Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q0Z944 (hemoglobin)
 63,986 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A competition radioimmunoassay for human superoxide dismutase (SOD-1) is described. Radioiodinated SOD-1 is incubated with unlabeled competitor and limiting antibody, then immune complexes are isolated using Staphylococcus aureus. The assay is sensitive (detecting 5 ng enzyme) and reproducible. Average values for SOD-1 in lysates of erythrocytes from normal individuals is 854 +/- 100 ng/mg hemoglobin and that of patients with trisomy-21 is 1313 +/- 110 ng/mg hemoglobin.
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PMID:A radioimmune assay for human cupro-zinc superoxide dismutase and its application to erythrocytes. 9 Jul 10

One and 24 hours after the administration of 63NiCl2 and 63Ni(CO)4 to mice 63Ni was present in association with both particulate and soluble cellular constituents in the lung, liver and kidney. After disruption of the cellular organells by sonication, a considerable part of the 63Ni was still bound to the cellular fragments. Sephadex G-75 chromatography of the cytosol of the lung showed that the largest proportion of 63Ni was eluted in the void volume and a smaller proportion was present in the salt volume. In the kidney, the proportions were reversed. Twentyfour hours after the injection of 63NiCl2 an intermediate 63Ni-containing peak, with an estimated molecular weight of about 30,000, was found in the lung and the kidney. In the liver of 63 NiCl2-injected mice, most of the nickel was recovered in the void volume, a lesser amount in the salt volume. There was no evidence that 63Ni was bound to metallothionein (induced by Cd-pretreatment) or to superoxide dismutase in the studied tissues. Pretreatments with non-labelled NiCl2 did not alter the elution profiles. In serum, most 63Ni was present in association with albumin. Gel-chromatograms of red blood-cell hemolysates from 63Ni(CO)4-injected mice showed 63Ni at an elution volume corresponding to hemoglobin, but 63Ni-binding ligands with higher and lower molecular weights were also present.
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PMID:Binding of 63Ni by cellular constituents in some tissues of mice after the administration of 63NiCl2 and 63Ni(CO)4. 11 36

Levels of erythrocyte superoxide dismutase (SOD) activitiy in a sample of Japanese people were determined. Blood samples were taken from new-born infants, preschool children, young and old people who had no apparent diseases and also from three anemic patients. Erythrocyte SOD activities in different age groups had a nearly normal distribution. Females had slightly lower activities than males, although the difference was statistically insignificant. The distributions of SOD activities were 12.6 +/- 2.7 (m +/- SD) unit/mg Hb in young people and 11.4 +/- 3.0 in old people, indicating that erythrocyte SOD activity falls with aging. Because of low concentration of hemoglobin, SOD activities of old people expressed as unit/ml blood were much lower than in young people. Three anemic patients had slightly lower SOD activity (unit/mg Gb), but the difference was not significant.
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PMID:Levels of erythrocyte superoxide dismutase activity in Japanese people. 15 24

The superoxide dismutase inhibitor diethyldithiocarbamate (DDC) was utilized to study the toxic effect of 1,4-naphthoquinone 2-sulfonate (NQ), a structural analog of the hemolytic drug, menadione, on red cells. NQ was shown to react with hemoglobin and result in the generation of superoxide anion (O2-). Red cells treated with NQ were found to undergo a gradual disappearance of their oxyhemoglobin and also hemolyze. Red cells pretreated with DDC to inhibit cellular superoxide dismutase were found to be markedly sensitive to oxyhemoglobin destruction and hemolysis in the presence of NQ. Superoxide dismutase-inhibited red cells were also found to undergo a slow autohemolysis in the absence of NQ. No evidence for lipid peroxidation was obtained for red cells treated with NQ either in the presence or the absence of DDC. Ghosts prepared from superoxide dismutase-inhibited red cells exposed to NQ were found to retain a green hemoglobin-derived pigment.
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PMID:Superoxide anion as a mediator of drug-induced oxidative hemolysis. 18 13

Superoxide anion, either generated during the autooxidation of dihydroxyfumaria acid or by the interaction of 1,4-naphthoquinone-2-sulfonate and intracellular hemoglobin in red cells pretreated with the intracellular superoxide dismutase inhibitor, diethyldithiocarbamate, produces structural changes in red cells hemoglobin and hypotonic lysis. No evidence for lipid peroxidation was found in red cells exposed to either 1,4 naphthoquinone-2-sulfonate in the presence of diethyldithiocarbamate or to dihydroxyfumaric acid, although the membranes of these cells exposed to either 1,4 naphthoquinone-2-sulfonate in the presence of diethyldithiocarbamate or to dihydroxyfumaric acid, although the membranes of these cells retained a green pigment. These results suggest that superoxide anion reacts with cellular hemoglobin to form hemoglobin breakdown products which bind to the red cell membrane and thereby increase the osmotic fragility of the cell.
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PMID:Superoxide anion and drug-induced hemolysis. 20 53

Activity of superoxide dismutase was studied in blood of children with various types of iron deficiency anemia. The enzymatic activity was increased in all the types of iron deficiency anemia studied (typical form, infectious anemia of premature children). This increase was especially distinct, when calculation was made per 1 mg of hemoglobin or 1 billion of erythrocytes. Alterations in superoxide dismutase activity and in content of blood hemoglobin were reciprocal in the anemias studied. Correlation was observed between the alteration in the enzymatic activity and a decrease in content of hemoglobin in prematurely born children with anemia.
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PMID:[Superoxide dismutase activity in the blood of children with iron deficiency anemia]. 44 89

Three experiments involving 52 baby pigs were conducted to determine the minimum copper requirement of baby pigs fed purified diets. Diets were supplemented with anhydrous cupric sulfate to yield the following copper concentrations (ppm, by analysis) when the three experiments were combined: 0.6, 0.9, 1.3, 1.9, 2.0, 2.8, 3.2, 4.0, 4.9, 5.6 and 9.3. Parameters examined include weight gain, hematocrit, hemoglobin concentration, mean corpuscular hemoglobin concentration, plasma ceruloplasmin activity, plasma copper concentration, copper balance, brain and erythrocyte superoxide dismutase activity, copper concentration of liver, kidney, spleen, heart, brain, femur and hair, liver ferritin-iron and total iron concentration, strength characteristics of the femur, and gross and histological appearance at necropsy. Weight gains were subnormal at dietary copper concentrations below 1.9 ppm; plasma ceruloplasmin activities, and plasma and tissue copper concentrations were depressed at dietary copper levels below 2.8 ppm. Bone histopathology was evident at dietary copper levels below 3.2 ppm, and copper balance was low at dietary copper levels below 4.9 ppm. Some evidence of anemia was present at dietary copper levels below 5.6 ppm. Under the conditions of this study, the copper requirement of the baby pig fed a purified diet was judged to be approximately 5.6 ppm (6 ppm copper, dry basis).
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PMID:Copper requirement of baby pigs fed purified diets. 44 53

Concentrations of a peroxidation product (malondialdehyde), fluorescent chromophores, lipofuscin-like fluorescent products, superoxide dismutase, catalase, glutathione peroxidase, and vitamin E in the maternal blood and the cord blood were determined and the results obtained were related to the estimation of lipid peroxidation and protective mechanism against uncontrolled oxidative processes in late pregnancy. Serum levels of fluorescent products were higher in the maternal blood than in the cord blood, indicating less frequent lipid peroxidation in the fetus than in the mother. In support of this assumption, the three protective enzymes and vitamin E were present in relatively lower concentrations in the cord blood. Sudden exposure of the newborn infant to a normobaric atmosphere after beginning breathing seems, therefore, to cause oxidation of red blood cell membrane, denaturation of the membrane, inducing hemoglobin breakdown, and consequently hemolysis.
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PMID:Lipid peroxidation in maternal and cord blood and protective mechanism against activated-oxygen toxicity in the blood. 48 29

Red cell superoxide dismutase (SOD) enzyme activity was determined in 58 cord blood specimens obtained from infants over a range of gestational ages. An inverse relationship between red cell SOD activity and gestational age was demonstrated. Red cell SOD activity showed a progressive fall from 263.1 +/- 30.5 units/mg non-hemoglobin protein (NHP) in infants of less than 29 weeks of gestation to 168.9 +/- 21.3 units/mg NHP in infants of more than 36 weeks of gestation (P less than 0.05). Infants treated for RDS showed an increase in red cell SOD activity which reached significance at 72 hr when compared to cord blood levels from the same population (P less than 0.05). No similar significant difference could be demonstrated in gestational age-matched control subjects over the same time period. However, initial cord blood SOD enzyme levels were lower in premature infants with RDS (229.5 +/- 30.6 units/mg NHP) than in premature infants without RDS (264.0 +/- 38.0 units/mg NHP). When infants with RDS were examined for oxygen toxicity and survival, red cell SOD levels were noted to decrease over 24 hr in four of five infants who died, three of whom developed bronchopulmonary dysplasia. In the surviving infants, red cell SOD levels showed a significant increase by 48 hr (P less than 0.05). None developed bronchopulmonary dyplasia and all survived.
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PMID:Neonatal red cell superoxide dismutase enzyme levels: possible role as a cellular defense mechanism against pulmonary oxygen toxicity. 55 82

The paper deals with the action of: primaquine, epinephrine, adrenochrome, acetylphenylhydrazine and sulphanilamide on the autoxidation of the isolated chains from human hemoglobin and on the precipitation which follows. The effect of superoxide dismutase and catalase on the drug induced autoxidation allows the assessment of the possible role of O2 derivatives (notably superoxide or peroxide) in the overall reaction mechanism. It is also shown that primaquine and acetylphenylhydrazine enhance precipitation of the isolated oxidized chains, while epinephrine and adrenochrome display a small inhibitory effect on precipitation. These effects do not involve O2 radicals, but have presumably to be related to a destabilizing (or stabilizing) action of the drugs on the structure of the protein.
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PMID:Effect of drugs on oxidation and precipitation of the isolated chains of human hemoglobin. 64 35


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