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)

Two patients with choreatic syndromes caused by polycythemia vera recovered after treatment of the polycythemia by only two venesections: this proves that the syndrome is due to reversible alterations. Investigations of the cerebral circulation in one of the patients showed that blood flow was lowest in the grey matter at the basal region of the brain: this suggests that the alterations might mainly occur there. However, investigation of erythrocyte rheology, glucose-6-phosphate dehydrogenase, serum concentrations of caeruloplasmin and serotonin, and urinary excretion of epinephrine, norepinephrine and vanillylmandelic acid gave normal results in both patients. There are therefore no indications as to the possible pathophysiology of these alterations. There are now 24 cases reported, including our 2 patients, which suggests that the association of these two diseases may not be so rare as supposed.
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PMID:Two cases of choreatic syndrome caused by polycythemia vera. 45 93

Phenotype and gene frequencies are presented for eight polymorphic systems among the Nubians of South Egypt, namely, acid phosphatase, glucose-6-phosphate dehydrogenase, adenylate kinase, 6-phosphogluconate dehydrogenase, esterase D, phosphoglucomutase I, peptidase A, and haptoglobin. Eleven systems, namely, albumin, ceruloplasmin, hemoglobin, lactate dehydrogenase, isocitrate dehydrogenase, phosphohexose isomerase, malate dehydrogenase, peptidase B and C, phosphoglucomutase II, and transferrin were found to be monomorphic. A single electrophoretic variant of phosphohexose isomerase were observed.
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PMID:The Nubians of Kom Ombo: serum and red cell protein types. 61 20

Despite similar vitamin E contents, erythrocytes of smokers have an increased tendency (P less than 0.01) to peroxidize in vitro compared with those of nonsmokers. This difference is abolished by vitamin E supplementation (1000 mg alpha-tocopherol acetate/d for 14 d). The increased susceptibility to erythrocyte peroxidation in the smokers may reflect lower glucose-6-phosphate dehydrogenase (P less than 0.02) and glutathione peroxidase (P less than 0.05) activities. Smokers seem to be under a sustained oxidant stress with increased plasma-conjugated dienes (P less than 0.01) and dehydroascorbate (P less than 0.05) and decreased ascorbate (P less than 0.06) concentrations. Additionally, plasma ceruloplasmin in smokers is elevated (P less than 0.01), consistent with an acute-stress response. Plasma total cholesterol is similar in smokers and nonsmokers and is unaffected by vitamin E supplementation. Indices of sustained oxidant stress in smokers are partially ameliorated by vitamin E supplementation.
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PMID:Effects of smoking and vitamin E on blood antioxidant status. 201 19

Early response to the exposure of cadmium includes the enhancement in lipid peroxidation with the concomitant impairment in antioxidative defence mechanism. This investigation deals with the delayed response of cadmium induced stimulation of endogenous defence response against its oxidative damage. The administration of cadmium led to an increase in the hepatic enzymatic and nonenzymatic defence armory in a dose dependent manner 72 hrs post its administration. This includes respectively an increase in the activities of superoxide dismutase, glutathione peroxidase, glucose-6-phosphate dehydrogenase and in the levels of glutathione, metallothionein and zinc. Cadmium administration also stimulated serum ceruloplasmin activity in a dose dependent manner. These changes are accompanied by the concomitant decrease in the peroxidative damage to lipids. Our results suggest the development of a delayed adaptive/defence response as a result of exposure to cadmium.
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PMID:Cadmium-mediated induction of cellular defence mechanism: a novel example for the development of adaptive response against a toxicant. 202 6

Many reports have pointed out that oxidative damage and disturbances in antioxidant defense systems of the lenses may play an important role in the development of cataract. In the present study the activities of glutathione peroxidase, glutathione reductase, glutathione-S-transferase, glucose-6-phosphate dehydrogenase, catalase and the level of glutathione and lipid peroxides were measured in red blood cells of galactosaemic children with cataract and without cataract. Furthermore the serum antioxidant activity and the level of uric acid. ceruloplasmin and transferrin in serum were estimated. It was found that in red blood cells of galactosaemic children with cataract the activity of glutathione reductase was slightly lower than in a control age-matched group of children and in galactosaemic children without cataract. The increase of serum antioxidant activity in both groups of galactosaemic children was also observed. Probably it could be due to the increase of the level of ceruloplasmin. Except glutathione reductase activity no other differences were found in the investigated components of the antioxidant defense systems of red blood cells and serum between galactosaemic children with cataract and those without cataract. Therefore it seems that red blood cells and serum metabolism are no good reflections of disturbances in antioxidant defense mechanisms which may be involved in the cataract development in galactosaemic children.
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PMID:Red blood cells and serum antioxidant defense systems of galactosaemic children. 208 Sep 1

The genetic structure of two Chukot Evens subpopulations (314 individuals) for electrophoretic protein systems and taste sensitivity to PTC was studied. 17 of the 39 loci were polymorphic (43.59%). The following systems were completely monomorphic: diaphorase NAD H (Dia); glucose-6-phosphate dehydrogenase (G-6-PD); glutamatoxalate transaminase (GOT); carbonic anhydrase (Ca-1); catalase (Ct), lactate dehydrogenase (loci LDH-A and LDH-B); leucine aminopeptidase (Lap); malate dehydrogenase (MDH); purine nucleoside phosphorylase (PNP); superoxide phosphorylase (PNP); superoxide dismutase (SOD); phosphoglucomutase-2 (PGM2); cholinesterase (locus E1); red cell esterase (4 loci); albumin (Alb); hemoglobin (Hb A and B); ceruloplasmin (Cp); and blood, gren, using the standard method. The following systems were polymorphic: red cell acid phosphatase (AcP); phosphoglucomutase-1 (PGM1); 6-phosphogluconate dehydrogenase (PGD); glutamatepyruvate transaminase (GPT); glyoxalase-1 (GLO-1); esterase (EsD); adenilatkinase (AK); alkaline phosphatase (Pp); cholinesterase (locus E2); haptoglobin (Hp); transferrin (Tf); group-specific component (Gc) and ABO, MN, Lewis, P blood groups and taste sensitivity to PTC. The following allele frequencies for polymorphic loci have been detected: AKI = 0.994; GLO = 1I = 0.082; GPT1 = 0.653; AcPA = 0.400; AcPB = 0.599; AcPC = 0.001; PGDA = 0.944; PGM1(1) = 0.906; EsD1 = 0.897; E2+ = 0.048; HpI = 0.394; GcI = 0,919; Tfc = 0.987; r(O) = 0.669; p(A) = 0.184; q(B) = 0.146; M = 0.711; Le = 0.411; P1+ = 0.521; t = 0.295. The genetic structure of Chukot Evens population is significantly nearer to that of the other ethnic groups of the North-East, in comparison with the genetic structure of Evenks of the Middle Siberia.
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PMID:[Genetic structure of the populations of native inhabitants in the northeastern USSR. V. The Chukot Evens]. 293 99

Serum protein (albumin, haptoglobin, ceruloplasmin, transferrin and group-specific component), haemoglobin, and red cell enzyme (glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, acid phosphatase, esterase D, adenylate kinase, glyoxalase I, phosphoglucomutase, lactate dehydrogenase, malate dehydrogenase, phosphohexose isomerase and superoxide dismutase) polymorphisms were studied among the Bengali Muslims of Bangladesh. In general, the gene frequencies of the polymorphic systems were similar to those in West Bengal and Assam. There appears to be a relatively strong Mongoloid influence in the present population as evidenced by the presence of HbE and TfDChi, higher frequencies of Hp1 and GcIF, and a lower AK2 frequency.
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PMID:Blood genetic markers in Bengali Muslims of Bangladesh. 295 66

The genetic structure of three Asiatic eskimos subpopulations (402 individuals), five coast chuckchies subpopulations (1793 individuals) and three reindeer chuckchies subpopulations (559 individuals) have been studied for 26 electrophoretic protein systems (33 loci). These are: adenilate-kinase (AK), diaphorase NAD X H (Dia), glyoxalase-1 (GLO-1), glucose-6-phosphate dehydrogenase (6GPT), glutamatpyruvate transaminase (GPT), glutamicoxalate transaminase (GOT), carbonic anhydrase-1 (Ca-1), catalase (Ct), acid phosphatase (AcP), lactate dehydrogenase (loci LDH-A and LDH-B), leucine aminopeptidase (Lap), malatedehydrogenase (MDH), purine nucleoside phosphorylase (PNP), superoxide dismutase (Sod), 6-phosphogluconate dehydrogenase (PGD), phosphoglucomutase (loci PGM1 and PGM2), cholinesterase (loci c1--c5), alkaline phosphatase (Pp), esterase D (EsD), red cell esterase (Est) - 4 loci, albumin (Alb), haptoglobin (Hp), hemoglobine (Hb A and B), group-specific component (Gc), transferrin (Tf), ceruloplasmin (Cp). In addition, AB0 and Rh system blood groups and phenyl thiocarbamide taste sensitivity (PTC) have been studied. 12 of 36 loci are polymorphic (33.33%), heterozygosity for all loci in eskimos, coastal and reindeer chuckchies being 0.118 +/- 0.005, 0.130 +/- 0.002 and 0.120 +/- 0.004, respectively. These estimates do not differ essentially from heterozygosity at these loci for mongoloid groups living further south. The test for interpopulation heterogeneity has permitted to estimate contribution of the loci to the differentiation of these populations. The least heterogeneity has been found at loci where gene frequency distribution is the most specific for these ethnic groups.
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PMID:[Genetic structure of the populations of native inhabitants in the northeastern USSR. III. Asiatic Eskimos and the coast and reindeer Chukchi]. 643 3

Intramuscular injections of the title drug in a dose of 5 mg/kg (5% of the LD50) during 10 days produced in the liver and blood serum of white rats a decrease in the activity of glucokinase, succinate dehydrogenase, glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, glutathione reductase, ATPase and ceruloplasmin. The urea content in total phospholipids rose, whereas the content of triglycerides and hexosamine diminished. Ten and 20 days after the drug was discontinued the majority of these characteristics returned to normal. The activity of glucosophosphate isomerase, transketolase, glucose-6-phosphatase, fructose-1,6-diphosphatase and lactate dehydrogenase as well as the content of total cholesterol, free fatty acids, tyrosine, hydroxyproline, total protein, RNA and DNA remained unchanged.
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PMID:[Effect of decane-1,10-bis[acetoxy-(N, N)-dimethyl-(N)-(diphenylmethoxy-2-ethyl) ammonium] dichloride on metabolism in white rats]. 651 57

The concentration of lipoperoxides (estimated as thiobarbituric acid-reactive material) and some components of the antioxidant defence system have been compared in various tissues of lean and congenitally obese mice. NADPH-stimulated lipoperoxide generation in vitro was significantly higher in microsomes (microsomal fractions) prepared from obese hepatic tissue than lean. Plasma, liver and brain lipoperoxide concentration was significantly higher in obese mice. In blood derived from obese mice the concentration of non-enzymic antioxidants including caeruloplasmin and vitamin A was higher, but hepatic retinol concentration was lower in these animals. In all the tissues assayed the glutathione peroxidase activity against H2O2 was less than its activity against cumene hydroperoxide. Assayed with either substrate, glutathione peroxidase activity was significantly higher in the brain and blood of obese mice than their lean counterparts. Conversely, liver glutathione peroxidase was decreased in obese animals, representing 43% of the activity of the lean-mouse liver enzyme against H2O2 and 81% of the cumene hydroperoxide-reducing activity. The liver of obese mice had significantly less, and the kidneys more, oxidized glutathione than the corresponding tissues of lean mice. Further investigations on hepatic tissue indicated that glutathione reductase activity was lower in the obese animals, but there was no significant difference between glucose-6-phosphate dehydrogenase activity in obese and lean mice.
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PMID:Abnormal antioxidant defence in some tissues of congenitally obese mice. 672 63


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