Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: C33C12 .10
63,145 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Serum trace elements (STE) were measured in 50 patients with chronic lymphocytic leukemia (CLL) and 100 normal subjects. Copper was higher in patients than in controls (1.50 +/- 0.06 versus 1.10 +/- 0.02 micrograms/ml, P less than 0.001), increased steadily from Stage 0 to Stage 4 (P = 0.002), and correlated with the lymphocyte count and serum lactate dehydrogenase (P less than 0.01) but not with acute phase reactants. Zinc was lower in patients than in controls (0.94 +/- 0.03 versus 1.10 +/- 0.02 micrograms/ml, P less than 0.001). Zinc (NS), selenium (P = 0.039), and calcium (P = 0.033), were decreased in Stages 3-4 as compared to Stages 0-2. The copper-to-zinc ratio (CZR) increased continuously from Stage 0 to Stage 4 (P less than 0.001). Discriminant analysis between two groups, Stage 0-2 and Stage 3-4, based on serum copper, zinc, calcium, and protein levels, allowed for a correct classification of 94% of the patients. Moreover, the clinical staging of the remaining 6% was modified retrospectively according to the results of discriminant analysis. It was concluded that (1) serum copper and CZR are useful indices of the extent of disease, (2) they are independent of a nonspecific acute phase reaction, (3) STE determination could be helpful in the staging of a limited number of CLL patients, and (4) zinc deficiency could contribute to immune dysfunction in CLL.
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PMID:Observations of serum trace elements in chronic lymphocytic leukemia. 365 10

Nickel subsulfide (Ni3S2), nickel chloride (NiCl2), nickel sulfate (NiSO4), and nickel oxide (NiO) are compounds of widely differing solubility encountered in the nickel-refining and electroplating industries. Inhalation is a common route of exposure and toxicity to the respiratory tract is possible. The purpose of this study was to evaluate the biochemical, cytological, and morphological changes in lung following administration of these compounds by intratracheal instillation. F344/Crl rats were administered a single dose of nickel compound containing 0.0, 0.01, 0.10, or 1.0 mumol Ni by intratracheal instillation. Rats were sacrificed at 1 or 7 days after compound administration, with half the animals in each exposure group taken for determination of nickel lung burden and the remaining half used for evaluation of biochemical, cytological, and histological changes. In the latter group, the right lung was lavaged and the fluid obtained was analyzed for indicators of pulmonary inflammation: lactate dehydrogenase (LDH), beta-glucuronidase (BG), total protein (TP), glutathione reductase (GR), glutathione peroxidase (GP), and sialic acid (SA). Total and differential cell counts on cells recovered in lavage fluid were also determined. The left lobe was examined for morphological changes. Clearance of nickel from the lung was most rapid for NiCl2 and NiSO4, followed by Ni3S2 and NiO. Minimal changes in all parameters were observed at 1 day after exposure. No significant changes in any parameter occurred in rats exposed to NiO, while Ni3S2, NiSO4, and NiCl2 caused increased in LDH, BG, TP, GR, SA, and total nucleated cells at 7 days.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparative acute toxicity of four nickel compounds to F344 rat lung. 375 51

Graded hepatic damage was induced in mature lactating dairy cows to measure the sensitivity of several hepatic diagnostic tests. In a preliminary study, cows were dosed with .05, .10 and .20 ml/kg body weight of carbon tetrachloride. Extreme changes occurred in hepatic tests by 24 h post-dosing, and all died by 35 h with massive diffuse centrilobular necrosis of hepatic cord cells. Dosing was decreased to induce non-fatal hepatic changes. Cows in Groups 1, 2, 3 and 4 were orally dosed with .002, .004, .006 or .01 ml/kg body weight of carbon tetrachloride, respectively. Serum enzymes of hepatic origin, bilirubin, plus bromosulfophthalein dye clearance were assayed before dosing and up to d 14 post-dosing. Liver biopsies were performed 24 h post-dosing for histological evaluation and cytochrome P-450 content. Hepatic concentrations of cytochrome P-450 were decreased in all the dosed cows. Serum activities of sorbitol dehydrogenase and gamma-glutamyl transferase were elevated in cows of Groups 3 and 4 and glutamic-oxaloacetic transaminase in cows of Group 4 by 24 h. Serum alkaline phosphatase, glutamic-pyruvate transaminase, lactate dehydrogenase, bilirubin, urobilinogen and bromosulfophthalein dye clearance were not significantly different. Mild to moderate diffuse centrolobular necrosis was observed in livers of cow of Groups 3 and 4, but no pathological changes were seen in Groups 1 and 2.
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PMID:Changes in hepatic function tests to induced toxicity in the bovine liver. 381 83

Enzymatic and histological features of muscular disorders associated with primary aldosteronism and glycyrrhizine-induced pseudoaldosteronism were studied. Among 10 patients with primary aldosteronism and 3 patients with pseudoaldosteronism, 5 patients were admitted to our hospital because of muscular weakness. The serum potassium (K) level was 1.86 +/- 0.21 mEq/l in a myopathy group on admission, a value significantly less than that of the 2.74 +/- 0.10 mEq/l in a non-myopathy group (p less than 0.01). Serum creatine phosphokinase (CPK), glutamate-oxyloacetate transaminase (GOT), and lactate dehydrogenase (LDH) were increased in the myopathy group compared to the non-myopathy group; serum CPK was 1412.6 +/- 902.6 vs. 22.8 +/- 5.0 mU/ml, serum GOT was 186.4 +/- 75.3 vs. 24.2 +/- 5.4 mU/ml (p less than 0.05), and serum LDH was 1133.4 +/- 377.3 vs. 387.6 +/- 42.5 mU/ml (p less than 0.05) in the groups with and without myopathy. Analysis of CPK isozymes revealed that the MM type exceeded 95%. The elevated serum CPK, GOT and LDH rapidly decreased to the normal range and muscular strength completely improved within 6 to 13 days after hospitalization, when the serum K level remained below than normal. Light microscopic finding of damaged muscle showed the diffuse necrosis and vacuolization of muscle fibers. Electron microscopic study clearly demonstrated complete dissolution of myofilaments with disappearance of sarcoplasmic reticulum and T-tubules in the necrotic muscle fibers. These results indicate that muscular lesions may occur in primary aldosteronism and pseudoaldosteronism when the serum K level is decreased to below 2.0 mEq/l. This myopathy is not periodic paralysis but hypokalemic myopathy. The mechanism by which K deficiency causes muscular damage remains unknown.
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PMID:Hypokalemic myopathy associated with primary aldosteronism and glycyrrhizine-induced pseudoaldosteronism. 391 13

1. Oxidized glutathione reacts or interacts with some erythrocytic enzymes (glucose 6-phosphate dehydrogenase, EC 1.1.1.49, aspartate aminotransferase, EC 2.6.1.10) but not with some others (lactate dehydrogenase, EC 1.1.1.27). 2. GSSG does not diminish the activity of any of these enzymes and is therefore not responsible for the decreased enzyme activities associated with older erythrocytes. 3. It may be that the reaction of aspartate aminotransferase with GSSG is the cause for the more rapid anodic electrophoretic mobility of this enzyme derived from human erythrocytes when compared with the mobility of the same enzyme from other human tissues. 4. A reinterpretation of some related, previously published, data with regard to the electrophoretic mobility of the above-mentioned enzymes from young and old erythrocytes is presented.
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PMID:Effect of oxidized glutathione on some enzymes of erythrocytes and its relation to erythrocytic enzyme activity and electrophoretic mobility. 438 18

Two enzymatic assay procedures for the measurement of 2,5-anhydrohexitol fructose analogs have been devised. Both procedures are based on the measurement of ADP formed during enzymatic phosphorylation of the analogs either by hexokinase or by fructokinase. The actual measurement makes use of the coupled assay system using pyruvate kinase, PEP, lactate dehydrogenase, and NADH. Both systems can be used to measure fructose and appropriate analogs at cuvette concentrations up to 0.10 mM. The hexokinase procedures allows the measurement of fructose, 2,5-anhydromannitol, and 2,5-anhydromannose. Glucose, which also reacts, can be removed by pretreatment of the samples with glucose oxidase. The fructokinase procedure allows the measurement of fructose, 2,5-anhydromannitol, 2,5-anhydroglucitol, and 2,5-anhydrotalitol.
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PMID:Enzymatic analysis of 2,5-anhydro-D-mannitol and related compounds. 641 7

The lactate dehydrogenase (LDH) isoenzyme pattern (expressed as the B:A subunit ratio) and two enzymes of the purine metabolism adenosine deaminase (ADA) and purine nucleoside phosphorylase (PNP) (expressed as the ADA/PNP ratio) were studied in human prenatal thymocytes, in subsets of human infant thymocytes, and in peripheral T lymphocytes. Prothymocytes were enriched by E rosette depletion, cortical thymocytes were enriched with a monoclonal antibody rosette technique using OKT6, and medullary thymocytes were enriched either with a monoclonal antibody rosette technique using OKT3 or with complement-mediated cytolysis using normal fresh rabbit serum. Peripheral T lymphocytes were isolated from normal adult peripheral blood by E rosette sedimentation. Prenatal thymocytes had the lowest B:A ratio. In the infant thymuses, prothymocytes had a lower B:A ratio (0.99 +/- 0.10) than the cortical thymocytes (1.04 +/- 0.08). The medullary thymocytes obtained either by OKT3 selection or normal rabbit serum cytotoxic treatment had higher B:A ratios (1.30 +/- 0.15 and 1.42 +/- 0.17, respectively). The highest B:A ratio is found in peripheral T lymphocytes (2.07 +/- 0.28) together with the lowest ADA/PNP ratio (0.50 +/- 0.07). The B:A ratios are paralleled by a progressive decrease in the ADA/PNP ratio. These findings indicate that during intrathymic T cell development, important changes occur not only in the activities of the enzymes of the purine metabolism but also in the distribution of the LDH isoenzymes.
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PMID:LDH analysis of human thymocytes and thymocyte subsets. 641 8

Cytoplasmic membranes were isolated from late-exponential phase Staphylococcus aureus 6539 P and the membrane proteins examined under non-denaturing conditions by thin-layer isoelectric focusing (TLIEF) in a pH 3.5-9.5 gradient. Isolated membrane preparations retained protein integrity as judged by the demonstration of membrane bound adenosine triphosphatase (ATPase) activity in addition to four other solubilized membrane enzyme markers. Membranes were effectively solubilized with 2.5% Triton X-100 (final concentration). Examination of Triton X-100 solubilized membrane preparations established the presence of 22 membrane proteins with isoelectric points between 3.7 and 6.0. The focused proteins displayed the following enzymatic activities and isoelectric points by zymogram methods: ATPase (EC 3.6.1.3), 4.20; malate dehydrogenase (EC 1.1.1.37), 3.90; lactate dehydrogenase (EC 1.1.1.27), 3.85; two membrane proteins exhibited multiple bands upon enzymatic staining NADH dehydrogenase (EC 1.6.99.3), 4.25, 4.35; succinate dehydrogenase (EC 1.3.99.1), 4.85, 5.10, 5.35.
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PMID:Analysis of Staphylococcus aureus cytoplasmic membrane proteins by isoelectric focusing. 645 26

Experiments were conducted to study the acute and subacute effects of intramuscularly injected T-2 toxin in rats and rabbits. The LD50 values of T-2 toxin were 0.85 +/- 0.03 and 1.10 +/- 0.08 mg/kg body wt in rats and rabbits, respectively. The intoxication was characterized by a consistent decrease in serum alkaline phosphatase (ALP) activity following either a single injection of 0.5, 0.6, or 0.9 mg/kg T-2 toxin in rats or daily injections of 0.2 mg/kg T-2 toxin for 10 days in rats and rabbits. Significant increases in bromosulfalein (BSP) retention and ALP activity were also observed in rabbits 24 hr following a single injection of 0.6 mg/kg T-2 toxin. The results indicated that the hepatobiliary system is a major target organ for T-2 toxin. Alterations in the activity of lactate dehydrogenase (LDH) and creatine kinase (CK) and in the hematocrit values were also observed.
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PMID:LD50 values and serum biochemical changes induced by T-2 toxin in rats and rabbits. 671 60

The L(+)-lactate dehydrogenase (EC 1.1.1.27) of Alcaligenes eutrophus catalyzes the NADH-dependent reduction of pyruvate and a few other 2-oxoacids. The Km values for NADH, NAD, pyruvate and L(+)-lactate are 0.075 mM, 0.130 mM, 0.820 mM and 7.10 mM, respectively. The reaction follows a rapid equilibrium ordered bi-bi mechanism and involves the formation of a dead-end EBQ complex. The competitive inhibition of pyruvate reduction caused by NAD (with respect to NADH) is regarded to be of physiological importance. The enzyme is strongly inhibited by oxaloacetate, oxalate and to a less extent by oxamate. Oxaloacetate was found to be the most powerful inhibitor of the enzyme and exerts an almost complete inhibition of the reduction of pyruvate and some 2-oxoacids at concentrations of 1 microM and less. At 0.1 microM oxaloacetate the inhibition of pyruvate reduction is about 90%. The kinetics of pyruvate reduction in the presence of oxaloacetate is characterized by a burst phase followed by a decreased steady-state velocity. During the burst phase, which lasts from several seconds to some minutes, the enzyme undergoes transition to a less active enzyme form. The inhibition studies revealed the lactate dehydrogenase to be a hysteretic enzyme, due to its slow response to the ligand. The characteristics of the transient were examined. The inhibition of lactate dehydrogenase from A. eutrophus by oxaloacetate is considered to be of great physiological importance, allowing its function only at a low oxaloacetate concentration and consequently at high NADH/NAD ratios.
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PMID:NAD-linked L(+)-lactate dehydrogenase from the strict aerobe alcaligenes eutrophus. 2. Kinetic properties and inhibition by oxaloacetate. 682 98


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