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)

All organisms are protected from harmful reactive oxygen which is produced also under physiological conditions by a complex antioxidative system. Our work was aimed at the ascertainment of the level of reduced and oxidated glutathione in erythrocytes of healthy people, the concentrations of ceruloplasmin (GSH) and transferrin (GSSG) in the serum, as well as the investigation of the relationship to antioxidative enzymes ---Cu, Zn-superoxide dismutase (SOD), catalase (CAT) and Se-glutathione-peroxidase (GPx) in erythrocytes. We discovered a mutual direct linear correlation between the levels of GSH, GSSG, CPL and TRF, indirect linear relation between the concentrations of TRF, GSH, GSSG and activities of SOD and GPx, between the concentrations of CPL and GPx activities, and a direct linear relation between concentrations of GSH and TRF with CAT activity. The results indicate to a mutual dependence of investigated nonenzymatic antioxidative factors and antioxidative enzymes. (Tab2, Fig. 4, Ref.13.).
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PMID:[Levels of erythrocyte glutathione and ceruloplasmin and transferrin in the serum and their role in antioxidant protection]. 868 24

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

The mechanism of increased susceptibility of red blood cells to oxidative haemolysis in the early post-burn period remains unclear. In this study it was revealed that the accumulation of lipofuscin products in red blood cells was accompanied by the elevation of oxidative haemolysis on the 24th hour after thermal trauma of rats (full thickness skin, on 20% of TBSA). Enhanced thiobarbituric acid reactive substrates (TBARS) and lowered levels of antioxidants such as alpha-tocopherol, ceruloplasmin and albumin were found in plasma. The activity of superoxide dismutase (SOD) and the concentration of alpha-tocopherol and reduced glutathione (GSH) in erythrocytes were also diminished. The results from this study suggest that plasma and intracellular antioxidant deficiency can potentiate oxidative membrane damage. There was a positive correlation (r = 0.72) between increased levels of lipofuscin products and oxidative haemolysis of red blood cells. The enhanced susceptibility of erythrocytes to oxidative haemolysis may be considered as an indirect but sensitive indicator of the impaired antioxidant defence of these blood cells following thermal skin injury. The decreased resistance of red blood cell to oxidative haemolysis under the conditions of reduced antioxidant defence of erythrocytes and blood plasma suggests that adequate antioxidant therapy could prevent all these complications after thermal skin injury.
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PMID:Lipofuscin product accumulation, insufficient antioxidant defence in erythrocytes and plasma and enhanced susceptibility to oxidative haemolysis after thermal trauma. 929 9

MeAN administration (40mg/kg body wt/day (i.e. 1/5 of LD50) resulted in increased levels of lipid peroxidation products, conjugated dienes and lipofuscin-like substances in rat liver. Significant decrease in GSH and a decreased activity of hepatic SOD, CAT and GPx were observed. There was also an increase in glutathione S-transferase and G6PD activities, decreased plasma ceruloplasmin and vitamin C implying oxidative stress caused by MeAN.
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PMID:Methacrylonitrile induced oxidative stress in rat liver. 959 37

Redox-active forms of iron are known to catalyze free radical mediated peroxidative reactions. There is scanty information on such effects at the sites of iron absorption. This was tested in iron-deficient WKY female rats supplemented for 15 days with FeSO4 equivalent to 8 mg of iron (D+) and compared with iron deficient (D) and iron adequate (C) rats. The levels of intestinal MDA and protein carbonyls and the activities of various antioxidant enzymes were estimated. As markers of functional integrity, the activities of alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were evaluated. In addition, we measured the concentrations of ferritin, transferrin, and ceruloplasmin levels in serum and in intestinal mucosa. It was observed that correction of iron deficiency resulted in significant increase in MDA and protein carbonyl formation. Activities of both alkaline phosphatase and Lys-Ala-dipeptidyl aminopeptidase were significantly decreased in D+ compared to C. The increase in catalase and decrease in Gpx was found to be sensitive to iron administration. Neither iron deficiency nor its correction had any effect on the activity of SOD and GSH levels. Iron supplementation has resulted in decreased mobilization of stored iron as reflected by increased mucosal ferritin level and decreased serum ceruloplasmin ferroxidase activity contributing to greater peroxidative stress in the intestine. These results suggest that iron-deficient intestine of rat is more susceptible to iron-mediated peroxidative damage and functional impairment during correction of deficiency with iron.
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PMID:Iron-deficient intestine is more susceptible to peroxidative damage during iron supplementation in rats. 980 Oct 65

Rheumatoid arthritis (RA) is a heterogeneous disorder with a spectrum of clinical severity ranging from mild arthritis to a crippling joint disease with involvement of internal organs. Carnitine is essential for muscle energy production and is required for the transport of long chain fatty acids and the acyl coenzyme A derivatives across the inner mitochondrial membrane. The levels of malondialdehyde (MDA), an index of lipid peroxidation, and the antioxidants copper-zinc superoxide dismutase (CuZnSOD), glutathione (GSH), ceruloplasmin (CP), catalase (CAT), and carnitine were assessed in 42 patients with RA and 24 control subjects. While plasma carnitine and erythrocyte CuZnSOD levels were significantly lower in the patients with RA compared with the control group (p<0.01 and p<0.001, respectively), the CAT level was not different from controls (p>0.05). Plasma MDA, CP, and erythrocyte GSH levels were significantly higher than in the control group (p<0.001, p<0.001 and p<0.01, respectively). MDA levels showed a positive correlation with CP and GSH levels (r=0.716, p<0.001 and r=0.492, p<0.01, respectively). However, MDA, GSH, and CP demonstrated a negative correlation with carnitine (r=-0.719, p<0.001; r=-0.559, p<0.01, and r=-0.635, p<0.001, respectively) in the patient group but not in controls. There was also a significant positive correlation between CP and GSH levels (r=0.561, p<0.01). However, neither CuZnSOD nor CAT levels demonstrated correlation withcarnitine, MDA, GSH, or CP levels. It was interesting that CAT activity was not altered and CuZnSOD activity decreased when compared with the control group. These results suggest that while CP, MDA and GSH levels increased, carnitine and CuZnSOD levels decreased, but CAT activity was unchanged.
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PMID:Carnitine and antioxidants levels in patients with rheumatoid arthritis. 985 15

The aim of this study was to measure the alterations in serum selenium (Se), copper (Cu), zinc (Zn), and iron (Fe) concentrations and their carrier proteins, ceruloplasmin (Cp), transferrin (Tf) albumin, and related antioxidant enzyme activities, erythrocyte Cu-Zn superoxide dismutase (Cu-Zn SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities in patients with cutaneous leishmaniasis (CL). Erythrocyte Cu-Zn SOD activities, serum Cu concentrations, and Cp levels were found to be significantly higher in the patients group than those of controls. However, GSH-Px and CAT activities and Se, Zn, Fe, and Tf levels were lower in patients than in the control subjects. There were positive important correlation's between Cu-Zn SOD and Cp, Cu-Zn SOD and Cu, Cp and Cu, GSH-Px and Se, and Fe and CAT in the patients group. Our results showed that serum essential trace elements Se, Zn, Cu, and Fe concentrations and their related enzymes Cu-Zn SOD, GSH-Px, and CAT activities change in CL patients. The changes may be a part of defense strategies of organism and are induced by the hormonelike substances.
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PMID:Alterations of serum selenium, zinc, copper, and iron concentrations and some related antioxidant enzyme activities in patients with cutaneous leishmaniasis. 989 99

Ceruloplasmin (CP) is a major multicopper-containing plasma protein that is not only involved in iron metabolism through its ferroxidase activity but also functions as an antioxidant. However, physiological substrates for CP have not been fully identified nor has the role of CP been fully understood. The reaction of nitric oxide (NO) with CP was investigated in view of nitrosothiol (RS-NO) formation. First, formation of heavy metal- or CP-catalyzed RS-NO was examined with physiologically relevant concentrations of NO and various thiol compounds (RSH) such as glutathione (GSH). Among the various heavy metal ions and copper-containing enzymes and proteins examined, only copper ion (Cu(2+)) and CP showed potent RS-NO (S-nitrosoglutathione)-producing activity. Also, RS-NO-forming catalytic activity was evident for CP added exogenously to RAW264 cells expressing inducible NO synthase in culture, but this was not the case for copper ion. Similarly, CP produced endogenously by HepG2 cells showed potent RS-NO-forming activity in the cell culture. One-electron oxidation of NO appears to be operative for RS-NO production via electron transfer from type 1 copper to a cluster of types 2 and 3 copper in CP. Neurological disorders are associated with aceruloplasminemia; besides RS-NO, S-nitrosoglutathione particularly has been shown to have neuroprotective effect against oxidative stress induced by iron overload. Thus, we suggest that CP plays an important catalytic role in RS-NO formation, which may contribute to its potent antioxidant and cytoprotective activities in vivo in mammalian biological systems.
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PMID:Nitrosothiol formation catalyzed by ceruloplasmin. Implication for cytoprotective mechanism in vivo. 1048 Sep 20

Increased free radical activity has been implicated in the pathogenesis of recurrent abortion. This investigation was conducted to determine if changes in some parameters of the antioxidant system contribute to this condition. Plasma ascorbic acid, alpha-tocopherol, total thiols, ceruloplasmin, uric acid, albumin, and erythrocyte glutathione (GSH) were assayed in 25 nonpregnant (NP) healthy women, 25 normotensive pregnants (NTP), and 120 women with recurrent abortion. Recurrent aborters were divided into four subgroups according to the etiology: autoimmune (AUTO, n=25), luteal phase defect (LPD, n=25), anatomical defect (AD, n=20) and unexplained (UNEx, n=50). Plasma levels of ascorbic acid, alpha-tocopherol, and erythrocyte GSH were significantly decreased in AUTO, UNEx and LPD subgroups than those in two control groups and the AD group (ANOVA). Plasma thiols of UNEx and AUTO aborters were diminished according to controls and other abortion subgroups (ANOVA). Ceruloplasmin levels showed a decline in AUTO and UNEx subgroups when compared to controls, AD and LPD aborters (ANOVA). When UNEx, AUTO and LPD recurrent abortion subgroups were compared with each other (Student's t-test) total thiols and erythrocyte GSH of UNEx and AUTO subgroups were diminished in comparison with LPD. We suggest that decreased concentrations of plasma ascorbic acid, alpha-tocopherol, total thiols and erythrocyte GSH in UNEx, AUTO and LPD reflect the increased oxidative stress, expressing a progress of the condition. Also, the imbalance between antioxidant defence and free radical activity is more evident in the AUTO subgroup. As a conclusion, although impaired antioxidant defence may be responsible for recurrent abortions, the recurrent abortions may also result in oxidative stress and depletion and weakness of antioxidant defence.
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PMID:Antioxidant defence in recurrent abortion. 1076 2


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