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)

We have previously shown that red blood cell (RBC) filtrability in uncontrolled insulin dependent diabetics is abnormal compared to healthy subjects, but is corrected by insulin added in vivo or in vitro. We have now found biophysical abnormalities of the RBC membrane in such patients: Fluorescence polarization value (p) evaluated using DPH as probe is significantly lower in patients; insulin added in vitro increases and normalises the p value of diabetic RBC membrane, and has no effect on normal RBC membrane. As there is a relationship between the lipid bilayer and membrane cytoskeleton proteins, this abnormality of RBC membrane fluidity, correctable by insulin, may be an important determinant of the rheological behaviour of the RBC. In parallel, biochemical abnormalities of the RBC membrane are shown in the same patients: Higher cholesterol/phospholipid ratio, lower content in unsaturated fatty acids and higher content in saturated fatty acids. Decreased activity of ouabaine sensitive Na+K+ ATPase and increased activity of Mg++ ATPase. All of these RBC biochemical abnormalities are corrected after 24 h of normoglycaemia obtained by insulin treatment given in vivo with a biostator. Our results show the importance to check the degree of control of glycaemia when studying rheological parameters in diabetes mellitus.
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PMID:Rapid modifications of biophysical and biochemical parameters of red blood cell membrane from insulin dependent diabetics after insulin administration. 302 39

Slowing of nerve conduction, a hallmark of both experimental and human diabetic neuropathy, is improved or corrected by aldose reductase inhibitors such as sorbinil. Animal experiments suggest that a myo-inositol-related defect in nerve sodium-potassium adenosine triphosphatase (ATPase) is responsible for the acute reversible slowing of nerve conduction in diabetes mellitus. This myo-inositol-related defect is at present viewed as a cyclic metabolic defect. Aldose reductase inhibitors have been shown to restore to normal both the myo-inositol content and the sodium-potassium ATPase activity of nerve. This suggests that the acute effects of aldose-reductase inhibitors on nerve conduction in both diabetic animals and human patients may be modified by the correction of an underlying myo-inositol-related defect of nerve sodium-potassium ATPase. Furthermore, this myo-inositol-related defect may contribute to other biochemical, functional and structural abnormalities of diabetic peripheral neuropathy.
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PMID:Sorbitol, myo-inositol and sodium-potassium ATPase in diabetic peripheral nerve. 302 50

The (Na+-K+)ATPase and (Mg2+)ATPase activities of erythrocyte membranes of Type 1 (insulin-dependent) diabetic patients were found to be significantly reduced compared to matched controls (p less than 0.005). On the contrary, erythrocyte Na+ and K+ contents were similar in diabetic patients and in normal subjects. When erythrocyte membranes from diabetic patients were incubated with their own plasma, a significant increase was observed in sodium-potassium ATPase activity (p less than 0.005), whereas (Mg2+)ATPase activity was not affected. The plasma stimulatory effect showed saturation kinetics. Maximum average stimulation was 96% (+/- 21.3). A similar stimulation pattern, although more limited in extent (maximum 48.3% +/- 12.2), was found when erythrocyte membranes from normal subjects were incubated with diabetic plasma. Normal plasma exhibited a modest stimulatory effect on erythrocyte (Na+-K+)ATPase activity. Similar stimulatory effects by diabetic plasma were observed on a (Na+-K+) ATPase preparation from beef heart. It is proposed that diabetic plasma contains a specific (Na+-K+)ATPase activator in a higher concentration than normal plasma. This may explain why a normal cellular electrolyte content was found in diabetic erythrocytes in spite of a reduced Na+-K+ pump activity. Purification experiments indicate that the plasma activator is a protein with a molecular weight greater than 50,000. Both the (Na+-K+)ATPase activity and the stimulatory effect of diabetic plasma were not influenced by the metabolic control, since they did not correlate significantly with fasting blood glucose and daily insulin dosage. Moreover, no correlation was found with duration of diabetes or age at diagnosis of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Reduction of erythrocyte (Na+-K+)ATPase activity in type 1 (insulin-dependent) diabetic subjects and its activation by homologous plasma. 302 45

The activity of Na+K+ ATPase in the endothelium and smooth muscle of the aortae of normotensive and hypertensive rats was investigated. The enzyme activity in the endothelium and smooth muscle of the spontaneously hypertensive rats (SHR) was 2.15 +/- 0.48 and 12.98 +/- 0.99 respectively. These values were significantly lower (P less than 0.05) than the enzyme activity in the corresponding tissues (10.10 +/- 1.78 for endothelium, 20.77 +/- 2.54 for smooth muscle) of the normotensive Wistar Kyoto (WKY) rats. However, with the low blood pressure spontaneously hypertensive rats (LBP-SHR) i.e. in those animals whose blood pressures were below 150 mm Hg, the enzyme activity in both tissues was not significantly different from those of the WKY. Since Na+ K+ ATPase is coupled to the sodium-potassium pump whose activity affects the functions of other pumps, the results indicate that the development of high blood pressure in the SHR may be related to an alteration in the transport of cations across the cell membrane.
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PMID:Decreased Na+K+ATPase activity in the aortic endothelium and smooth muscle of the spontaneously hypertensive rats. 304 Mar 3

In recent years several different tests of cations in human cells have been studied to detect and to define possible roles in the development of essential hypertension. The goal of this report is to summarize what has been learned in genetic and epidemiological studies of human populations. The seven tests reviewed in greatest detail include sodium-lithium countertransport, intraerythrocytic sodium, sodium (or lithium)-potassium cotransport, lithium leak, sodium-potassium ATPase pump, sodium pump sites (ouabain binding), and circulating sodium pump inhibitor ('digoxin-like factor' in some studies). Countertransport, intraerythrocytic sodium and cotransport consistently show different values in hypertensives compared to normotensives and even in normotensives with a positive family history of hypertension when compared to controls without a positive family history. Thorough genetic studies have been carried out only for sodium-lithium countertransport and intraerythrocytic sodium. Both of these tests are highly heritable with a combination of both polygenic and major gene effects. Cotransport, leak, and pump sites also seem to be quite significantly heritable whereas the ATPase pump activity and the circulating pump inhibitor seem to be largely determined by nongenetic factors. Some of the most dramatic changes in these tests have been observed during pregnancy. Significant increases are seen in countertransport, cotransport, ouabain binding sites, and digoxin-like factor. Oral contraceptives also seem to affect at least cotransport. Plasma triglyceride level and body weight are some of the strongest correlates of countertransport, cotransport, and lithium leak. Cotransport increases with higher dietary sodium intake and decreases with the use of the diuretic medication. In the current developmental stage these tests have several significant limitations. In most population studies there is a considerable overlap of test values between persons with high and normal blood pressure. There are substantial variations in the methods used by different laboratories for the same tests. They are expensive, complex and usually must be done on fresh cells. There are conflicts between the results of several different reported studies that could be due to the way in which their subjects were selected, the effects of medications or other uncontrolled variables, or even due to the differences in laboratory methodologies.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetic and epidemiological studies on electrolyte transport systems in hypertension. 306 Feb 95

Inhibition of poly (ADP-ribose) synthesis by agents such as 3-aminobenzamide (3-AB) potentiates the cytotoxic, carcinogenic, and clastogenic effects of certain DNA-damaging agents. Experiments were carried out in Chinese hamster ovary cells to compare chromosome aberration production and cytotoxicity with the induction of somatic mutations at the hypoxanthine-guanine phosphoribosyltransferase (HGPRT) and sodium-potassium ATPase loci after treatment with 3-AB in combination with certain monofunctional alkylating agents. On its own, 1 to 10 mM concentrations of 3-AB were not mutagenic, reduced plating efficiencies only slightly, and produced a small elevation in the frequency of chromatid aberrations. In combination with ethyl methanesulfonate (EMS), 3-AB increased cytotoxicity and the frequency of alkylation-induced chromatid aberrations. 3-AB also increased the frequency of EMS and N-methyl-N'-nitro-N-nitrosoguanidine-induced 6-thioguanine-resistant cells (a marker for the HGPRT- phenotype). It had no effect on the frequency of EMS-induced ouabain-resistant cells (a marker for ATPase mutations). All the effects were dose dependent. Larger absolute increases were found with 10 mM 3-AB as compared with 1 mM 3-AB and with 2 mM EMS as compared to 1 mM EMS. The 3-AB-mediated increases in 6-thioguanine-resistant cells, which are often deletion mutations, and the lack of any increase in the frequency of ouabain-resistant cells, which can only arise through point mutation induction, along with the increases in chromosome aberration frequency, suggests that 3-AB increases the frequency of deletion mutations by increasing the frequency and duration of DNA strand breaks.
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PMID:Comutagenic effects of 3-aminobenzamide in Chinese hamster ovary cells. 397 24

Vitamin E is known to have an interaction with pyridoxine. To understand the functional significance of this interaction a study was carried out on the effect of simultaneous administration of vitamin E and pyridoxine on erythrocyte membrane Na+K+ ATPase activity. Adult male volunteers belonging to low socio-economic class with prior consent were used as subjects for the study. The results of the study have shown that administration of vitamin E alone brings about a transient increase in the total and ouabain insensitive Na+K+ ATPase. Administration of B6 along with vitamin E brought about an increase in the total and true Na+K+ ATPase activity. B6 administration alone showed a statistically insignificant increase in true ATPase activity. The results of the study are interpreted to show that administration of vitamin E along with B6 is beneficial to membrane function.
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PMID:Effect of simultaneous administration of vitamin E and pyridoxine on erythrocyte membrane Na+K+ ATPase activity. 609 64

Release of noradrenaline (NA) from isolated rat iris during perfusion in K+-free medium was confirmed. Direct biochemical measurement of different cation-activated ATPases did not reveal any definite relationship between Na+K+ ATPase and NA release. A significant increase in Ca++Mg++ ATPase activity was found on termination of NA release obtained by reintroduction of K+ to the medium. Criticism of the model for studying enzymatic control of transmitter release under physiological conditions is presented. It is suggested that removal of intracellular Ca++ ions by a calcium pump is directly associated with termination of transmitter release.
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PMID:The role of cation-activated ATPases in transmitter release from the rat iris. 625 6

Nerve conduction impairment in experimental diabetes has been empirically but not mechanistically linked to altered nerve myo-inositol metabolism. The phospholipid-dependent membrane-bound sodium-potassium ATPase provides a potential mechanism to relate defects in diabetic peripheral nerve myo-inositol-phospholipid metabolism, impulse conduction, and energy utilization. Therefore, the effect of streptozocin-induced diabetes mellitus and dietary myo-inositol supplementation on rat sciatic nerve sodium-potassium ATPase was studied. ATPase activity was measured enzymatically in sciatic nerve homogenates from 4-wk streptozocin diabetic rats and age-matched controls either fed a standard or 1% myo-inositol supplemented diet. The sodium-potassium ATPase components were assessed by ouabain inhibition or the omission of sodium and potassium ions. Diabetes reduced the composite ATPase activity recovered in crude homogenates of sciatic nerve. The 40% reduction in the sodium-potassium ATPase was selectively prevented by 1% myo-inositol supplementation (which preserved normal nerve conduction). Thus, in diabetic peripheral nerve, abnormal myo-inositol metabolism is associated with abnormal sodium-potassium ATPase activity. The mechanism of the effect of dietary myo-inositol to correct diabetic nerve conduction may be through changes in a sodium-potassium ATPase, possibly via changes in myo-inositol-containing phospholipids.
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PMID:Impaired rat sciatic nerve sodium-potassium adenosine triphosphatase in acute streptozocin diabetes and its correction by dietary myo-inositol supplementation. 630 4

Adenosine has been reported by several investigators to stimulate corneal deturgescence, but the actual biochemical mechanism of this effect remains unknown. Effects observed include increased magnitude and rate of corneal thinning, increased endothelial fluid transport rate, support of adenosine triphosphate (ATP) levels, stimulation of magnesium activated ATPase (Mg++ATPase) and sodium-potassium activated ATPase (Na+K+ ATPase) activities in endothelium whole cell preparations, but a lack of stimulation of Mg++ATPase and Na+K+ATPase activities in endothelial plasma membrane preparations. This study examined the possibility that adenosine alters the corneal endothelial levels of two biochemical effectors: adenosine 3',5'-cyclic monophosphate (cAMP) and guanosine 3',5'-cyclic monophosphate (cGMP). Bovine corneal endothelium was studied as fresh tissue and after growth in tissue culture. The samples were processed both at room temperature and in liquid nitrogen. Incubation of fresh and cultured endothelia in media containing adenosine was found to have no effect on the cAMP and cGMP levels regardless of the processing method. The data suggest that cyclic nucleotides do not mediate adenosine-stimulated corneal deturgescence.
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PMID:Null effect of adenosine on cyclic nucleotides of the corneal endothelium: possible implications for adenosine-stimulated corneal deturgescence. 632 99


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