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 elasmobranch rectal gland has served as a useful model to study features of Na-K-Cl cotransport that are common to many chloride-transporting epithelia. These include: (1) dependence on a Na+ gradient created by Na-K-ATPase; (2) high intracellular Cl- concentration; (3) characteristic inhibitor profile including inhibition by loop diuretics and barium but not by amiloride, SITS, DIDS, or carbonic anhydrase inhibitors; and (4) remarkable energy efficiency of transepithelial transport (25-30 NaCl/l 02). The mechanism by which this is accomplished is clarified by kinetic analysis of experiments with isolated perfused rectal glands of Squalus acanthias in which perfusate concentrations of Na and Cl are systematically varied. These show a Hill coefficient of one for Na+ and two for Cl-, suggesting that one Na+, one K+, and two Cl- interact with the cotransport carrier. Nitrate can substitute for Cl- to some extent, and it itself weakly transported. The loop diuretic bumetanide behaves like a competitive inhibitor of Cl-. The teleological significance of the neutral cotransport of two Cl- with one Na+ and one K+ is that it enables transporting epithelia like the rectal gland, cornea, salivary gland, and thick ascending limb of Henle's loop to double the efficiency of their Na-K-ATPase pump.
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PMID:Na-K-Cl cotransport in chloride-transporting epithelia. 241 26

Experimental alkali-burns rabbit corneas present a neovascularisation. Six weeks later the corneas have been processed for ATPase Cytochemistry, allowing the observation of Langerhans cells. We observed an increase in the number of Langerhans cells that was statistically significant in alkali-burned corneas when compared to unburned corneas in the peripheral and midperipheral cornea.
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PMID:[Langerhans cells and corneal neovascularization in experimental alkali burns]. 244 50

Activities of different enzymes (acid glycosidases, phosphatases, Na+ - K+ -dependent ATPase, proteases, dehydrogenases) and acid glycosaminoglycans were studied by histochemical methods in sections of rabbit anterior eye segments after experimental alkali burn and treatment with aprotinin, an inhibitor of plasmin and other serine proteinases. Solutions of sodium hydroxide (0.25-1.0 M) were applied on corneas using 12-mm-diameter plastic tube for 15-60 s. After wiping with cotton and rinsing with tap water aprotinin solutions were applied in saline (in experimental animals) and saline (in control animals) dropwise in 12-h intervals for a month. Within the first two weeks aprotinin was used at a concentration of 5000 IU/ml. During the subsequent two weeks the aprotinin concentration was reduced to 2500 IU/ml. Striking differences in enzyme activities and in the healing between treated and untreated eyes were found. Without aprotinin, ulcers developed in most corneas within 3 weeks and plasmin was regularly demonstrated in tears and in the aqueous. When aprotinin treatment was started within 24 h after the burn, the number of enzymatically active inflammatory cells was significantly lower, not only in the cornea itself but also in the whole anterior eye segment. With aprotinin treatment no ulcerations and no plasmin in tears and the aqueous were observed and the corneas healed within a month. The healing process started from the zone of enzymatically activated corneal cells in the unburned zone at the corneal periphery. In the regenerating epithelium and endothelium high activities of Na+ -K+ -dependent ATPase, gamma-glutamyltransferase, lactate and succinate dehydrogenases appeared very soon.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histochemical study of alkali-burned rabbit anterior eye segment in which severe lesions were prevented by aprotinin treatment. 247 20

The Na+, K+-ATPase pump site density on corneal endothelial cells from Fuchs' endothelial dystrophy corneas has been shown to be drastically decreased in end-stage disease (McCartney et al, Invest Ophthalmol Vis Sci 28:1955, 1987) and significantly increased in the early stages (Geroski et al, Ophthalmology 92:759, 1985) as compared to normal endothelium. In order to provide values for corneas between these two extremes, eye bank corneas from donors with no evidence of corneal edema but with guttata across the extent of the cornea were processed for autoradiography as well as immunohistochemistry. Pump site density was increased compared to end-stage disease but was less than values reported for either functional tissue or early stage disease. Similarly, immunohistochemistry results showed the amount of Na+, K+-ATPase antibody localization to be increased in respect to end-stage disease, but reduced as compared to functional tissue. These results suggest that pump site density on endothelial cells affected with Fuchs' endothelial dystrophy follows a gradual decline towards end-stage disease values as opposed to a sudden sharp deterioration after an initial increase.
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PMID:Moderate Fuchs' endothelial dystrophy ATPase pump site density. 254 44

Our studies, as reviewed here, clearly show that in the cornea, and possibly in other ocular tissues, arachidonic acid derivatives other than the classical PGs or the more recently discovered leukotrienes can be formed, and that at least some of the AA metabolites produced via the cytochrome P450 system have potent biological activities. In fact, two of these metabolites, 12(R)-HETE (compound C) and 12-hydroxyeicosatrienoic acid (compound D; Fig. 1), appear to be much more potent than classical PGs with respect to their effect on active ion transport systems, vasodilation, or the breakdown of the blood-aqueous barrier. The fact that 12(R)-HETE was found to be a potent inhibitor of Na+-K+-ATPase activity without appreciable vascular effects or effects on barrier permeability, while compound D was found to have a potent effect on the last two parameters without any influence on the first, suggests that products of the cytochrome P450 system are capable of inducing or modulating highly specific functions.
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PMID:Novel cytochrome P450-dependent arachidonic acid metabolites and their ocular effects. 255 70

The authors compared on the rabbit eye the tolerance of hydrophilic contact lenses with equal parameters (0.2 mm central and peripheral thickness, 7.4 radius, 15 mm diameter) with a different degree of hydration (37% H2O-Hema), (55% and 65% H2O-Hema-Degma) during continuous wear for a period of two weeks (1, 2, 3, 4, 7 and 14 days). Special attention was devoted to changes in the transparency of the cornea. Changes of the transparency due to wearing of contact lenses were due to changes of corneal hydration. The cause of increased corneal hydration were metabolic and later also morphological disorders in the corneal endothelium. The activity of Na+-K+-dependent adenosine triphosphatase and gamma-glutamyl transferase were reduced, followed by a change in the shape and size of endothelial cells. Later the activities of both enzymes were reduced also in the epithelium. Keratocytes had reduced alkaline phosphatase and gamma-glutamyl transferase activities. The staining properties of glycosaminoglycans in the stroma remained, however, unaltered, similarly as the activity of acid glycosidases and other investigated lysosomal enzymes. The onset of increased corneal hydration caused by a disorder of the active water ion transport and of metabolites in the cornea depended on the percentage of water in hydrophilic contact lenses. It was observed latest after application of contact lenses with 65% water.
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PMID:[Comparison of tolerance to hydrophilic contact lenses made of Hema (37% H2O) and Hema-Degma (55%, 65% H2O) in the rabbit eye. I. Changes in corneal transparency due to disturbed hydration]. 257 15

The etiology of keratoconus is still unclear. This study presents a new clinical sign, Thalasselis' syndrome, defined as: an association between keratoconus, magnesium deficiency, type-A behavior and allergy. Also, it introduces the hypothesis that magnesium deficiency could affect pathologically the osmotic mechanism of the cornea, specifically the Na-K and/or Ca-ATPase pumps; the collagen structure by alteration of the adenylate cyclase activity; and other mechanisms as well. Furthermore, we propose the Thalasselis' syndrome is compatible with previous theories on keratoconus. In addition to the other therapeutic measures, such as contact lenses and keratoplasty, this study suggests a clinical, nutritional, psychological, and immunological treatment for keratoconic patients.
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PMID:Thalasselis' syndrome and other theories on keratoconus. 258 91

When corneal microsomes were incubated with arachidonic acid in the presence of an NADPH-generating system, four polar metabolites (compounds A-D) were formed. Synthesis of these metabolites could be inhibited by carbon monoxide, SKF 525A, and anti-cytochrome c reductase antibodies. One of the metabolites, compound C, was found to inhibit partially purified Na+,K+-ATPase from the corneal epithelium in a dose-dependent manner with an ID50 of approximately 50 nM. After compound C was purified by TLC and HPLC, it was found to have a UV absorption spectrum with a maximum absorbance at 236 nm suggesting the presence of a conjugated diene. Mass spectrometric analysis using positive- and negative-ionization modes was carried out on derivatized compound C that had been synthesized from a mixture of specifically labeled ([5,6,8,9,11,12,14,15-2H8]arachidonic acid) and unlabeled arachidonic acid. Abundant fragment ions were consistent with compound C being a monooxygenated derivative of arachidonic acid with a hydroxyl substituent at carbon-12 of the icosanoid backbone; all deuterium atoms from [2H8]arachidonate were retained in the structure. Oxidative ozonolysis yielded products indicating double bonds between carbons at positions 10 and 11 and positions 14 and 15 of the 20-carbon chain. Compound C was, therefore, characterized as a 12-hydroxyicosatetraenoic acid. However, only 12(R) isomer was found to be an inhibitor of the Na+,K+-ATPase from the corneal epithelium, suggesting that the biologically active compound C was 12(R)-hydroxy-5,8,10,14-icosatetraenoic acid. Such an inhibitor of Na+,K+-ATPase synthesized in the cornea may have an important role in regulating ocular transparency and aqueous human secretion.
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PMID:12(R)-hydroxyicosatetraenoic acid: a cytochrome-P450-dependent arachidonate metabolite that inhibits Na+,K+-ATPase in the cornea. 282 78

Cells of the thick ascending limb of the loop of Henle (TALH) metabolize arachidonic acid (AA) via the cytochrome P450 monooxygenase system to biologically active products that are resolved into two peaks, P1 and P2, on reverse-phase HPLC. Each peak contains materials that have characteristic biological activity. P1 contains a material that relaxes blood vessels and is structurally similar to a vasodilator, the 5,6 epoxyeicosatrienoic acid (EET). P2 contains a material that inhibits cardiac Na+-K+-ATPase, the major component of which has been identified as the 11,12 dihydroxyeicosatrienoic acid. In mTALH cells obtained from rabbits made hypertensive by aortic coarctation, there was a selective increase in P1 and P2 formation compared to other renomedullary cells. We have identified AA metabolites in bovine corneal epithelium with biological properties and chemical features similar to those of mTALH cells. 12(R)hydroxyeicosatetraenoic acid (12(R) HETE) a possible derivative of the 11,12-EET, is produced by the cornea and also has been shown to inhibit Na+-K+-ATPase activity. Renal microsomes obtained from spontaneously hypertensive rats (SHRs) also metabolize AA via a cytochrome P450 monooxygenase pathway to three principal biologically active metabolites that are formed in increased amounts during the developmental phase of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Novel renal arachidonate metabolites. 283 48

Epithelial sheets from the limbus, cornea, and third eyelid of Hereford and non-Hereford cattle were examined for the presence of Langerhans cells (LC) using the membrane enzyme ATPase as a marker for LC. The aim of the study was to test the hypothesis that differences in LC density exist between the various ocular epithelia of these animals producing depressed immune surveillance in the case of Hereford cattle. The presence of LC in ocular tissues was confirmed by parallel studies which detected epithelial cells bearing T6, an antigen expressed by human LC. Studies using serial sections demonstrated that T6+ cells also reacted with an anti-human HLA-DR monoclonal antibody. The detection of T6+, DR+ and ATPase+ cells in ocular epithelium in the absence of infiltrating macrophages suggested that LC are present in these tissues. While there were no significant differences in the density of T6+ cells between non-Hereford and Hereford cattle, in the latter ATPase+ cells were significantly fewer in the lateral, medial, and upper limbus.
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PMID:Differential distribution of ATPase- and T6-positive cells (Langerhans cells) in the limbus and cornea of Hereford and non-Hereford cattle. 295 Jun 48


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