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

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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)

Wilson disease (WD) is an autosomal recessive disorder due to the defect in ATP7B gene characterized by excessive accumulation of copper in the liver with progressive hepatic damage and subsequent redistribution to various extrahepatic tissues including the brain, kidneys, and cornea. Strikingly, the total serum copper concentration is always low in WD, even though the non-ceruloplasmin copper level is still expected to be high. To assess the role of free radical reactions catalyzed by non-ceruloplasmin copper, we investigated erythrocyte metabolism and oxidative stress as a mechanism for hemolysis in eight WD patients during episodes of acute hemolysis and compared them with eight follow-up cases of WD on d-penicillamine therapy and eight healthy, age-matched children. Elevated levels of non-ceruloplasmin copper were found in all the WD patients during an episode of hemolytic anemia. There was marked inhibition in erythrocyte enzymes, namely, hexokinase, total adenosine triphosphatase (ATPase), and glucose-6-phosphate dehydrogenase (G-6-PD) from WD patients compared with patients on penicillamine and healthy children, indicating altered erythrocyte metabolism during a hemolytic crisis. Antioxidant status was also found to be compromised as is evident from decreased glutathione (GSH) levels, decreased antioxidant enzymes (namely, superoxide dismutase, catalase, glutathione peroxidase, and glutathione reductase), increased lipid peroxidation, and deranged plasma antioxidants. Uric acid showed maximum decrease followed by ascorbic acid. These findings suggest that the free radical production by elevated non-ceruloplasmin copper through transition metal catalyzed reactions leads to oxidative injury resulting in altered erythrocyte metabolism and severely compromised antioxidant status of WD patients during hemolytic anemia.
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PMID:Erythrocyte metabolism and antioxidant status of patients with Wilson disease with hemolytic anemia. 1654 36

Inhibition of either the insulin-like or target of rapamycin (TOR) pathways in the nematode Caenorhabditis elegans extends life span. Here, we demonstrate that starvation and inhibition of the C. elegans insulin receptor homolog (daf-2) elicits a daf-16-dependent up-regulation of a mitochondrial superoxide dismutase (sod-3). We also find that although heat and oxidative stress result in nuclear localization of the DAF-16 protein, these stressors do not activate a SOD-3 reporter, suggesting that nuclear localization alone may not be sufficient for transcriptional activation of DAF-16. We show that inhibition of either TOR activity or key components of the cognate translational machinery (eIF-4G and EIF-2B homologs) increases life span by both daf-16-dependent and -independent mechanisms. Finally, we demonstrate that at least one nematode hexokinase is localized to the mitochondria. We propose that the increased life spans conferred by alterations in both the TOR and insulin-like pathways function by inappropriately activating food-deprivation pathways.
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PMID:daf-16 protects the nematode Caenorhabditis elegans during food deprivation. 1672 Jul 40

Honeybees, Apis mellifera, gradually increase their rate of forage uptake as they gain foraging experience. This increase in foraging performance has been proposed to occur as a result of learning; however, factors affecting flight ability such as changes in physiological components of flight metabolism could also contribute to this pattern. Thus, the purpose of this study was to assess the contribution of physiological changes to the increase in honeybee foraging performance. We investigated aspects of honeybee flight muscle biochemistry throughout the adult life, from non-foraging hive bees, through young and mature foragers, to old foragers near the end of their lifespan. Two-dimensional gel proteomic analysis on honeybee thorax muscle revealed an increase in several proteins from hive bees to mature foragers including troponin T 10a, aldolase and superoxide dismutase. By contrast, the activities (V(max)) of enzymes involved in aerobic performance, phosphofructokinase, hexokinase, pyruvate kinase and cytochrome c oxidase, did not increase in the flight muscles of hive bees, young foragers, mature foragers and old foragers. However, citrate synthase activity was found to increase with foraging experience. Hence, our results suggest plasticity in both structural and metabolic components of flight muscles with foraging experience.
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PMID:Lifetime performance in foraging honeybees: behaviour and physiology. 1698 99

Determination of erythrocyte number and their indices and enzymatic activity of: glucose-6-phosphate dehydrogenase (G-6PD), superoxide dismutase (SOD), acetylcholinesterase (AchE), glutathione reductase (GR) and hexokinase (Hx) in peripheral blood erythrocytes of workers chronically exposed to mercury vapours during the production of chloride (the mercuric electrolysis method). The studied workers were equipment operators, electricians and electrolysis maintenance men at the chloride production department using the mercuric electrolysis method. The study involved 46 men, aged 21 to 56, (x = 39 +/- 10.4) exposed to mercury vapours for the period from 7 months to 32 years (x = 14.7+/-10.8), working in a three shift system, for 8 hours a day. Smokers constituted 50% of the studied group (23 men). Urine mercury concentrations of workers exposed to mercury vapours were in the range from 10 to 215 microg/dm3 (x = 81,4 +/- 72,9) and in blood in range 4 do 72 microg/dm3 (x=16.3 +/- 15,0). Controls were 46 men aged 20-54, (x=33.6 +/- 9.8), workers and voluntary blood donors, who never experienced occupational exposure to mercury vapours or other chemicals, and to physical agents. The percentage of smokers in the control group was 34.7% (16 men). Basic haematological determinations (hematocrit - Hct, Hb concentration, erythrocyte number in mm3 of blood, mean red cell hemoglobin concentration (MCHC), mean red cell volume (MCV) and enzymatic studies (activity of G-6PD, SOD, AchE, GR, Hx) in peripheral blood samples obtained from workers and controls were performed. Hematological parameters of the peripheral blood were determined using AVL 808 hematological counter, following the manufacturer's instructions. Activity of the studied enzymes was estimated by the spectrophotometric method described by Beutler, following the recommendations of the International Committee for Standardisation in Hematology. Values of Ht were higher in all the subgroups exposed to Hg workers (divided according to duration of exposure or urine mercury concentrations) in comparison to the control group. The erythrocyte number in mm3 of peripheral blood was also higher in the exposed workers group than in controls. MCHC in the total group exposed to mercury vapours was lower than in the controls. In the subgroup exposed to mercury vapours for < 10 years, the value of this parameter was lower than in the control group; whereas in the subgroups separated in respect to mercury concentration in the urine, it was lower only in workers showing the highest urine concentration of this metal. In workers exposed to mercury vapours, MCV index values were lower than in the controls. In the subgroups of workers who smoked and those who did not smoke, they were also lower than in the controls; whereas in the group of the longest exposed workers from 21 to 35 years, it was found to be higher than in controls. The activity of G6PD was lower in the group of subjects occupationally exposed to mercury vapours than in the control group - 5.60 +/- 1.60 and 7.41 +/- 0.43 IU/gHb respectively. When comparing the subgroups of smokers and non-smokers with the controls, workers showed lower G6PD activity than in the matching control subgroups - 6.24 +/- 1.97 and 7.44 +/-0.22 IU/gHb in the subgroups of smokers and 4.97 +/- 0.72 and 7.38 +/- 0.18 IU/gHb in non-smokers respectively. Erythrocyte G6PD activity was lower in all studied groups separated in respect to exposure time - 5.54 +/- 1.75, 6.02 +/- 2.05 and 5.54 +/- 1.05 IU/gHb respectively. The same pattern of changes was observed in the subgroups separated in respect to mercury concentration in the urine compared to the controls. The lowest enzyme activity was found in the subgroups showing the highest mercury concentration in the urine wnen compared with the subgroup with the lowest urine concentration of this metal - 5.19 +/- 1.50 and 6.00 +/- 1.84 IU/gHb respectively SOD activity in the group of workers exposed to mercury was lower compared to the controls - 2289.97 +/- 122.31 and 2418.03 +/- 60.28 IU/gHb respectively. The smoking and non-smoking workers showed respective SOD activities on - 2305.43 +/- 102.75 and 2274.50 +/- 124.5 IU/gHb; whereas in the matching subgroup of controls - 2452.11 +/- 88.72 and 2382.09 +/- 91.22 IU/gHb, respectively. The activity of this enzyme in all investigated groups selected in respect to length of employment, revealed lower values when compared with the controls - 2271.20 +/- 115.23 in the group with under 10 years of exposure, 2335.11 +/-167.71 IU/gHb in those exposed for 11-20 years, and 2290.40 +/- 26.12 IU/gHb in the subgroup exposed for the longest period of time. Similar changes were observed in the activity of this enzyme in the subgroups separated in respect to mercury concentration in the urine when SOD activity was compared with the controls. The AchE activity was higher in the group exposed to mercury vapours compared to the controls and the respective values were - 50.22 +/- 14.44 and 36.87 +/- 2.92 IU/gHb. In the subgroups separated in respect to length of exposure, the activity of this enzyme was statistically significantly higher than in the control group. The GR activity levels were lower in the exposed group - 8.01 +/-2.54 IU/gHb, compared to the controls - 10.24 +/- 1.24 IU/gHb. In the subgroups of smokers and non-smokers, GR activity was lower, 8.48 +/- 2.37 and 7.54 +/- 2.68 IU/gHb, compared to smokers and non-smokers in the control group, 10.26 +/- 1.01 and 10.16 +/- 1.03 IU/gHb, respectively. The GR activity was also statistically significantly lower in all groups separated in respect to duration of exposure, with the values of 8.56 +/-2.39, 8.26 +/- 2.38, 7.06 +/- 2.75 IU/gHb, respectively in subject groups and 10.24 +/- 1.35 in the control group. Similar changes were noticed in the subgroup separated in respect to mercury concentration in the urine. The Hx activity was lower in the group exposed to mercury vapours - 1.08 +/-0.11. compared with the controls - 1.21 +/- 0.16 IU/gHb. The enzyme activity showed a similar pattern in the subgroups separated in respect to duration of exposure when they were compared with the control group. Exposure to mercury vapours present changes in the red blood cells, manifested by increased (when compared with the control group), number of erythrocytes in peripheral and decreased mean cell volume and mean cell hemoglobin concentration values, as well as changes in the metabolic processes occurring in the erythrocytes. In subjects exposed to mercury vapours some metabolic processes may be additionally modified by addiction to cigarette smoking.
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PMID:[Red cell system and selected red cell enzymes in men occupationally exposed to mercury vapours]. 1778 49

Alkyl-lysophospholipids (ALPs), developed initially to be antitumor agents, have proved highly effective in the treatment of visceral leishmaniasis, a disease caused by the species making up the protozoan complex Leishmania donovani. Although their effectiveness is known, the mode of action against this parasite is not completely understood. In the present work, we have studied the effect of 3 derivatives, edelfosine, miltefosine, and ilmofosine. Using nuclear magnetic resonance spectroscopy ('H-NMR), we have examined the excreted catabolites from glucose metabolism in the promastigote forms treated with these compounds. The ALPs at concentrations of 19 and 38 microM inhibit the excretion of acetate, succinate, and pyruvate. The effect of edelfosine, miltefosine, and ilmofosine on the activity of the enzymes hexokinase, glycerolkinase 3-PD, phosphoglucose isomerase, superoxide dismutase, and phospholipase C were also examined. Glycerolkinase 3-PD and phosphoglucose isomerase are generally insensitive to the compounds, whereas hexokinase and superoxide dismutase are inhibited by miltefosine and ilmofosine. The ALPs exhibited an activated effect against the phospholipase C activity. Alkyl-lysophospholipids were shown to have a significant effect on several enzymes in important biochemical pathways indispensable for the survival of L. donovani promasigotes.
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PMID:Effect of alkyl-lysophospholipids on some aspects of the metabolism of Leishmania donovani. 1816 58

Gentamicin (GM) is an effective aminoglycoside antibiotic against severe infections but nephrotoxicity and oxidative damage limits its long term clinical use. Various strategies were attempted to ameliorate GM nephropathy but were not found suitable for clinical practice. Green tea (GT) polyphenols have shown strong chemopreventive and chemotherapeutic effects against various pathologies. We hypothesized that GT prevents GM nephrotoxicity by virtue of its antioxidative properties. A nephrotoxic dose of GM was co-administered to control and GT-fed male Wistar rats. Serum parameters and enzymes of oxidative stress, brush border membrane (BBM), and carbohydrate metabolism were analyzed. GM increased serum creatinine, cholesterol, blood urea nitrogen (BUN), lipid peroxidation (LPO) and suppressed superoxide dismutase (SOD) and catalase activities in renal tissues. Activity of hexokinase, lactate dehydrogenase increased whereas malate dehydrogenase decreased. Gluconeogenic enzymes and glucose-6-phosphate dehydrogenase were differentially altered in the cortex and medulla. However, GT given to GM rats reduced nephrotoxicity parameters, enhanced antioxidant defense and energy metabolism. The activity of BBM enzymes and transport of Pi declined by GM whereas GT enhanced BBM enzymes and Pi transport. In conclusion, green tea ameliorates GM elicited nephrotoxicity and oxidative damage by improving antioxidant defense, tissue integrity and energy metabolism.
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PMID:Protective effect of green tea extract on gentamicin-induced nephrotoxicity and oxidative damage in rat kidney. 1942 67

Total sleep deprivation (TSD) induces a broad spectrum of cognitive, behavioral and cellular changes. We previously reported that long term (5-11 days) TSD in the rat, by the disk-over-water method, decreases the activity of the antioxidant enzyme superoxide dismutase (SOD) in the brainstem and hippocampus. To gain insight into the mechanisms causing cognitive impairment, here we explore the early associations between metabolic activity, antioxidant responses and working memory (one form of cognitive impairment). Specifically we investigated the impact of short-term (6h) TSD, by gentle handling, on the levels of the endogenous antioxidant, total glutathione (GSHt), and the activities of the antioxidative enzymes, SOD and glutathione peroxidase (GPx). Short-term TSD had no significant impact on SOD activity, but increased GSHt levels in the rat cortex, brainstem and basal forebrain, and GPx activity in the rat hippocampus and cerebellum. We also observed increased activity of hexokinase, (HK), the rate limiting enzyme of glucose metabolism, in the rat cortex and hypothalamus. We further showed that 6h of TSD leads to increased exploratory behavior to a new environment, without impairing spontaneous alternation behavior (SAB) in the Y maze. We conclude that acute (6h) sleep loss may trigger compensatory mechanisms (like increased antioxidant responses) that prevent initial deterioration in working memory.
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PMID:Short-term total sleep deprivation in the rat increases antioxidant responses in multiple brain regions without impairing spontaneous alternation behavior. 1985 85

Oxidative phosphorylation and/or glycolysis provide energy, mainly in the form of ATP, which ensures proper functioning of immune cells such as CD4(+) T lymphocytes. However, the main substrates, namely oxygen and glucose, are known to remain for a relatively short time in the inflamed tissue and in other clinical situations where immune cells need to function properly. Therefore, we examined the effect of hypoxia and/or lack of glucose on cellular energy metabolism and on cytokine secretion in stimulated human CD4(+) T lymphocytes. Human CD4(+) T cells were MACS-isolated using peripheral blood obtained from healthy donors. Stimulated cells were incubated in medium with or without glucose for 6h in a sealed chamber which led to cumulative hypoxia. During this incubation period, (i) oxygen saturation was measured continuously using a Clark-type electrode, and (ii) samples were taken at different time points in order to quantify for each the viability of cells, intracellular reactive oxygen species (iROS), ATP levels, glycolytic enzyme activity, mRNA expression of hexokinase-1 and superoxide dismutase-1, and concentrations of several different cytokines. Stimulated CD4(+) T cells which were incubated under normoxic conditions served as controls. Under hypoxic conditions, lack of glucose exerted a biphasic effect on cellular oxygen consumption: initially higher but later lower respiration rates were measured when compared to conditions where glucose was available. Lack of glucose strongly increased the number of dead cells and the formation of iROS under normoxia but not under hypoxia. Under both normoxic and hypoxic conditions, intracellular ATP levels remained almost unchanged during the incubation period if glucose was present, but decreased significantly in the absence of glucose, despite the enhanced glycolytic enzyme activity. Measurements of stimulated cytokine production demonstrated (i) that cumulative hypoxia stimulates especially the secretion of IL-1beta, IL-10 and IL-8, and (ii) that lack of glucose results in lower cytokine concentrations. We demonstrate that CD4(+) T cells are highly adaptive in bioenergetic terms which ensure their proper function under extreme conditions of glucose and/or oxygen availability as found under physiological and pathophysiological conditions. Hypoxia seems to facilitate inflammatory reactions and angiogenesis.
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PMID:Effects of hypoxia and/or lack of glucose on cellular energy metabolism and cytokine production in stimulated human CD4+ T lymphocytes. 2020 8

The present study aims to evaluate the antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic male Wistar rats. To induce diabetes mellitus, rats were injected with streptozotocin intraperitoneally at a single dose of 40mg/kg. Streptozotocin induced diabetic rats showed significant (P<0.05) increase in the levels of blood glucose, glycosylated haemoglobin and significant (P<0.05) decrease in the levels of plasma insulin, body weight and total haemoglobin. Diabetic rats also showed significant (P<0.05) decrease in the activity of hepatic hexokinase and significant (P<0.05) increase in the activities of glucose-6-phosphatase and fructose-1, 6-bisphosphatase. The pancreatic thiobarbituric acid reactive substances and lipid hydroperoxides were significantly (P<0.05) increased and the activities of pancreatic superoxide dismutase, catalase and glutathione peroxidase were significantly (P<0.05) decreased in diabetic rats. Oral treatment with gallic acid (10 and 20mg/kg) daily for a period of 21days showed significant (P<0.05) protective effects on all the biochemical parameters studied. Histopathology of pancreas confirmed the protective effects of gallic acid in diabetic rats. In vitro study also revealed the potent antioxidant effect of gallic acid. Thus, the study shows the antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic rats. The effect exerted by 20mg/kg body weight of gallic acid was more effective than 10mg/kg body weight of gallic acid.
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PMID:Antihyperglycaemic, antilipid peroxidative and antioxidant effects of gallic acid on streptozotocin induced diabetic Wistar rats. 2086 84

Nonylphenol is known to have estrogenic properties and has been reported to cause health hazards to animals and humans. The effects of nonylphenol on pancreas are not clearly elucidated. In this study, we sought to evaluate the effects of nonylphenol on the oxidative status of pancreas and consequential effects of nonylphenol on some of the end points of carbohydrate metabolism in the female rats. Rats were administered nonylphenol orally at the doses of 1.5, 15, and 150 mg/kg of body weight per day for 7 days. After 24 h of last dosing, the animals were sacrificed by cervical dislocation. The activities of pancreatic superoxide dismutase and catalase were significantly decreased with a concomitant increase in the levels of H2O2 and lipid peroxidation. Nonylphenol increased plasma insulin levels with a concomitant decrease in the levels of plasma glucose as compared to the control groups of rats. A dose-dependent increase in the activities of liver hexokinase and phosphofructokinase was recorded along with decreased activity of glycogen phosphorylase in liver. Western blot analysis revealed a significant decrease in the levels of GLUT-2. These results show that nonylphenol causes oxidative stress in pancreas and impairs liver glucose homeostasis.
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PMID:Short-term exposure to nonylphenol induces pancreatic oxidative stress and alters liver glucose metabolism in adult female rats. 2147 97


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