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:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The morphological and biochemical changes that occur during chemical hypoxic injury in a neural cell line were studied in the presence and absence of calcium. Oligodendroglial-glioma hybrid cells (ROC-1) were subjected to inhibitors of glycolytic and oxidative ATP synthesis (chemical hypoxia). Complete respiratory inhibition depleted [ATP] to less than 5% of control by 4 min. Blebs appeared on the cell surfaces and cells began to swell within a few minutes of ATP depletion. A 200% increase in cell volume and bleb coalescence preceded irreversible cell injury (lactate dehydrogenase release) which began at approximately 20 min with 50% cell death by 40 min. In energized cells an equivalent degree of osmotic swelling induced by ouabain inhibition of the Na+, K(+)-ATPase pump did not produce blebbing or cell death. Partial inhibition of respiration decreased [ATP] to approximately 10% of control by 40 min. Blebbing and swelling began at 40 min and bleb coalescence preceded plasma membrane disruption which began at approximately 55 min. ATP depletion, blebbing, swelling, and death followed similar time courses in the presence or absence of extracellular calcium ([Ca2+]e). Intracellular calcium ([Ca2+]i) was measured using fura-2. In calcium-containing medium metabolic inhibition caused a transient increase in resting [Ca2+]i (100 +/- 17 nM) followed by a low steady-state level preceding plasma membrane disruption. Following deenergization in calcium-free medium, [Ca2+]i remained below 60 nM throughout injury and death. These data suggest that decreased ATP initiates a sequence of events including bleb formation and cell swelling that lead to irreversible cell injury in the absence of large increases in [Ca2+]i.
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PMID:Cell swelling, blebbing, and death are dependent on ATP depletion and independent of calcium during chemical hypoxia in a glial cell line (ROC-1). 161 11

Recent studies indicate that in animals with marked cardiac hypertrophy, there is depressed function of Ca2+ sequestration by myocardial sarcoplasmic reticulum (SR) because of down regulation of the Ca(2+)-ATPase gene. However, in several animal models we have observed enhancement of myocardial Ca2+ sequestration in response to chronic cardiac stimulation. We tested the hypothesis that in animals with mild cardiac hypertrophy, there is enhanced Ca(2+)-cycling activity by the SR Ca2+ pump and Ca(2+)-release channel. Because creatine kinase activity is consistently decreased in cardiomyopathy, we also determined whether enhanced Ca2+ cycling was accompanied by down regulation or inhibition of the creatine kinase system. Mild cardiac hypertrophy was induced by volume overload; 2% salt was added to the diet of 2-week-old turkey poults for 4 weeks. Compared with age-matched controls, volume overload resulted in 14.3% increase in heart weight and 21.5% increase in heart-to-body weight ratios. The hypertrophied heart had approximately 20% increased activities of the SR Ca2+ pump and the SR Ca2+ channel. Net Ca2+ transport was increased by 16.5%. Compared with controls and in contrast to several other myocardial enzymes, creatine kinase activity was diminished in the hypertrophied hearts by 23% and creatine content was decreased by 8%. Differences between groups were not detected for lactate dehydrogenase, aspartate transaminase, and alanine transaminase. We concluded that an early adaptation of the myocardium undergoing hypertrophy in compensatory response to functional overload is an enhancement of Ca2+ cycling activity by the Ca2+ pump and Ca2+ channel of the SR.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of mild cardiac hypertrophy, induced by volume overload in turkeys, on myocardial sarcoplasmic reticulum calcium-pump and calcium-channel activities and on the creatine kinase system. 165 61

The orientation of the enzyme Mg(2+)-ATPase (EC 3.6.1.3) in the transverse tubule (TT) membranes of skeletal muscle was investigated using highly purified chicken and rabbit TT vesicles. The percentage of sealed vesicles present in these preparations averaged 88 and 78%, respectively, as calculated from the detergent-induced increase in ouabain-sensitive (Na+, K+)-ATPase activity, ATP-dependent ouabain binding, and lactate dehydrogenase activity (sarcoplasmic enzyme trapped in the TT vesicles). Sidedness of the sealed vesicles, estimated from latency of 5'-nucleotidase, acetylcholinesterase, and adenylate cyclase, was predominantly right-side out (69-76%, chicken TT and 62-70%, rabbit TT). In both chicken and rabbit native vesicles, high Mg(2+)-ATPase activity was detected by addition of ATP to the extravesicular medium; this activity was increased 14-12% by alamethicin pointing to the external localization of the active site. Furthermore, the enzymatic activity resulted partially inhibited by treatment of the chicken TT vesicles with proteinase K or p-hydroxymercuribenzoate. Concanavalin A stimulated 4-fold the chicken TT Mg(2+)-ATPase activity, an effect not potentiated by detergent permeabilization of the intact vesicles, indicating that lectin-binding sites were also solvent accessible. This stimulatory effect was not observed in native or permeabilized rabbit TT vesicles. From these results we conclude that the TT Mg(2+)-ATPase is an ectoenzyme with its nucleotide-hydrolyzing site and glycosylated regions facing the extracellular space. Inhibitors of ion-motive ATPases did not modify the enzyme activity, suggesting a different physiological role for the TT Mg(2+)-ATPase which may be involved in the regulation of muscle fiber functions affected by extracellular ATP levels.
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PMID:Transverse tubule Mg(2+)-ATPase of skeletal muscle. Evidence for extracellular orientation of the chicken and rabbit enzymes. 166 Apr 76

1. This experiment was designed to study the effects of fasting and enforced exercise on the physiological, biochemical and physical characteristics of duck muscle. 2. Sixty 75-d-old male ducks weighing 3.0 +/- 0.2 kg were assigned to three treatments: a control, and an 8 and 24 h fast plus enforced exercise for 10 min. The ducks were then sacrificed and the carcass stored at 4 degrees C for 24 h. 3. Although the pH and serum lactate contents gradually increased with fasting time the responses were not significant. The ultimate pH was elevated and the lactate of breast and thigh muscles was lower in stressed birds. 4. The activity of lactic dehydrogenase was significantly increased by the stress, and the activities of creatine phosphokinase and alkaline phosphatase were also increased slightly. However, no effect was found on the ATPase activity of the myofibrillar protein of either breast or thigh muscle as a result of the stress. The ATPase activity of myofibrillar protein of breast muscle significantly increased with storage time. 5. The extractability of myofibrillar protein increased with storage time for all treatments. The SDS-PAGE patterns of myofibrillar proteins were also studied. 6. Consequently DFD-like muscle was observed in the breast and thigh muscles of ducks which had been stressed.
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PMID:Effect of stresses before slaughter on changes to the physiological, biochemical and physical characteristics of duck muscle. 166 82

Na-K ATPase activity in the brain decreased significantly after diabetes was induced with streptozotocin in rats. Largest decreases were observed in the hippocampus (-30%) and the cerebral cortex (-26%). Smaller decreases were observed in the thalamus (-13%), hypothalamus (-11%) and brain stem (-10%). Na-K ATPase activity in the striatum and the cerebellum were not significantly decreased. The varied decreases suggest that the regional variation of the enzyme is enhanced in the diabetic state. The enzymes of glucose metabolic pathway, namely hexokinase, lactate dehydrogenase and citrate synthase in the brain regions largely remained unchanged although increases in lactate dehydrogenase were observed in some regions. Acetylcholinesterase activity, a marker for the cholinergic system, remains unaltered in the brain during diabetes. The results are discussed with respect to the possible metabolic factors which alter the Na-K ATPase in the brain and its comparison with the peripheral nerve.
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PMID:Diabetes induced by streptozotocin causes reduced Na-K ATPase in the brain. 166 46

Primary cultures of renal rabbit proximal tubule cells were initiated from a pure suspension of proximal tubule fragments. Proximal tubule cells were grown in a hormone-supplemented, serum-free medium containing low concentrations of antibiotics. Confluent monolayers exhibited multicellular dome formation, indicating the presence of transepithelial solute and water transport. Ultrastructural examination revealed a monolayer of polarized epithelial cells with tight junctions and sparse membraneous microvilli facing the culture medium. Time course biochemical characterization was performed using a palette of 12 enzymes, representative of important metabolic functions or pathways. Brush-border-associated enzymes (gamma-glutamyl transpeptidase and alanine aminopeptidase) were moderately reduced throughout the culture whereas alkaline phosphatase was markedly decreased at confluency. Mitochondrial and lysosomal marker enzymes were well preserved over the culture period. Glutathione-S-transferase activity remained stable during the 16-day culture period investigated. Glycolysis enzyme activities (lactate dehydrogenase and hexokinase) were enhanced, as a function of culture age. Na(+)-K(+)-ATPase activity rise was concomitant with the increase of glycolysis marker enzymes. In contrast, the gluconeogenesis marker enzyme, glucose-6-phosphatase, fell dramatically to reach a low level equivalent to 4% of the activity measured in isolated proximal tubules. Primary cultures exhibited several differentiated functions of the proximal tubule cell: (a) PTH alone was able to induce a significant stimulation of adenylate cyclase activity, unlike isoproterenol, thyrocalcitonin, and arginine vasopressin, and (b) sodium-dependent alpha-methylglucoside (AMG) transport was detected. This AMG uptake was selectively inhibited by phlorizin (5 X 10(-3) M), which is a competitive inhibitor of glucose uptake at the apical membrane. Complete characterization made it possible to investigate hitherto unexplored aspects of in vitro cultured proximal tubule cells. This primary culture model could provide a useful and reliable tool to investigate in vitro renal proximal tubule function, under normal conditions or after a drug-induced toxicity.
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PMID:Biochemical, functional, and morphological characterization of a primary culture of rabbit proximal tubule cells. 167

A study was made of the role of prolactin (PRL) in the regulation of thyroid function in intact animals and in those exposed to stress (swimming was used as physical exercise). A single daily dose of 125 micrograms of PRL per 100 g of body mass was injected subcutaneously in 0.5 ml of saline solution during a week to male rats (control: intact rats; injection of 0.5 ml of saline solution subcutaneously). Redox enzymes; succinate dehydrogenase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, NAD.H2 and NADP.H2, ATPase and monoamine oxidase, total protein, RNA and glycogen in glandular cells were investigated histochemically 24 h after the last injection of PRL or saline, 30 min., 1, 2, 3, 5 and 7 hours after swimming or right after complete fatigue (in the presence of experimental hyperprolactinemia). A conclusion has been made that one of the most important mechanisms of the adaptive effect of PRL is its ability to suppress thyroid function, thus decreasing the metabolism level, which results in reduction of oxygen consumption and improves body tolerance to stress.
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PMID:[Metabolism of thyroid gland cells as affected by prolactin and emotional-physical stress]. 178 Feb 95

A study is performed on the long-term effect of the chloracetanilide herbicide "Acetochlor" in doses 21.0; 10.6: 5.5 and 2.6 mg/kg-1 in conditions of 6-month oral application and 2-month rehabilitation period on the metabolite processes and the balance of the connective-tissue components in the myocardium and aorta of male white rats. A complex of biochemical and histological methods are performed (activity of succinate dehidrogenase, lactate dehydrogenase, glucose-6-phosphate dehydrogenase, adenosin triphosphatase, cytochrome oxidase, fructoso-1,6-diphosphatase, level of the thiol groups, soluble globular, elastine, collagen fractions, insoluble collagen and elastine, general and sulphated glucosamino glycanes). The dose 21.0 mg/kg-1 leads to blocking of the thyol groups, inactivation of succinate dehydrogenase, cytochrome oxidase, adenosin triphosphatase, fructose-1,6-diphosphatase, glucose-6-phosphate dehydrogenase, activation of lactate dehydrogenase, decrease of the soluble globular, elastine, and collagen fractions and increase of the glucoseaminoglycanes in the heart muscle and aorta. The changes established in the heart muscle at 10,6 mg/kg-1 certify for stronger sensitivity of the organ of the aorta wall. The presence of single changes in the examined indices, their complete dying out after the rehabilitation period and absence of structural changes in the myocardium and aorta permit the dose of 5.5 mg/kg-1 to be accepted as not effective in the conditions of chronic experiment concerning the cardiovascular system.
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PMID:[The effect of the acetanilide herbicide Acetochlor on the cardiovascular system of white rats]. 179 94

A number of chemicals are known to potentiate the hepatotoxicity of carbon tetrachloride. The halocarbon trichloroethylene was shown in a previous study to enhance both carbon tetrachloride-induced toxicity and lipid peroxidation in isolated hepatocytes. In this study three other chlorocarbons have been investigated in order to determine whether this interaction was peculiar to trichloroethylene or common to chlorinated solvents. Hepatocyte suspensions were exposed to carbon tetrachloride at subthreshold levels of toxicity and various concentrations of 1,1,1-trichloroethane, tetrachloroethylene, and chloroform over an eightfold concentration range. Plasma membrane preparations were exposed to tetrachloroethylene and carbon tetrachloride and effects on Mg(2+)- and Na(+)-K(+)-ATPase activities determined. None of the treatments alone caused statistically significant toxicity. Combined treatments resulted in toxicity as demonstrated by potassium ion, alanine aminotransferase, and lactate dehydrogenase leakage from the cells on coincubation of carbon tetrachloride with each of the other halocarbons studied. Only tetrachloroethylene and chloroform were found to potentiate lipid peroxidation, however. In liver plasma membranes no changes in Na(+)-K(+)-ATPase were observed with any of the treatments and only the highest dose of tetrachloroethylene was able to inhibit Mg(2+)-ATPase activity. There was no increase in this inhibition on coincubation with carbon tetrachloride, which does not support involvement of ATPases in combined halocarbon toxicity. In conclusion, the data suggest a mechanism of action common to this class of chemical although its specific nature remains to be established.
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PMID:Potentiating effects of chlorinated hydrocarbons on carbon tetrachloride toxicity in isolated rat hepatocytes and plasma membranes. 182 22

Adult rats injected with streptozotocin during the neonatal period displayed in the fed state moderate hyperglycemia. However, the percentages of glycated hemoglobin in erythrocytes and glycated lactate dehydrogenase in liver and pancreatic islets, as well as the sorbitol and glycogen content of the islets, were not significantly increased. Likewise, in intact islets, the ouabain-sensitive inflow of 86Rb+, and the ratio between 3H2O production from D-[2-3H]glucose and D-[5-3H]glucose were not different in control and streptozotocin-injected rats. These findings suggest that the alteration in both the mitochondrial catabolism of D-glucose and secretory response to the hexose previously documented in the islets of the latter animals are not attributable to factors such as the excessive nonenzymatic glycation of cytosolic proteins, sorbitol or glycogen accumulation, or impaired Na+, K(+)-adenosine triphosphatase (ATPase) activity. Although a contributive role of glucotoxicity in the impaired function of beta cell in this model of non-insulin-dependent diabetes should not be ruled out, it is speculated that streptozotocin might also cause a long-term damage of key mitochondrial dehydrogenases in the pancreatic beta cells and, possibly, their precursor cells.
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PMID:Neonatal streptozotocin injection: a model of glucotoxicity? 183 15


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