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)

Ouabain-sensitive Na+-K+-stimulated ATPase was measured in red cell membranes using a spectrophotometric assay. The mean enzyme level in patients in the depressed state (1.2 nM/mg protein per min +/- 0.18 SEM) was lower lower than that in well-state patients (2.0 +/- 0.26) and hypomanic patients (2.4 +/- 0.31). Lithium treatment itself did not alter ATPase levels. Levels in patients in the well state were not significantly different from controls and thus ATPase does not constitute a "trait" marker for affective illness. Plasma cortisol level was higher in well-state patients (15.9 micrograms/dl +/- 1.46) than in controls (11.5 +/- 0.75). There were no significant differences in cortisol in these single morning samples during different mood states. Cortisol level correlated negatively with ATPase level in the total group of patients (r = 0.42, p less than 0.005), especially in those who were euthymic. These data indicate a relationship between cortisol and ATPase levels in affectively ill patients. Ouabain-sensitive NaK ATPase may be useful as an indicator of state in affective illness; plasma cortisol may be continuously elevated in some individuals with affective disorder.
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PMID:Red cell ouabain-sensitive Na+-K+-adenosine triphosphatase: a state marker in affective disorder inversely related to plasma cortisol. 629 47

Cortisol (0.28 mumol X L-1) applied to lobster (Homarus americanus) neuromuscular preparations produces a hyperpolarization in muscle fibers and an increase in amplitude of excitatory postsynaptic potentials. The effect appears to be surface-mediated, because of its rapid onset (within seconds). It is also Na+-K+ ATPase dependent, because ouabain blocks the effects. The effects are relatively short-lasting, and gradually subside within 15 min. The increase in excitatory postsynaptic potentials is attributed in part to increased quantal output of transmitter, and not to changes in muscle fiber membrane resistance. The effects of cortisol on neuromuscular transmission and membrane potential indicate that cortisol may have a physiological role in crustaceans.
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PMID:Lobster muscle and synapse respond to cortisol, a vertebrate hormone. 631 72

Changes in plasma cortisol and glucose concentration were studied in carp during acclimation from fresh water (FW) to 1.5% salt water and vice versa. There was an increase in cortisol and glucose concentration during acclimation from FW to salt water which lasted for several days. Reacclimation to FW did not cause clear changes in cortisol and glucose levels. One single injection of cortisol (0.2 mg/100 g or 1 mg/100 g) and additional transfer to salt water (1.5% for carp and 2.7% for tilapia) altered the changes caused by acclimation alone of cortisol, glucose, Na+ concentration, and the osmolality in plasma. Gill Na-K-ATPase activity was also influenced. The effects of cortisol on electrolyte concentrations during acclimation and on Na+-K+-ATPase activity differed in both types of fish. Cortisol clearly lowered the increase in plasma Na+ concentration of the stenohaline carp and increased the ATPase activity. The changes in plasma Na+ concentration of the euryhaline tilapia was not clearly altered and the enzyme activity was inhibited. The significance of these cortisol effects is discussed.
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PMID:The significance of cortisol for osmoregulation in carp (Cyprinus carpio) and tilapia (Sarotherodon mossambicus). 632

P-glycoprotein (P-gp) is a membranous ATPase responsible for the multidrug resistance (MDR) phenotype. Using membrane vesicles prepared from the highly resistant cell line DC-3F/ADX we studied the influence of P-gp ATPase activity of four progesterone derivatives which specifically bind to P-gp and reverse MDR. Progesterone and desoxycorticosterone stimulate P-gp ATPase activity with, respectively, apparent concentrations giving half-maximal activation of 20-25 microM and 40-50 microM, and activation factors of 2.3 (at 100 microM progesterone) and 1.8 (at 170 microM desoxycorticosterone). Hydrocortisone above 100 microM stimulates P-gp ATPase activity while corticosterone has no apparent stimulating effect. Our data are consistent with the location of the binding sites for the progesterone derivatives on the P-gp membranous domain. The effects of these steroids on verapamil-stimulated P-gp ATPase activity support a non-competitive mechanism, i.e. the binding sites for verapamil and steroids are mutually non-exclusive for P-gp ATPase modulation. A similar non-competitive inhibition of progesterone-stimulated P-gp ATPase activity by desoxycorticosterone or by corticosterone leads to the conclusion that these steroids, although sharing related structures, have distinct modulating sites on P-gp. As expected from their mutually non-exclusive interactions on P-gp, progesterone and verapamil when mixed induce a synergistic modulation of P-gp ATPase activity. Since drug transport by P-gp is believed to be coupled to its ATPase activity, a corresponding synergistic effect of these two modulators for the inhibition of P-gp-mediated drug resistance can be expected.
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PMID:Effects of steroids and verapamil on P-glycoprotein ATPase activity: progesterone, desoxycorticosterone, corticosterone and verapamil are mutually non-exclusive modulators. 871 80

The potential roles of growth hormone (GH) and insulin-like growth factor I (IGF-I) in seawater (SW) acclimation of juvenile Atlantic salmon (Salmo salar) were examined. Compared to controls, fish in 12 ppt seawater given one or three injections (2-6 days) of GH (ovine, 0.2 microgram.g-1) or IGF-I (recombinant bovine, 0.05-0.2 microgram.g-1) had significantly greater salinity tolerance as judged by lower plasma sodium, osmolality, and muscle moisture content following transfer to 34 ppt. Single injections of GH and IGF-I in fish in fresh water failed to improve salinity tolerance following transfer to 25 ppt SW. Treatment of fish in 12 ppt with GH or IGF-I for 2-6 days did not increase gill Na+, K(+)-ATPase activity, but treatment with GH prevented decreases in gill Na+, K(+)-ATPase activity that occurred in controls following transfer to 34 ppt seawater. Fish in fresh water administered GH by implants (5.0 microgram.g-1) or osmotic minipumps (0.5 micrograms.g-1 day-1) for 7-14 days had greater gill Na+, K(+)-ATPase activity and salinity tolerance than controls. IGF-I administered by implants (0.5-1.0 microgram.g-1) or osmotic minipumps (0.1 microgram.g-1 day-1) for 4-14 days did not increase salinity tolerance or gill Na+, K(+)-ATPase activity. Cortisol implants (50 micrograms.g-1) also increased gill Na+, K(+)-ATPase activity and salinity tolerance after 14 days, and in combination with GH had a synergistic effect, Although IGF-I and cortisol implants had no significant effect after 7 days, in combination they significantly increased gill Na+, K(+)-ATPase activity. The results indicate that GH and cortisol can increase salinity tolerance and gill Na+, K(+)-ATPase activity of Atlantic salmon and together act in synergy. Although IGF-I can increase salinity tolerance in short-term treatments (2-6 days) in 12 ppt, it is less effective than GH in increasing salinity tolerance and gill Na+, K(+)-ATPase activity in long-term treatments (7-14 days) and in interacting with cortisol.
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PMID:Effects of growth hormone and insulin-like growth factor I on salinity tolerance and gill Na+, K+-ATPase in Atlantic salmon (Salmo salar): interaction with cortisol. 871 39

To clarify the involvement of cortisol in functional differentiation of branchial chloride cells, cellular gene expression and localization of cortisol receptor were examined in chum salmon (Oncorhynchus keta) fry in freshwater (FW) and those adapted to seawater (SW) by in situ hybridization and immunocytochemical staining. Sodium-potassium adenosinetriphosphatase (Na+,K(+)-ATPase) activity in the whole gill homogenate was significantly higher in SW fish than in FW fish. There were no significant differences in plasma cortisol levels nor in the expression of cortisol receptor mRNA, examined by Northern blot analysis, between SW and FW fish. The receptor gene expression, examined by in situ hybridization with biotin-labeled synthetic oligonucleotide probe, and specific immunostaining with anticortisol receptor serum were found in two types of chloride cells distributed in the gill filaments and lamellae, which were also labeled with anti-Na+,K(+)-ATPase serum, indicating that cortisol may be one of the important factors regulating chloride cell functions. Gene expression of cortisol receptor in filament chloride cells, which were highly activated in SW-adapted fry, was significantly greater in the fry adapted to SW than in FW-adapted fry, reflecting their specific role in salt secretion in SW. Cortisol receptors were also present in undifferentiated cells in the interlamellar regions adjacent to the central venous sinus, also suggesting the involvement of cortisol in the functional differentiation of chloride cells.
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PMID:Localization of cortisol receptor in branchial chloride cells in chum salmon fry. 947 62

We analyzed muscle area in CT and muscle pathology in a patient with isolated ACTH deficiency who started with the difficulty of elevation of both arms. Cortisol treatment resulted in full recovery from severe muscle atrophy and contracture of major joints. Change of volume of major muscles in arm, thigh and calf was followed. Major muscles were identified in CT and the area of each muscle was calculated with computer assistance. The increase of total muscle area in sequential 3 times in CT was up to 74% after prednisolone treatment. This indicates that the deficiency of cortisol resulted in 42% reduction of muscle volume. This also suggests that reduction of muscle volume induces the limitation of range of motion of shoulder joint. ATPase of muscle biopsy revealed the influence on fiber type proportion; type 1 : type 2A : type 2B = 29.6 : 6.0 : 64.4% and 35.7 : 17.6 : 46.7% in pre-treatment and post-treatment of cortisol, respectively. Mean diameters of muscle fibers in type 1, type 2A and type 2B was 41.8, 41.8, 39.1 microns and 46.2, 44.0, 37.2 microns in pre-treatment and post-treatment of cortisol, respectively. These suggest that deficiency of glucocorticoid introduces the reduction of the activity of the motor neurons innervating type 1 and type 2A muscle fibers.
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PMID:[Muscle atrophy in isolated ACTH deficiency]. 978 7

Glucocorticoid levels increase greatly at the time of birth in humans and sheep, coinciding with an increased ability of the kidney to reabsorb sodium. Cortisol induces proximal tubule apical membrane Na+/H+ exchanger maturation in near-term fetal sheep. Proximal tubule salt transport is ultimately dependent on Na+ pump activity, so we studied the effects of cortisol treatment on renal cortical Na+-K+-ATPase. We first looked at six 140 day gestation fetal sheep (term is 145) and compared their renal cortical Na+-K+-ATPase to that of six 1-day-old lambs. Na+-K+-ATPase activity increased 80% after birth. Then nine pairs of twin fetal sheep were chronically instrumented at 127 days gestation. After 72 h recovery, one twin was given a 48-h continuous intraperitoneal infusion of cortisol. Both twins were then killed, and their renal cortices were studied. Na+-K+-ATPase activity increased 122% with cortisol treatment; activity equaled that of 1-day-old lambs. Protein abundance of the alpha1-subunit of the Na+-K+-ATPase increased 19%; the beta1-subunit increased 39% with cortisol treatment. mRNA abundance of the alpha1-subunit increased 58%; the beta1-subunit increased 72%. These results indicate that cortisol matures Na+-K+-ATPase activity.
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PMID:Role of glucocorticoids in the maturation of renal cortical Na+-K+-ATPase during fetal life in sheep. 1036 66

The yolk diameter of cortisol-treated tilapia (Oreochromis mossambicus) larvae, immersed in freshwater (FW) containing 10 mg L-1 cortisol from 48 h postfertilization to 12 d posthatching, was significantly larger than that of control larvae after 8 d of treatment, suggesting that inhibition on larval growth occurred only after a long-term treatment with cortisol. Tilapia embryos or larvae treated with 1-10 mg L-1 cortisol for 1-2 d and then transferred to 20-30 g L-1 seawater (SW) showed reduced cumulative larval mortality in SW compared with controls. Moreover, 4-5 d of cortisol treatments significantly diminished the degree of increase in larval body Na content after the transfer to SW. Significant effect of cortisol on body Na content of larvae occurred as early as 4-8 h after the transfer to SW, while no significant difference was found in the ouabain binding of yolk-sac epithelia between control and cortisol-treated larvae even 12 h after the transfer. Cortisol may be involved in the early phase of SW adaptation in developing larvae, and this mechanism may be achieved by other means than increasing the Na-K-ATPase of yolk-sac epithelia.
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PMID:Effects of cortisol on ion regulation in developing tilapia (Oreochromis mossambicus) larvae on seawater adaptation. 1043 77

We determined whether two naturally occurring steroids, cortisol and 17beta-estradiol (E2), can rapidly modulate the activity of an important membrane protein, human erythrocyte (RBC) Na+,K+-ATPase, an enzyme that does not bind either hormone directly. We also determined the membrane binding locations for cortisol and E2 and their effects on membrane molecular structure and fluidity. Direct application of both steroids to intact human RBC significantly altered maximum ouabain-sensitive 86Rb uptake within 5 min: Cortisol decreased it by 24%, whereas E2 increased it by 18%. As determined by small angle x-ray diffraction, these steroids occupied distinct time-averaged binding locations in the RBC membrane, cortisol localizing near the bilayer surface, 14-29 A from the bilayer center, and E2 localizing deep within the hydrocarbon core, 0-7 A from the bilayer center. Neither steroid significantly changed overall bilayer width or membrane fluidity. These data suggest that cell membrane protein function can be altered rapidly and differentially by naturally occurring steroids. This effect did not appear to be related to the different binding locations of the steroids in the membrane or to their influence on membrane fluidity.
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PMID:Rapid and opposite effects of cortisol and estradiol on human erythrocyte Na+,K+-ATPase activity: relationship to steroid intercalation into the cell membrane. 1050 40


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