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)

Distinct impairments were found in membranes of rat myocardium and liver tissue in animals kept on food, which was deficient in retinol, tocopherol, ascorbic acid and essential amino acids lysine, methionine and threonine. Deficiency in these dietary components led to a decrease in content of phosphatidyl ethanolamine and phosphatidyl serine and in activity of total ATPase and Ca2+-ATPase in membranes of myocardial sarcoplasmic reticulum as well as to decrease Na+, K+-ATPase activity in liver plasmatic membrane.
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PMID:[Effect of diet on transport ATPase activity in myocardial and liver membranes]. 300 33

Undernutrition during the suckling period imposed by maternal protein deficiency during lactation resulted in elevated inositol triphosphatase activity (units per gram of wet tissue) in the ileum and lower phytase activity in the duodenum and jejunum. Activities of inositol triphosphatase in the duodenum and jejunum and phytase in ileum were unaffected. Postweaning nutritional rehabilitation resulted in elevated specific activities of both enzymes in all segments; however, activities of whole segments were similar to the corresponding control values. Elevation of inositol triphosphatase (ileum) and decline of phytase (duodenum and jejunum) activities due to undernutrition were reversed by the administration of hydrocortisone or thyroxine during undernutrition. These results suggest that maturation of activities of inositol triphosphatase in ileum (by hydrocortisone) and phytase in all segments (by both hydrocortisone and thyroxine) is under hormonal regulation, and the effects of neonatal undernutrition may be partly due to hormonal imbalances.
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PMID:Effects of neonatal undernutrition and subsequent nutritional rehabilitation or administration of thyroxine and hydrocortisone on the inositol phosphatase activities in rat intestine. 302 Feb 20

To investigate the effect of chronic protein-calorie malnutrition on intestinal repair after an enteric infection, we examined small intestinal structure, enzyme activity, and sodium transport in undernourished piglets during the acute and convalescent phases of a viral enteritis, transmissible gastroenteritis (TGE). Gnotobiotic pigs, nutritionally deprived from the age of 7 days, gained less weight than dietary controls from 14 days of age until the end of the study. Animals from malnourished and control diet groups were inoculated with TGE virus at 22-23 days and studied during the acute (40 h) and convalescent (4, 10, and 15 days) stages of this experimental enteritis along with noninfected dietary controls. After TGE infection, we observed a further decrease in weight gain and an increased mortality only in undernourished pigs. In jejunum and ileum of both dietary groups at 40 h after TGE infection, we observed comparable structural lesions, similar decreased activities of mucosal enzymes (sucrase, lactase, sodium-potassium-dependent ATPase), and increased thymidine kinase activities. Also we noted comparable diminution of glucose-stimulated jejunal sodium absorption in both dietary groups at 40 h. In control diet pigs, transport abnormalities recovered by 4 days after TGE infection and normal mucosal structure and enzyme activity returned over 4-15 days. In undernourished piglets, structural repair and enzyme abnormalities were prolonged when compared with the control diet group; glucose-stimulated sodium transport did not recover until 10 days after infection and never regained the enhanced activity seen in noninfected undernourished controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impact of chronic protein-calorie malnutrition on small intestinal repair after acute viral enteritis: a study in gnotobiotic piglets. 392 24

Muscle ion composition, Na-K-ATPase activity, tissue respiration, and transmembrane potential differences were measured after 28 and 56 days of ethanol consumption (6.2 g X kg-1 X day-1) or an isocaloric amount of glucose in 12 and 4 dogs, respectively. Ethanol and glucose were given as supplements to an otherwise nutritious diet. After 28 and 56 days of alcohol consumption, skeletal muscle contents of phosphorus, magnesium, and potassium were significantly reduced as compared with either the control values or those in glucose-fed animals. In alcohol-fed animals, muscle sodium chloride, and calcium were significantly elevated. Ethanol consumption also resulted in hyperpolarization of the resting transmembrane potential of skeletal muscle fibers and a significant increase in Na-K-ATPase activity. No change was noted in Mg-ATPase activity. The increase in Na-K-ATPase activity was accompanied by increased sodium transport-dependent respiration. These results indicate that a subclinical myopathy may be induced by alcohol in the dog. Malnutrition did not appear to be a factor in this study, and thus the changes observed are believed to be due to ethanol per se. The magnitude and direction of these changes are similar to those observed in the skeletal muscle of chronically alcoholic humans. The changes in Na-K-ATPase activity and sodium transport-dependent respiration may represent adaptive responses of the muscle cell to ion transport or membrane disorders induced by ethanol.
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PMID:Derangements of muscle composition, ion transport, and oxygen consumption in chronically alcoholic dogs. 623 59

In the United States and other developed countries thiamin deficiency is often related to chronic alcoholism. A number of mechanisms may be involved in the pathogenesis of thiamin deficiency in the alcoholic population. An important cause is inadequate intake of thiamin. Moreover, there may be decreased converstion of thiamin to the active coenzyme, reduced hepatic storage of the vitamin in patients with fatty metamorphosis, ethanol inhibition of intestinal thiamin transport, and impaired thiamin absorption secondary to other states of nutritional deficiency. The present discussion focuses on the mechanism of ethanol-related thiamin malabsorption. Under normal conditions thiamin transport in animals and humans is biphasic. At low or physiological thiamin concentrations, transport is a saturable, carrier-mediated, active process; but at higher concentrations, the transport of thiamin is predominantly passive. Ethanol reduces the rate of intestinal absorption and the net transmural flux of thiamin. Furthermore, ethanol inhibits only the active and not the passive component of thiamin transport by impeding the cellular exit of thiamin across the basolateral or serosal membrane. The impairment of thiamin movement out of the enterocyte correlates with a fall in the activity of Na-K ATPase. Bound to the basolateral membrane, Na-K ATPase is believed to be involved in the kinetics of active transport. Ethanol also increases the fluidity of enterocyte brush border and basolateral membranes. Since ethanol increases membrane fluidity it is possible that tahe impairment of thiamin transport and the diminution of Na-K ATPase activity may be related, at least partly, to a physical perturbation of the enterocyte membrane.
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PMID:Mechanisms of thiamin deficiency in chronic alcoholism. 625 54

Na+,K+-ATPase was studied in developing rat brain during undernutrition. The activity of Na+,K+-ATPase was significantly lower in animals that were undernourished from 6 to 17 days after birth than in well-nourished controls. The decreased activity of the enzyme was partially recovered after 4 weeks of rehabilitation. No change in the cation contents of brain following undernutrition was observed. The decrease in Na+,K4-ATPase activity was possibly due to the reduction in cholesterol contents and could be responsible for the observed functional changes associated with malnutrition or undernutrition during development.
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PMID:Na+,K+-ATPase in developing rat brain during undernutrition. 625 82

Previous results suggested a possible association between brain serotonin (5-HT) and Na+-K+-ATPase, in vivo. We extended the study to the developmental response of this enzyme to early 5-HT changes induced by early malnutrition and by a serotonin agonist. Agonist treatment produced a response of the enzyme activity at early stages of development in normal and malnourished brains. The induction of 5-HT changes through malnutrition could be playing an important role in the development and maturation of Na+-K+-ATPase activity, and brain 5-HT receptors could possibly be involved in such a response.
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PMID:Effects of malnutrition and quipazine on rat cerebral cortex ATPase activity during development. 625 73

The present study ascertained the influence of litter-size-induced perinatal nutritional modification on cardiac contractile protein enzymatic activity and isomyosin composition. Myofibrillar enzyme activities for Mg2+ -ATPase, Ca2+ -ATPase, and creatine kinase (CK) in the weanling heart were unaltered by nutritional modification. However, these enzyme activities were all significantly augmented in the adult heart. Hill plot analyses of Mg2+ -ATPase activities indicated that myofibrillar calcium regulation was not influenced by either nutritional modification or the weanling-to-adult developmental progression. Isomyosin V1 composition (90 +/- 1%) correlated with plasma thyroid hormone level in normal-growth (8/litter) weanlings. Undernutrition retarded conversion of V3 isomyosin to the V1 species while overnutrition enhanced isomyosin conversion. Isomyosin composition in weanling rats subjected to perinatal nutritional modification was independent of thyroid status. In the adult rat, plasma thyroxine levels were increased, whereas V1 isomyosin remained unchanged (88 +/- 2%) compared with that of the weanling groups. Discrepancies in the relationship between contractile protein enzymatic activities, myosin composition, and heart function are apparent between both the litter-size-adjusted weanling rats and between weanling and adult animals. These discrepancies indicate the complex relationship between heart function and contractile protein properties.
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PMID:Perinatal nutritional modification of weanling rat heart contractile protein. 650 43

The hypothesis that during the promotion phase of carcinogenesis a second rare event leads to a promoter-independent tumour cell was tested in an initiation-promotion-initiation type of experiment. Precancerous (island) cells induced in rat liver by 10 mg/kg N-nitrosodiethylamine given 24 h after partial hepatectomy were promoted by a protocol consisting of 2-acetylaminofluorene/partial hepatectomy. Administration of 25-100 mg/kg N-ethyl-N-nitrosourea served as second initiater. Microscopic foci of neoplastic cells were observed within the precancerous islands 66 days later; no such foci were noted in the appropriate controls. Deficiency of adenosine triphosphatase and glucose-6-phosphatase marker enzymes in the foci was more pronounced than in the surrounding island cells; glycogen storage was decreased and cytoplasmic basophilia slightly increased; gamma-glutamyltranspeptidase staining was negative or decreased with respect to the surrounding island cells, which exhibited a partially positive reaction. We conclude that a secondary change produced by N-ethyl-N-nitrosourea in precancerous island cells leads to focus-forming cells which grow, in the absence of promoter, into foci of neoplastic phenotype. Similar rare, initiation-like events might be involved in the process of tumour promotion in general.
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PMID:Initiation-promotion-initiation. Induction of neoplastic foci within islands of precancerous liver cells in the rat. 653 10

The interactions of Mg and K in cardiovascular disease are diverse and complex. However, Mg deficiency and loss from the heart and arteries, caused e.g. by dietary deficiency or imbalance, or by diseases and their treatment, can contribute to cardiovascular damage, and to functional abnormalities. Although Mg deficiency interferes with K retention, it is seldom measured in routine clinical practice, and the need to correct low Mg levels, in order to replete K, is rarely considered. The heart, with its high metabolic activity, is particularly vulnerable to Mg deficiency or loss because of the importance of Mg in mitochondrial structure and enzymatic function. The need for Mg to activate Na/K ATPase has long been known. Mg has also been shown to be structurally part of the enzyme in cardiac mitochondria. Additionally, Na/K exchange occurs in association with phosphorylation and dephosphorylation, reactions that are also Mg-dependent. The demonstration that Mg modulates K+/proton (H+) exchange, and that cation selectivity in Na+ and K+ exchange for H+ is highly dependent on the concentration of Mg++, provides new insights into how Mg protects against K loss. The loss of myocardial K that results from Mg deficiency contributes to electrophysiologic changes, as can the Ca shifts of Mg loss. A high Ca/Mg ratio also predisposes to arterial spasms, and increases catecholamine release. Thus the arrhythmogenic potential of Mg deficiency can be related to imbalances between Mg and K or between Mg and Ca, or both. Electrical or K-induced catecholamine release is increased by a low Mg/Ca ratio, as are increased fatty acids and lipids and intravascular hypercoagulability. K or Ca loading of the patient with undiagnosed Mg inadequacy is not only often unsuccessful, but it may carry inherent risks. It can intensify the Mg depletion, the arterial contractility, and ECG abnormality. In the patient receiving digitalis, Mg deficiency can increase drug toxicity. In the case of myocardial infarction, Mg deficiency can increase the risk of malignant ventricular arrhythmias and sudden cardiac death. In the absence of alcoholism or gastrointestinal disease, the use of loop diuretic therapy for congestive heart failure, especially in elderly patients, is the most common cause of Mg depletion. A high concurrence of hypomagnesemia with hypokalemia, from whatever cause, has been documented. However, systemic Mg deficiency can exist despite normal Mg serum levels. Methodological difficulties hamper direct detection of cellular Mg deficiency, but patients can be indirectly evaluated by use of Mg-loading tests, which may be of combined diagnostic and therapeutic value.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Interactions of magnesium and potassium in the pathogenesis of cardiovascular disease. 653 39


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