Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.1.1 (hexokinase)
 5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The activity of hexokinase, glucose-6-phosphoric dehydrogenase, lactic dehydrogenase, succinic dehydrogenase, acid and alkaline phosphatases was determined in the rat kidney tissue with phenylhydrazine anemia and posttransfusion polycytemia. The blood supply of the cortical and medullary layers of the kidneys was studied at the same time. The purpose of this work was to ascertain possible connections between the changes in the activity of the enzymes under study with the renal erythropoietin producing function of the kidneys. The blood supply of the kidneys of rats with phenylhydrazine anemia was sharply decreased, but it was markedly elevated in case of posttransfusion polycytemia. There were no significant changes in the activity of the mentioned enzymes. These data suggest that the activity of the kidney enzymes is not a controlling factor in the renal erythropoietin production.
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PMID:[Activity of kidney tissue enzymes in phenylhydrazine anemia and post-transfusion polycythemia]. 89 Jan 28

The oxidative injury to erythrocytes, red blood cell (RBC) rigidity and splenic hemolysis was assayed in 17 chronically hemodialyzed patients before and during recombinant erythropoietin (EPO) treatment. When a stable hematocrit between 30 and 35% had been established for at least 4 months, a statistically significant increase in RBC volume, hemoglobin concentration, hematocrit, reticulocyte count, and several RBC enzymes (2,3-diphosphoglycerate, glucose 6-phosphate dehydrogenase, pyruvate kinase, hexokinase) was noted. This indicated significant RBC rejuvenation under the influence of EPO. However, no significant improvement in the RBC oxidative sensitivity, RBC deformability, splenic RBC volume, slow mixing splenic RBC volume, and the intrasplenic RBC transit time could be disclosed. These data confirm the existence of an extra-erythrocytic factor in uremic plasma, which is partly responsible for a reduced RBC life span in hemodialysis patients despite EPO treatment.
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PMID:Oxidative injury to erythrocytes, cell rigidity and splenic hemolysis in hemodialyzed patients before and during erythropoietin treatment. 824 95

Aluminium (Al.) is an ubiquitous element found in every food product. The sources of Al. are especially corn, yellow cheese, salt, herbs, spices, tea and tap water. In household Al.-made ware is a major source of the element. Al. may cause diseases in humans, especially hampers many metabolic processes especially turnover of calcium, phosphorus and iron. Salts of Al. may bind to DNA, RNA, inhibit such enzymes as hexokinase, acid and alkaline phosphatases, phosphodiesterase and phosphooxydase. Al. salts are especially harmful to nervous, hematopoietic systems and to skeleton. Al. gets to organism with food, water, cosmetics, from aluminium ware and containers. Toxicity comes from substitution of Mg and Fe ions effecting in disturbances in intracellular signaling, excretory functions and cellular growth. Neurotoxic action of Al. probably comes from substitution of Mg ions in ATP, what finally influences function of every ATP using-enzymes. There are observations in experimental models proving Al. salts are responsible for Alzheimer disease development. Toxicity of Al. to skeletal system results in diminished resistance thus tendencies to breaking, and comes from lower collagen synthesis and slowing down of mineralisation. Low erythropoietin production, inhibition of hem-synthesing enzymes and binding of Al. to transferrin, effects in anaemia. Carcinogenic effects of Al. were nor proved nor denied, but high concentrations of Al. were found in many neoplastic cells. In conclusion, we should introduce prophylactic measures effecting in less Al. intake esp. avoiding use of Al.-made ware nad controlling food for Al. content.
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PMID:[Aluminum--occurrence and toxicity for organisms]. 1129 16

Recombinant human erythropoietin (epoetin) is widely used for the treatment of renal anemia. The aim of our study was to determine the influence of epoetin on erythrocyte metabolism. Thirty-six hemodialysis patients (22 men, 14 female), aged from 17 to 64 years (mean age 43) and 30 healthy volunteers (12 men, 18 female), aged from 25 to 65 years (mean age 40) were studied. Epoetin (Eprex, Janssen-Cilag) was administered subcutaneously with the starting dose of 2000 IU three times per week for twelve months (range from 75 to 133 IU/kg/week, mean dose 102+/-21 IU/kg/week). Laboratory markers of: hematological response, iron status and erythrocyte metabolism were measured before epoetin administration. Afterwards the markers were controlled every three months. During epoetin treatment a significant increase in hemoglobin concentration was observed (100% patients responded in a positive way to epoetin). The following changes in erythrocyte metabolism were noticed: 1) in glycolytic enzymes: a significant increase in the activity of hexokinase and that of lactate dehydrogenase, 2) in glycolytic intermediates: a significant increase in the 2,3-diphosphoglycerate and adenosine triphosphate concentrations, 3) a significant increase sodium, potassium adenosine triphosphatase concentration, 4) the glucose uptake by erythrocytes significantly decreased while the lactate production remained stable. During anemia treatment with epoetin in hemodialysis patients not only quantitative but also qualitative changes in erythrocytes were observed.
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PMID:Erythrocyte metabolism during renal anemia treatment with recombinant human erythropoietin. 1563 50

Adaptations to chronic hypoxia involve changes in membrane transport proteins. The underlying mechanism of this response may be related to concomitant occurring changes in erythropoietin (Epo) levels. We therefore tested the direct effects of recombinant human erythropoietin (rHuEpo) treatment on the expression of muscle membrane transport proteins. Likewise, improvements in performance may involve upregulation of metabolic enzymes. Since Epo is known to augment performance we tested the effect of rHuEpo on some marker enzymes that are related to aerobic capacity. For these purposes eight subjects received 5,000 IU rHuEpo every second day for 14 days, and subsequently a single dose of 5,000 IU weekly for 12 weeks. Muscle biopsies were obtained before and after 14 weeks of rHuEpo treatment. The treatment increased hematocrit (from 44.7 to 48.8%), maximal oxygen uptake by 8.1%, and submaximal performance by approximately 54%. Membrane transport systems and carbonic anhydrases involved in pH regulation remained unchanged. Of the Na(+), K(+)-pump isoforms only the density of the alpha2 subunit was decreased (by 22%) after treatment. The marker enzymes cytochrom c and hexokinase remained unchanged with the treatment. In conclusion, changes in muscle membrane transport proteins and selected muscle enzymes do not contribute to the Epo-induced improvement in performance.
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PMID:Effects of prolonged recombinant human erythropoietin administration on muscle membrane transport systems and metabolic marker enzymes. 1788 50