to that observed in the 35- to 39-year age group (0.24 +/- 0.21; Student's t-test, t = 0.68, p > 0.05). Levels of the antioxidants glutathione peroxidase (GPx EC 1.11.1.9), catalase (CAT; EC 1.11.1.6) and caeruloplasmin (CPL; EC 1.16.3.1) were significantly elevated in the 75- to 80-year age group, compared to the 35- to 39-, 50- to 54- and 65- to 69-year age groups. Levels of bilirubin (BR) were reduced in the 75- to 80-year age group, the decrease being contributed by the female subjects. No differences in levels of superoxide dismutase (SOD; EC 1.15.1.1) or uric acid (UA) were found between the 4 age groups. Following treatment of lymphocytes with H2O2, we did not find any difference in the susceptibility of lymphocytes to DNA damage in the 75- to 80-year age group, compared to the other age groups. The DNA repair capacity in lymphocytes from individuals in the 75- to 80-year age group was similar to that of the 35- to 39-year age group, for all time points assessed. These results highlight the importance of DNA repair processes and antioxidant defence systems for maintaining genomic stability in vivo.
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PMID:In vivo antioxidant status, DNA damage, mutation and DNA repair capacity in cultured lymphocytes from healthy 75- to 80-year-old humans. 921 88

Rats were injected 21 mg/kg dimethylhydrazine (DMH), in a single dose, subcutaneously (experimental run I), or 5 times at weekly intervals (experimental run II) to measure free-radical process indices in blood serum, liver and large bowel 24 hr after a single exposure and 6 months after 5 exposures. Run I identified marked DMH inhibition of blood-serum level of active forms of oxygen (AFO). However it did not involve any changes in the concentrations of such products of lipids peroxidation (LP) as dien conjugates, Schiff's bases and protein peroxides (PP). Neither did total antioxidation activity (TAA) or that of Cu, Zn-superoxydismutase (SOD) change. However, nitrite levels increased while those of ceruloplasmin decreased significantly. AFO levels also dropped in the liver, following a single injection of DMH, with TAA and SOD activity decreased significantly. No changes were observed in AFO generation processes in the bowel which was targeted by DMH treatment. A slight decrease in TAA, a rise in PP and diverse changes in the enzymatic system of antioxodation protection were recorded: decreased SOD activity and an insignificant rise in catalase level (like in the liver). Run II showed an intensification of peroxidation in blood serum and bowel in animals bearing intestinal tumors. However, no distinct changes occurred in the liver. The results point to a tendency of free-radical processes being intensified during DMH-induced carcinogenesis in rats.
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PMID:[Free-radical processes in blood serum, liver and large bowel during 1,2-dimethylhydrazine-induced carcinogenesis in rats]. 947 64

Changes in the concentrations of antioxidant (Cu, Zn superoxide dismutase catalase, ceruloplasmin, and transferrin) and recently discovered pro-oxidant (cytochrome B-558 I-IV and suprol, a superoxide producing lipoprotein) metalloproteins and cytochrome B-5 were assessed in the blood of anesthesized and control rats. The concentrations of antioxidant and pro-oxidant metalloproteins varied. They were not changed during anesthesia, except suprol. As for the qualitative changes, phospholipid composition was altered, superoxide production decreased, and lipid peroxidation of suprol increased during anesthesia. The authors propose using antioxidant metalloproteins for decrease of the undesirable consequences of halothane anesthesia in experimental medicine.
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PMID:[Level of blood metalloproteins during fluothane anesthesia in experimental animals]. 951 Dec 41

Molecular mechanisms of the trauma stress of different origins in children to some extent is related to the quantitative changes of blood superoxide dismutase, catalase, ceruloplasmin, transferrin, cytochromes b5, b558III, b558IV and suprol. Non adequate changes of antioxidant (superoxide dismutase, catalase, ceruloplasmin, transferrin) and newly discovered prooxidant (cytochromes b5, b558III, b558IV, suprol) metalloproteins, as well as serum and erythrocyte cytochrome b5 depend on characteristic and duration of trauma stress caused by extremity fractures in children. This is due to the different mechanisms of adaptation to trauma stress.
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PMID:[Disturbance of equilibrium between blood levels of antioxidant and prooxidant metalloproteins in pain stress in children]. 960 48

The data obtained from the author's laboratory were used to make this review. The author's classification of free radicals, approaches, the origin and metabolism of primary radicals, the contribution of iron ions to the production of secondary radicals and the mechanisms of antioxidative protection of cells and tissues from damage are considered. According to the classification proposed, the radicals may be divided into primary (superoxide, semiquinones and nitric oxide), secondary (hydroxyl and lipid radicals) and tertiary (radicals of antioxidants). The primary radicals are formed by enzymatic systems and perform biologically important functions. The secondary radicals are formed from hydroperoxides in the reactions of divalent iron ions and damage to cell structures. In the cells and blood plasma, there is a complicated system of antioxidants that prevent the production of secondary radicals. All antioxidants may be arbitrarily divided into water-soluble and hydrophobic. The first group involves the enzymes catalase and glutathione peroxidase, iron ion chelators (such as ceruloplasmin and transferrin in the blood and carnosine in other tissues), and, probably, hydroxyl radical traps, such as uric acid and ascorbate. The hydrophobic antioxidants include primarily the free radical traps alpha-tocopherol, flavonoids, and carotenes. Studies of lipid peroxidation kinetics in the membranous structures, carried out by chemiluminescence and mathematical modeling of the reactions have shown that the radicals of antioxidants (such as alpha-tocopherol) enter the further reactions in the lipid phase, including those with lipid hydroperoxides.
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PMID:[Free radicals and antioxidants]. 972 Apr 15


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