Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

---

Query: EC:2.7.1.1 (hexokinase)
5,274 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The hexokinase method and a method using glucose dehydrogenase are compared. In general, the two methods show good agreement. The samples were not deproteinized and were obtained from fasting patients of the medical, surgical, rheumatological and hemodialysis clinics. The possible influence of anticoagulants, preservatives and hemoglobin on the determination of glucose with glucose dehydrogenase was checked; there was no evidence of interference. Among the carbohydrates which were tested, only 2-deoxyglucose gave a positive reaction. In addition, this is a reliable and cheap method. The multiplication factor for the photometric analysis remains stable for seven days with a linearity between 0.55 and 44.4 mmol/1 glucose.
...
PMID:[Investigation of a new method for the determination of glucose, using the Greiner Selective Analyzer II (GSA II) (author's transl)]. 85 3

The erythrocytes of 350 pigtailed macaques (Macaca nemestrina) were examined for electrophoretic variation of hemoglobin and 26 enzymes. Seven enzymes showed variation in more than 1% of individuals: phosphoglucose isomerase, phosphoglucomutase-1, soluble NADP-dependent isocitric dehydrogenase, peptidase A, peptidase C, 2,3-diphosphoglycerate mutase, and acid phosphatase. Variation with lesser frequency was found in soluble glutamic-oxalacetic transaminase, phosphoglycerate kinase, lactic dehydrogenase, and hemoglobin. Only eight samples were tested for esterase D, and one of these had a variant phenotype. Enzymes with no clear variation were adenylate kinase, adenosine deaminase, phosphofructokinase, hexokinase, pyruvate kinase, glyceraldehyde 3-phosphate dehydrogenase, aldolase, phosphoglycerate mutase, phosphopyruvate hydratase (enolase), phosphoglucomutase-3, and superoxide dismutase. There was father-to-son transmission of PGI, PGM-1, peptidase C, 6PGD, 2,3-DPGAM, NADP-ICD, and acid phosphatase variants, suggesting that these loci are autosomal as in man.
...
PMID:Intraspecific red cell enzyme variation in the pigtailed macaque (Macaca nemestrina). 114 87

In this paper we report the purification of pig erythrocyte hexokinase type III, at preparative level, using 52 liters of starting material (hemolysate). This was possible using a new efficient anion exchanger support, the Toyopearl DEAE 650 M which allows completely to change the strategy of removing hemoglobin from hemolysates, permitting to handle large amounts of starting material and reducing work would have required months using conventional anion exchanger supports, to only 2-3 days. Furthermore, we have tested the binding of other red blood cell enzymes to the Toyopearl DEAE 650 M, showing a wider potential use of this chromatographic support for their purification at a preparative level.
...
PMID:Preparative purification of pig red blood cell hexokinase type III using a new efficient chromatographic support. 162 Jun 86

1. Thioridazine and trifluoperazine, which have been previously found in this laboratory to be the most effective calmodulin antagonists in treatment of burns, are shown here to be also effective in the treatment of frostbite. 2. Electron microscopic studies have revealed a complete reversal of both the vascular and skin tissue damage induced by frostbite. 3. The reversal of the vascular damage was also demonstrated by the ability of these compounds to abolish the increase in hemoglobin content in the skin. 4. The reversal of the skin tissue damage was also revealed by the ability of these compounds to raise the decreased ATP level and the reduced activities of 6-phosphogluconate dehydrogenase and mitochondrial and soluble hexokinase in skin, induced by frostbite, to normal control levels.
...
PMID:Treatment of frostbite with the calmodulin antagonists thioridazine and trifluoperazine. 260 33

1. Several calmodulin antagonists abolished the decrease in ATP level and in the activities of 6-phosphogluconate dehydrogenase and mitochondrial and soluble hexokinase, induced by burns in the rat skin. 2. These antagonists had also a protective action on the blood capillaries and erythrocyte membrane, as judged by the electron microscopic appearance, as well as the abolishment of hemoglobin increase and burn edema. 3. Of all the compounds investigated here, the most effective were trifluoperazine and thioridazine, which are also known as the more potent calmodulin antagonists. 4. The present experiments suggest that calmodulin antagonists may be effective drugs in treatment of burns, having both therapeutic and prophylactic action.
...
PMID:Therapeutic and prophylactic treatment of skin burns with several calmodulin antagonists. 271 15

The effects of vitamin B6 on erythrocyte metabolism, erythrocyte hemoglobin O2 affinity (P50), and nonenzymatic glycosylation were studied in 15 Caucasian men with type II (non-insulin-dependent) diabetes mellitus. A control group of 13 healthy Caucasian men was also evaluated. Before treatment, diabetic subjects had low mean cell hemoglobin concentration values and increases in both erythrocyte 2,3-diphosphoglycerate (2,3-DPG) levels and erythrocyte hexokinase activities. Although all three of these changes are associated with a decrease in hemoglobin O2 (Hb-O2) affinity, P50 values were normal in diabetic subjects. Moreover, P50 values normalized to pH 7.4 (P50(7.4] were inversely related to the level of glycosylated hemoglobin (HbA1c). Both erythrocyte 2,3-DPG and erythrocyte ATP were also inversely related to HbA1c. Vitamin B6 nutriture, as determined by erythrocyte aspartate aminotransferase (AST) and alanine aminotransferase (ALT) activities, was normal in all diabetic subjects before vitamin B6 therapy. Nonetheless, HbA1c levels decreased after 6 wk of treatment with 150 mg/day pyridoxine and increased again during placebo administration. These changes were not explained by changes in fasting blood glucose. Pyridoxine therapy also decreased P50(7.4) values and increased erythrocyte AST and ALT activities but had no effect on 2,3-DPG, ATP, or the activities of hexokinase, glucose-6-phosphate dehydrogenase, and 6-phosphogluconate dehydrogenase. These observations suggest that 1) nonenzymatic glycosylation may play a role in regulating both erythrocyte metabolism and Hb-O2 affinity in diabetic subjects, and 2) vitamin B6 therapy may modify nonenzymatic glycosylation of hemoglobin in this population.
...
PMID:Erythrocyte O2 transport and metabolism and effects of vitamin B6 therapy in type II diabetes mellitus. 273 64

The erythrocyte metabolism of two patients with nonspherocytic hemolytic anemia caused by a hexokinase deficiency, and a pyruvate kinase deficiency, respectively, were studied with NMR. The complexing of ATP and 2,3-diphosphoglycerate (2,3-DPG) with Mg2+ and hemoglobin (Hb) was determined using 31P-NMR on oxygenated and deoxygenated cells to investigate the influences of these enzyme defects on intracellular magnesium distribution and on Hb oxygen dissociation. In the pyruvate kinase-deficient red blood cells, the 2,3-DPG concentration was almost twice the normal value and the ATP concentration was near the lower limit of the normal range. In the hexokinase-deficient red cell population, the predominance of young cells masked the deficiency. Therefore, reticulocyte control cells were included in this study. In the oxygenated pyruvate kinase-deficient cells, the fraction of ATP that is complexed to magnesium as well as the free Mg2+ concentration were normal, despite the abnormal concentration of 2,3-DPG. In the deoxygenated cells the free Mg2+ concentration was lower than in normal cells. The fraction of Hb complexed with 2,3-DPG was higher than normal in both oxygenated and deoxygenated pyruvate kinase-deficient cells, in accordance with the high p50 of the oxygen-hemoglobin dissociation curve. In hexokinase-deficient cells, two major abnormalities are found: when the cells were deoxygenated, the concentration of ATP and 2,3-DPG fell. This was not observed for any other sample and could, therefore, be a consequence of the hexokinase deficiency. Despite almost normal levels of magnesium-binding metabolites, the free Mg2+ concentration in oxygenated and deoxygenated cels is much lower than in normal cells. This could be a cell-age-related phenomenon, since lower free Mg2+ concentrations were also found in reticulocyte control cells.
...
PMID:Intracellular free magnesium and phosphorylated metabolites in hexokinase- and pyruvate kinase-deficient red cells measured using 31P-NMR spectroscopy. 292 Jan 77

Hemoglobin affinity to oxygen, enzyme activity and metabolite concentration of carbohydrate metabolism were determined in erythrocytes of rats which were administered insulin solution. A valid decrease of the hemoglobin value P50 (pressure of hemoglobin half-saturation with oxygen), as well as a decrease of the enzyme activity of 2,3-diphosphoglycerate shunt and increase of the activity of regulatory glycolysis enzymes--hexokinase and pyruvate kinase in erythrocytes with multiple introduction of hormones to animals have been established. Such changes in rat erythrocytes were registered with the simultaneous effect of insulin and hypoxic hypoxia evoked by the "lift" of rats in the altitude chamber to the conditional altitude of 9000 m. It is found out that preliminary injection of insulin considerably increases survivability of rats under hypoxic hypoxia at great altitudes.
...
PMID:[Oxygen-transport function and carbohydrate metabolism in rat erythrocytes during hypoxic hypoxia and treatment with insulin]. 307 Aug 87

We studied the interactions of the A- variety of glucose-6-phosphate dehydrogenase (G6PD) deficiency and sickle cell anemia (HbSS) to see if G6PD deficiency influenced laboratory and clinical features of HbSS. A total of 801 male patients over age 2 had G6PD electrophoresis on cellulose acetate membranes. Assays of both G6PD activity and hexokinase activity were then done on all samples that had an electrophoretic pattern other than the normal wild type (GdB). The collection of clinical data used a standardized protocol. Using cluster analyses we classified 10.4% males to be G6PD deficient, while 18.4% had the functionally normal GdA+ enzyme. The prevalence of G6PD deficiency did not change significantly when age was stratified by decade, suggesting little survival advantage or disadvantage of the combination of G6PD deficiency and HbSS. Compared to patients who were not G6PD deficient, there were no significant differences in the hemoglobin concentration, mean corpuscular volume, reticulocyte count, bilirubin, or SGOT level in patients with HbSS who had G6PD deficiency. The incidence of painful episodes, sepsis, or acute anemic episodes was similar in both groups. Our results are consistent with recent studies of smaller numbers of patients that have found little influence of G6PD deficiency upon HbSS. Specifically, we found no evidence that G6PD enhanced the severity of hemolysis or increased the incidence of acute anemic episodes or sepsis in HbSS.
...
PMID:Effects of glucose-6-phosphate dehydrogenase deficiency upon sickle cell anemia. 334 44

This study was performed to examine the relationship between postmortem biochemical values and cause of death. The follow samples were taken from 399 corpses: cerebrospinal fluid (CSF; n = 376, suboccipital), blood (n = 158, femoral vein), and urine (n = 101, at autopsy). (See Table 1 for causes of death) All samples were stored at -80 degrees C. A further 100 samples of blood were later taken and stored at +4 degrees C before testing. Biochemical determinations made were: glucose in CSF, blood, and urine (hexokinase method); lactate (LDH/GPT) and free acetone (HS-gas chromatography) in CSF; hemoglobin A1 in blood (microcolumn technique). In 34 cases fatal diabetic coma was considered verified by morphological and chemical findings. One hundred cases of sudden cardiac death were chosen as the main control group. In 32 of the 34 cases defined above, the value of the formula of Traub (glucose + lactate in CSF) exceeded 415 mg/dl. It is not influenced significantly by hyperglycemia or hyperlactatemia due to factors other than diabetes (i.e., carbon monoxide, asphyxia). After death the value rose till the 30th hpm, then remained stable for at least 1 week. Fatal coma was defined as the ketoacidotic form if free acetone in CSF ranged above 21 mg/l. In these cases, CSF glucose and free acetone correlated positively. Hemoglobin A1 remained stable after death. Its amount was independent from postmortem blood glucose, postmortem interval and total hemoglobin. Furthermore, the manner of storage (-80 degrees or +4 degrees C) had no significant influence on its values. In 29 of 34 cases of fatal coma, Hb A1 exceeded 12.1%. Analysis of urine glucose showed elevated levels (over 500 mg/dl) in diabetic comas. On conclusion, fatal diabetic coma seems indicated as the cause of death if measured values of postmortem biochemistry exceed the following limits: CSF-Traub 415 mg/dl, free acetone (CSF) 21 mg/l; Hb A1 12.1%; urine glucose 500 mg/dl. Most important are the Traub formula and hemoglobin A1. Usually, in fatal coma both values are elevated. If both of them are normal, diabetic coma can nearly be excluded. Combined evaluation of all values is absolutely necessary. Morphology must also always be taken into account. Consequently, a diagnosis of fatal coma can be obtained by a process of elimination.
...
PMID:[Biochemical measurements of glucose metabolism in relation to cause of death and postmortem effects]. 376 99


<< Previous 1 2 3 4 5 6 7 8 9 Next >>

---