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)

Sodium-potassium-activated adenosine triphosphatase (Na-K-ATPase) is associated with electrolyte transport in many tissues. To help delineate its role in intestinal transport, changes in rat intestinal electrolyte and water transport induced by injecting methylprednisolone acetate 3 mg/100 g or deoxycorticosterone acetate (DOCA) 0.5 mg/100 g per day for 3 days were correlated with changes in Na-K-ATPase activity. Methylprednisolone increased sodium and water absorption, potassium secretion, transmural potential difference, and Na-K-ATPase activity in the jejunum, ileum, and colon. Examination of isolated epithelial cells demonstrated that the jejunal and ileal increase in Na-K-ATPase occurred in both the villus tip and crypermeability, Mg-ATPase, and adenylate cyclase activities were unchanged by methylprednisolone. DOCA increased sodium and water absorption, potassium secretion, transmural potential difference, and Na-K-ATPase activity in the colon alone. Colonic Mg-ATPase and adenylate cyclase activities were unaffected. Jejunal and ileal enzyme activity, electrolyte transport, and permeability were unchanged by DOCA. Methylprednisolone and DOCA were not additive in their effect on colonic Na-K-ATPase activity. Methylprednisolone and DOCA increased electrolyte and water transport and Na-K-ATPase activity concomitantly in specific segments of small intestine and colon. These data are consistent with an important role for Na-K-ATPase in intestinal electrolyte and water transport.
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PMID:Na+-K+-activated adenosine triphosphatase and intestinal electrolyte transport. Effect of adrenal steroids. 12 64

The hypothesis that colchicine and vinblastine, which are commonly used for therapeutic purposes and known to cause diarrhoea, decrease intestinal water transport by inhibition of Na-K-ATPase activity was tested in rats. Net fluid transport by jejunal segments was measured four hours after intraperitoneal injection of either 0.15 M NaCl (0.5 ml/100 g), colchicine (0.5 mg/100 g b.w.), or vinblastine (1.0 mg/100 g b.w.). Colchicine and vinblastine decreased net fluid transport: 3.0 +/- 0.9 (SE) and 4.6 +/- 0.4 (SE) respectively, as compared to that transported by segments from rats injected with 0.15 M NaCl, 8.6 +/- 0.7 (SE) g fluid/hour/g. Methylprednisolone (3.0 mg/100 g b.w.) abolished the inhibitory effect of cholchicine and vinblastine on fluid transport. Colchicine and vinblastine were found to decrease significantly mucosal Na-K-ATPase activity, 18.2 +/- 4.9 (SE); 25.2 +/- 2.4 (SE) respectively, as compared to that measured in rats injected with saline 40.6 +/- 3.4 (SE) mumol/mg protein/hour. Pretreatment with methylprednisolone prevented the decrease in enzyme activity observed in rats injected with colchicine and vinblastine. The degree of inhibition in intestinal Na-K-ATPase activity was similar to that observed in fluid transport following colchicine and vinblastine. It is thus suggested that colchicine-induced inhibition of water transport is caused by inhibition of Na-K-ATPase activity, an effect which can be prevented by pretreatment with methyl-prednisolone.
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PMID:Effect of colchicine and vinblastine on rat intestinal water transport and Na-K-ATPase activity. 15 Mar 64

We measured the effect of pharmacological doses of glucocorticoid on piglet jejunal structure and function during acute viral diarrhea. Weaned piglets, infected experimentally with transmissible gastroenteritis virus, a coronavirus that induces a diarrheal illness similar to human rotavirus infection, received methylprednisolone (30 mg/kg) or saline intramuscularly at 48 and 72 h after infection; noninfected littermate controls were similarly injected with methylprednisolone. Animals were killed at 96 h, at the height of diarrhea, and jejunal epithelium was studied in vitro. Transmissible gastroenteritis, as expected, induced structural, enzyme, and Na transport abnormalities. Methylprednisolone did not affect small intestinal structure or function of noninfected control piglets. In transmissible gastroenteritis-infected piglets, jejunal villi were longer and glucose-facilitated Na absorption was greater after methylprednisolone than after saline treatment. Increased glucose stimulation of Na flux in vitro in the methylprednisolone-treated infected group was not attributable to enhanced Na+-K+-ATPase activity and occurred despite persistence of the virus within mucosal cells, shown by immunofluorescence microscopy. In this piglet model of viral diarrhea, early regeneration of absorptive surface that precedes recovery of disaccharidase function is accelerated by glucocorticoid therapy.
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PMID:Effect of glucocorticoid on piglet jejunal mucosa during acute viral enteritis. 283 16

In the isolated human lens, short circuit current was inhibited by pharmacological concentrations of 6-methylprednisolone and opacities occurred in the posterior subcapsular region in some lenses. The effect was seen only when the anterior (epithelial) surface of the lens was exposed. There was an increase of the short circuit current in the rabbit lens by 6-methyl-prednisolone and the lenses remained clear. Methylprednisolone effects were seen in spite of Na-K-ATPase inhibition by ouabain. Aldosterone had no effect on the translenticular potential difference, short circuit current and transparency. The data are discussed with respect to corticosteroid receptors in the lens epithelium and to the pathogenesis of steroid-associated cataract in man.
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PMID:Effect of corticosteroids on electrolyte transport of the isolated human and rabbit lens. 401 35

Studies were performed to determine relationships among Na+, K+-ATPase, the transmucosal Na+ gradient, and bile-acid transport in metabolically viable cells isolated from rat ileum. Incubation of cells with 0, 10(-6), 10(-5), 10(-4) and 10(-3) M ouabain resulted, respectively, in a 0, 10.3, 42.1, 97.0, and 100% decrease in glycocholate uptake and a 0, 10.7, 46.4, 76.8, and 100% decrease in Na+, K+-ATPase activity. Thus, one-half maximal inhibition of glycocholate uptake and Na+, K+-ATPase activity occurred at 5.5 x 10(-5) M and 1.7 x 10(-5) M ouabain, respectively. A change in glycocholate uptake was correlated with a change in Na+, K+-ATPase activity after daily injections of methylprednisolone. After 4 days treated animals showed a 26% and 36% increase in glycocholate uptake and Na+, K+-ATPase activity, respectively, over pair-fed saline-treated controls (p less than 0.001). Methylprednisolone did not significantly alter the activity of (Mg++)-ATPase when compared with controls (p greater than 0.05). Glycocholate uptake was reduced by the omission of Na+ from the incubation medium. Preincubation of cells at 37 degrees C with gramicidin D, 10 micrograms/ml, to alter membrane permeability to Na+, resulted in a significant rise in cell Na+ (p less than 0.01) and a significant fall in glycocholate uptake from values in untreated cells (p less than 0.01) to approach values for glycocholate uptake at 0 degrees C. These data suggest that Na+, K+-ATPase may play a role in a bile-acid uptake into ileal cells possibly by maintaining a Na+ electrochemical potential gradient for coupled Na+-bile-acid transport.
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PMID:Studies of relationship among bile-acid uptake, Na+, K+-ATPase, and Na+ gradient in isolated cells from rat ileum. 616 41

Thirty minutes after experimental spinal cord contusion (500 gm-cm) injury, cats were treated with an initial intravenous dose of either vehicle (V) or 30 mg/kg of Solu-Medrol sterile powder (methylprednisolone sodium succinate; MPSS). Two hours later, cats received a second intravenous injection of either V or 15 mg/kg MPSS, giving three treatment groups: V/V; MPSS/V; MPSS/MPSS. At 4 1/2 hours following injury of the cat lumbar spinal cord, the gray and white matter neurofilament protein content was reduced by over 70% within the injured segment of V/V-treated animals. The three major cat spinal cord neurofilament protein subunits of 200,000, 152,000, and 76,000 daltons were reduced in parallel by the injury. Treatment of cats with a single 30-mg/kg dose of MPSS (MPSS/V) provided a clear, although not significant, protection against neurofilament degradation compared with V/V-treated cats when measured at 4 1/2 hours after injury. The lactic acid content of the injured spinal cord segment at 4 1/2 hours after injury was significantly elevated in both V/V- and MPSS/V-treated cats, while the adenosine triphosphate (ATP) content, total adenylates, and energy charge were significantly reduced. The administration of a second intravenous 15-mg/kg dose of MPSS 2 hours after the initial 30-mg/kg dose (MPSS/MPSS) provided complete (p less than 0.01) preservation of neurofilaments within the injured spinal cord segment measured at 4 1/2 hours after injury. The levels of lactate, ATP, total adenylates, and tissue energy charge in MPSS/MPSS-treated cats were not different from those of uninjured spinal cords following laminectomy. The (Na+ + K+)-ATPase activity in the injured spinal segment was enhanced, although highly variable, in MPSS/V-treated animals. On the other hand, spinal cord enzyme activity was significantly and consistently elevated in the MPSS/MPSS-treated group. The results demonstrate that a 30-mg/kg dose of MPSS followed at 2 hours by a 15-mg/kg dose provides significantly better protection against injury-induced ischemia and Ca++-dependent neurofilament degradation than a single 30-mg/kg dose. These findings are in agreement with the spinal cord tissue pharmacokinetics and time-action characteristics of methylprednisolone observed in earlier studies.
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PMID:Effects of multi-dose methylprednisolone sodium succinate administration on injured cat spinal cord neurofilament degradation and energy metabolism. 653 14

The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K+/Mg+2 ATPase EC 3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings are determined in rat spinal cord at the early stage of trauma produced by a surgical clip on the thoracal 2-7 segments. The effect of treatment with intravenous methylprednisolone (MP) was evaluated the basis of these biochemical alterations and ultrastructural findings in the same model. The specific activity of the membrane bound enzyme Na(+)-K+/Mg+2 ATPase was promptly reduced in as early as ten minutes following spinal cord injury and remained at a level lower than the levels in the control group and in the sham-operated group. Methylprednisolone treatment immediately after the trauma attenuated the inactivation of Na(+)-K+/Mg+2 ATPase. On the other hand, there was significant difference in lipid peroxide content between the sham-operated and the injured animals. Methylprednisolone treatment reduced thiobarbituric acid reactive substance (TBARS) content in Group IV. We determined a positive relationship among membrane-bound enzyme Na+K+/Mg+2 ATPase activity, malondialdehyde (MDA) content and early ultrastructural changes in the traumatized and treated groups.
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PMID:Correlation of alterations on Na(+)-K+/Mg+2 ATPase activity, lipid peroxidation and ultrastructural findings following experimental spinal cord injury with and without intravenous methylprednisolone treatment. 756 28

Using Ehrlich ascites tumour cells, the short-term effects of the therapeutic glucocorticoid Methylprednisolone (MP) on the cellular energy metabolism were studied. ATP-consuming processes involved in the rapid MP effects were identified indirectly from the effects of MP on cellular oxygen consumption related to the inhibition of respiration by selective inhibitors of Ca(2+)-ATPase and protein synthesis. The effects of MP on plasma membrane permeability for Ca2+ ions and phospholipid turnover were studied directly by using confocal laser scanning microscopy and tracerkinetic measurements, respectively. MP inhibited cellular oxygen consumption, suppressed the inhibitory effect of lanthanum but not that of cycloheximide on oxygen consumption, blocked the [Ca2+]i rise in response to calcium ionophore A 23187, and decreased phospholipid turnover. MP acted instantly in a dose-dependent manner. The observed effects of MP are discussed in relation to the hypothesis that the drug has direct membrane effect affecting plasma membrane permeability and function.
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PMID:The influence of methylprednisolone on the energy metabolism of Ehrlich ascites tumour cells. 762 79

The short-term effects of high concentrations of Methylprednisolone (MP) on the energy metabolism of quiescent and Concanavalin A-stimulated rat thymocytes were investigated in vitro. Concanavalin A (ConA) stimulated the respiration rate of quiescent thymocytes by 35%. Addition of more than 0.15 mg MP/10(7) cells to ConA-stimulated cells reversed this respiratory stimulation; in addition, higher concentrations of MP caused a similar progressive decrease in the rate of respiration of both quiescent and ConA-stimulated cells. Similarly, the stimulation of respiration by ConA was greatly reduced in MP-treated cells. MP addition lowered cytoplasmic [Ca2+] and, at high concentrations, abolished the ability of ConA to increase [Ca2+]. Thus MP both reverses and prevents the immediate stimulation of thymocytes by ConA. In quiescent thymocytes, MP strongly inhibited that part of the oxygen consumption used to drive the cycle of Na+ influx across the plasma membrane and Na+ efflux on the Na+K(+)-ATPase, but did not inhibit oxygen consumption used to drive protein synthesis. In ConA-stimulated thymocytes MP had the same effects and also strongly inhibited oxygen consumption dependent on the cycle of Ca2+ influx across the plasma membrane and Ca2+ efflux on the Ca(2+)-ATPase, but had little effect on oxygen consumption used to drive RNA and DNA synthesis. These results show that MP prevents cation cycling in thymocytes (either by preventing cation influx or by inhibiting cation pumps) and prevents mitogenic stimulation of the cells. The high MP concentration required and the speed of onset of the effects (less than 30 s) provide strong evidence that these effects of MP are not mediated by glucocorticoid receptors and subsequent activation of gene expression. They may be caused by direct effects of MP on the properties of the plasma membrane. These effects are considered to be, at least partially, responsible for the beneficial results that currently have been obtained using MP megadoses in various clinical situations.
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PMID:Effects of methylprednisolone on the energy metabolism of quiescent and ConA-stimulated thymocytes of the rat. 768 56

The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K(+)/Mg(+2) ATPase EC.3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings were determined in rat brain at the acute stage of ischaemia produced by permanent unilateral occlusion of the middle cerebral artery (MCA). The effects of the pretreatment with intravenous high-dose methylprednisolone (MP) on these biochemical indices and ultrastructural findings were also evaluated in the same model. The rats were divided into four groups. In group I, 10 rats were used to determine Na(+)-K(+)/Mg(+2) ATPase activity and the extent of lipid peroxidation by measuring the malondialdehyde (MDA) content and normal ultrastructural findings. In group II on 20 rats, only subtemporal craniectomy was done in order to determine the effects of the surgical procedure on these indices and findings. This group was treated intravenously with saline solution before occlusion. In group III with MCA occlusion, saline solution was administered intravenously to 20 rats in the same amount of methylprednisolone used in group IV, ten minutes before the occlusion. In Group IV, a single high-dose (30 mg/kg) of methylprednisolone was administered intravenously, ten minutes before occlusion in 20 rats. After occlusion of the middle cerebral artery, Na(+)-K(+)/Mg(+2) ATPase activity was decreased promptly in the first ten minutes in the ischaemic hemisphere and remained at a lower level than the contralateral hemispheres in the same group and the normal levels in group I, during 120 minutes of ischaemia. A single dose methylprednisolone pretreatment prohibited the inactivation of Na(+)-K(+)/Mg(+2) ATPase. On the other hand, there was significant difference in malondialdehyde content between group I and group III. Malondialdehyde levels were significantly increased following ischaemia and a non-significant increase was observed in the contralateral hemisphere. Methylprednisolone treatment significantly decreased malondialdehyde content on the side of the ischaemic hemisphere. We conclude that there is a positive relationship between membrane-bound enzyme Na(+)-K(+)/Mg(+2) ATPase activity, malondialdehyde content and early ultrastructural changes in the treated group with MP. These data suggest that the pretreatment injection of high doses (30 mg/kg) methylprednisolone contribute to the protection of the brain from ischaemia with stabilization of the cell membrane by effecting the lipid peroxidation and the activation of Na(+)-K(+)/Mg(+2) ATPase.
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PMID:The effects of the pretreatment of intravenous high dose methylprednisolone on Na(+)-K(+)/Mg(+2) ATPase and lipid peroxidation and early ultrastructural findings following middle cerebral artery occlusion in the rat. 886 4


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