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 mean orientations of the transition dipole moments associated with vibrational modes of the proteins and phospholipids of sarcoplasmic reticulum were determined on dry and hydrated membrane multilayers deposited on germanium or zinc selenide crystals, using polarized infrared attenuated total reflectance spectroscopy (P-IR-ATR). For preservation of the enzymatic activity of the Ca(2+)-ATPase the films were prepared from solutions containing 0.05 M KCl, 5 mM imidazole (pH 7.4), 0.5 mM MgCl2, 1-10 mM trehalose and dithiothreitol. The anisotropy was highest in dry films containing congruent to 7.5 micrograms protein/cm2, and decreased with increasing membrane thickness or hydration. The dichroic ratio of the CH2 vibrations (2923 cm-1) of extracted sarcoplasmic reticulum phospholipids on Ge plate was 1.56, compared with a dichroic ratio of 1.68 obtained on dry films of whole sarcoplasmic reticulum. The dichroic ratios of the amide I band (1650 cm-1) of the Ca(2+)-ATPase in the Ca2-E1 state and in the EGTA and vanadate stabilized E2-V state were nearly identical (1.60 vs. 1.62). The dichroism of the amide I, amide II and lipid CH2 vibrations was not affected by changes in the concentration of KCl (25-100 mM) or Ca2+ (approximately equal to 10(-8)-10(-4) M) and by the addition of vanadate (1 mM) or Pi (5 mM) in a calcium-free medium containing 0.5 mM EGTA. The dichroic ratio of the C-C (1033 cm-1) or CO stretching band (1046 cm-1) of trehalose incorporated into SR films was 1.2 on Ge plate; this corresponds to a mean angle of approximately 70 degrees between the plane of the trehalose ring and the normal of the film plane, suggesting that the trehalose molecules are surprisingly well oriented in the polar headgroup region of the phospholipids. The orientation of the trehalose was not affected by the presence of Ca(2+)-ATPase.
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PMID:Polarized infrared attenuated total reflectance spectroscopy of the Ca(2+)-ATPase of sarcoplasmic reticulum. 183 64

The purpose of this study was to determine if the dietary antioxidant selenium could inhibit hepatocarcinogenesis induced by peroxisome proliferators, which are hypothesized to induce tumors by increased production of hydrogen peroxide or other reactive oxygen species. Rats were fed diets containing the peroxisome proliferator ciprofibrate and one of three concentrations (0.04, 0.2, or 1.0 ppm) of selenium for 6 or 21 months. The incidence of hepatic tumors and the number and volume of gamma-glutamyl transpeptidase-positive, ATPase-negative, glucose-6-phosphatase-negative, and glucose-6-phosphatase-positive foci at 21 months were lower in rats fed higher levels of selenium (no foci or tumors were seen at 6 mo). Indices of oxidative damage in the liver (thiobarbituric acid reactants, conjugated dienes, and lipid-soluble fluorescence products), however, were not decreased in rats fed the high-selenium diet. Therefore, selenium was protective against ciprofibrate-induced hepatocarcinogenesis, but not by reducing the degree of oxidative damage. The liver selenium and glutathione concentrations, and liver selenium-dependent glutathione peroxidase activity, increased as dietary selenium increased. Therefore, inhibition of carcinogenesis by selenium was correlated with increased levels of glutathione and glutathione peroxidase, but these did not inhibit the indices of oxidative damage. Peroxisomal beta-oxidation also increased with the dietary selenium content; it therefore does not appear to be a factor in the inhibition of hepatocarcinogenesis in rats fed higher levels of selenium.
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PMID:Effect of dietary selenium on the induction of altered hepatic foci and hepatic tumors by the peroxisome proliferator ciprofibrate. 208 22

A decrease in activity of Na+, K(+)-ATPase, estimated in erythrocytes of women at the second half of pregnancy, served as a criterion in screening of the risk group tended to development of late toxicoses. In the risk group of women with pregnancy activity of glutathione peroxidase and content of selenium were studied in blood, simultaneously with estimation of osmotic resistance of erythrocytes. A decrease in activity of Na+, K(+)-ATPase was shown to be a reliable prognostic criterion in pregnant women with tendency to late toxicoses. At the same time, a decrease in glutathione peroxidase activity should be used as a distinct prognostic pattern only if content of selenium was as low as 95 pg/ml in blood of women with pregnancy. Alimentary and metabolic deficiency of selenium appears to be responsible for limitation of the glutathione peroxidase activity at the preclinical step of late toxicosis development.
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PMID:[Metabolic status of selenium in pregnant women from a risk group of developing late toxemia]. 256 Aug 72

Cell culture conditions were devised that selectively supported growth of 13 or 14 gestation day F344 rat ureteric bud, the renal collecting duct anlagen. These same conditions also inhibited the growth of metanephrogenic mesenchyme, precursor of structures proximal to the duct. Isolated buds were cultured in Ham's F12 medium supplemented with epidermal growth factor, selenium, insulin, hydrocortisone, prostaglandin E1, transferrin, and triiodothyronine; fetal bovine serum (1%) was required for continuous propagation. Cultured cells were epithelial in morphology and formed domes. By electron microscopy, many structural characteristics of highly differentiated cells were evident: numerous mitochondria, Golgi apparatus, extensive endoplasmic reticulum, an occasional cilium, intracytoplasmic filaments, polarized formation of microvilli, and gap junctions. Histochemistry revealed considerable functional differentiation as well. Cultured bud cells, adult collecting duct, and fetal duct anlagen were positive for acid phosphatase, membrane-localized ATPase, and nonspecific esterase. Bud cells and fetal duct anlagen expressed high levels of gamma-glutamyl transpeptidase activity while adult collecting duct exhibited slight activity. In addition, immunocytochemical observation of intermediate filament expression revealed the presence of epithelial cytokeratins but absence of mesenchymal vimentin in cultured bud cells and fetal and adult collecting ducts. These results indicate that the culture conditions described can maintain the partially differentiated fetal collecting duct anlagen in a state consistent with its embryonal derivation, and therefore may be useful in culture studies of renal differentiation.
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PMID:Selective growth in culture of fetal rat renal collecting duct anlagen. Morphologic and biochemical characterization. 286 2

Keshan disease (KD) is a cardiomyopathy endemic in certain areas of China, characterized by severe deterioration and multiple focal necrosis. In the present paper we describe abnormalities of the structure and function of myocardial mitochondria from patients with subacute Keshan disease. Activities of succinate dehydrogenase, succinic oxidase, cytochrome c oxidase, H(+)-ATPase and its sensitivity to oligomycin and the response of membrane potential to energization by ATP were significantly decreased. However, the spectrum of reduced-minus-oxidized cytochromes in patients' mitochondria showed no obvious difference in the content of cytochrome c oxidase (aa3). There was also a marked decrease in lipid fluidity of affected mitochondria, and an abnormal amount of moderately electron dense amorphous inclusions. Electron-microscopic x-ray microanalysis and exposure to protein digestion reagent demonstrated that these inclusions are not Ca3(PO4)2, but are, probably, proteinaceous in nature. Affected mitochondria had markedly decreased selenium content. The defects in myocardial mitochondria from patients with chronic Keshan disease were less extensive than those in patients with subacute Keshan disease. We propose that Keshan disease be classified as a form of "mitochondrial cardiomyopathy".
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PMID:Keshan disease--an endemic mitochondrial cardiomyopathy in China. 290 94

Urodiolenone is a substance that appears as the glucuronide in the urine of 1 in 3 hypertensive subjects. It is a potent inhibitor of Na+, K+-ATPase in kidney tissue of the guinea pig, as measured by cytochemical assay. Chemical and mass spectrometric evidence is presented, from which it is concluded that urodiolenone is a sesquiterpenoid substance, is a bicyclic enone with a vicinal diol side chain, and has molecular formula C15H24O3.
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PMID:Observations on the chemical and physiological properties of urodiolenone, an urinary compound found in hypertension. 298 48

Sodium selenite has been shown to inhibit Na,K-ATPase. Glutathione, at sufficient excess, is able to prevent or reverse the inhibition. Dithiothreitol can also reverse much of the inhibition, but KCN cannot. Selenomethionine does not inhibit Na,K-ATPase. The interactions of sodium selenite with Na,K-ATPase and glutathione may aid in understanding the early events in selenium cataractogenesis.
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PMID:Inhibition of Na,K-ATPase by sodium selenite and reversal by glutathione. 302 32

A large amount of biochemical, physiological, and pharmacological data has been obtained which supports a mechanistic role of oxygen free radical-induced lipid peroxidation (LP) in post-traumatic spinal cord degeneration. Biochemical evidence of early and progressive lipid peroxidative reactions occurring in the injured spinal cord includes: an increase in polyunsaturated fatty acid peroxidation products (e.g., malonyldialdehyde), a decrease in cholesterol and the appearance of cholesterol oxidation products, an increase in cyclic GMP presumably due to free radical activation of guanylate cyclase, a decrease in tissue anti-oxidant levels (e.g., alpha tocopherol, reduced ascorbate), and inhibition of membrane-bound enzymes such as Na+ + K+-ATPase. In vitro CNS tissue studies have provided support for the possibility that LP may contribute to other early post-traumatic events including intracellular calcium accumulation and arachidonic acid release. Moreover, spinal tissue lactic acidosis, which occurs early after injury, can exacerbate LP reactions. The involvement of LP in the development of progressive post-traumatic spinal white matter ischemia has been strongly inferred from pharmacological studies in cats with known inhibitors of LP. For example, the dose-response curves for the ability of the glucocorticoid methylprednisolone (MP) to inhibit post-traumatic LP and to retard ischemia development are identical. This relationship between LP and post-traumatic ischemia is more directly implied from studies showing that pretreatment of cats with high doses of anti-oxidants (e.g., d-alpha tocopherol plus selenium p.o. or 1-ascorbic acid i.v.) can also significantly antagonize the progressive decrease in spinal cord blood flow that follows severe blunt injury. However, a similar efficacy of certain calcium and prostaglandin antagonists suggests an interrelationship between aberrant calcium fluxes, vasoconstrictor/platelet aggregating prostanoids, and LP in the post-traumatic ischemic phenomenon. In addition to a role of LP in ischemia development, the action of intensive d-alpha tocopherol and selenium pretreatment to retard anterograde cat motor nerve fiber degeneration after nerve section suggests that LP may also be a fundamental mechanism of "Wallerian" axonal degeneration after neural injury. Finally, a critical role of LP in the acute pathophysiology of CNS injury in general has been supported by the finding of an excellent correlation, in terms of efficacy and potency, between the action of glucocorticoid and nonglucocorticoid steroids to inhibit neural tissue LP in vitro and to promote early neurological recovery in severely head-injured mice.
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PMID:Role of lipid peroxidation in post-traumatic spinal cord degeneration: a review. 355 50

Intestinal absorption of selenate and selenite in rats was investigated in vitro by using everted sacs of the duodenum, jejunum and ileum. Only the ileal sacs incubated with selenate accumulated selenium in the serosal fluid during the incubation. Selenium transport across the ileum did not occur against a concentration gradient when selenite instead of selenate was present in the incubation medium. Sulfate and thiosulfate significantly inhibited ileal selenate transport. Decreasing the activity of the Na+,K+-ATPase, by the addition of ouabain, resulted in a significant reduction of concentrative selenate transport by the ileum. Furthermore L-leucine, but not D-glucose and D-galactose, significantly reduced selenium absorption by ileal sacs incubated with selenate. It is concluded from these results that selenate is transported actively by the ileal mucosa and that a common transport mechanism for selenate and sulfate exists. The Na+-gradient across the intestinal brush border membrane seems to be capable of energizing active ileal selenate transport.
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PMID:Active absorption of selenate by rat ileum. 403 68

1. ATP sulphurylases were partially purified (20-40-fold) from leaf tissue of Astragalus bisulcatus, Astragalus racemosus (selenium-accumulator species) and Astragalus hamosus and Astragalus sinicus (non-accumulator species). Activity was measured by sulphate-dependent PP(i)-ATP exchange. The enzymes were separated from pyrophosphatase and adenosine triphosphatase activities. The properties of the Astragalus ATP sulphurylases were similar to the spinach enzyme. 2. The ATP sulphurylases from both selenium-accumulator and non-accumulator species catalysed selenate-dependent PP(i)-ATP exchange; selenate competed with sulphate. The ratio of V(selenate)/V(sulphate) and K(m)(selenate)/K(m)(sulphate) was approximately the same for the enzyme from each species. 3. Sulphate-dependent PP(i)-ATP exchange was inhibited by ADP, chlorate and nitrate. The kinetics of the inhibition for each enzyme were consistent with an ordered reaction mechanism, in which ATP is the first substrate to react with the enzyme and PP(i) is the first product released. 4. Synthesis of adenosine 5'-[(35)S]sulphatophosphate from [(35)S]sulphate was demonstrated by coupling the Astragalus ATP sulphurylases with Mg(2+)-dependent pyrophosphatase; the reaction was inhibited by selenate. An analogous reaction using [(75)Se]selenate as substrate could not be demonstrated.
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PMID:Comparative enzymology of the adenosine triphosphate sulphurylases from leaf tissue of selenium-accumulator and non-accumulator plants. 437 98


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