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)

It has been shown that, changes in the structure of the cardiac glycoside, are related to changes in their biological effects. In the present study we compared the effects of two structurally different digitalis compound (ouabain and ouabagenin), on K+ induced vascular relaxation as an index of the Na+K+ ATPase activity. Ouabain was the most potent compound tested, and had vasoconstrictor effect on the rat aortic rings, as, well as inhibitory effect on the K(+)-induced relaxation. Ouabagenin did not affect either the vascular tone or K(+)-induced relaxation. It is well known that changes in the part of the structure of the cardiac glycoside that contain the sugar, are important to maintain some of their biological effects. In this paper we demonstrate that elimination of the 1-rhamnose in ouabagenin reduces its vascular effects associated to the inhibition of the Na+ K+ ATPase pump.
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PMID:[The effects of digitalis compounds on K(+)-induced relaxation in aortic rings]. 772 85

We evaluated whether fish oil or vitamin E administration affected ethanol-induced changes in membrane ATPases. Male Wistar rats (225-250 g) were fed, through a gastric tube a liquid diet containing fish oil (25% of calories) and ethanol for one month. Another group of animals was given supplemental vitamin E (300 u/kg). In the pair-fed control animals, ethanol-derived calories were replaced with dextrose. The blood ethanol levels were maintained between 150 and 350 mg/dL. At sacrifice, the red cells were immediately washed with ice-cold saline, membranes were prepared and ATPases measured. These was no difference in the Na+K+ ATPase, Ca2+ ATPase and Mg2+ ATPase activities between the fish oil-dextrose and corn oil-dextrose groups. A decrease in Ca2+ ATPase and an increase in Na+K+ ATPase was seen with ethanol feeding; these change are similar to those seen in corn oil-ethanol fed rats. In contrast, Vitamin E administration prevented the ethanol-induced changes in ATPase. This observation provides support for the role of lipid peroxidation in alcohol-induced changes in cell membrane ATPase activities.
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PMID:Effect of fish oil and vitamin E on ethanol-induced changes in membrane ATPases. 805 50

The genetically obese Zucker rat (fa/fa) is an animal model with severe insulin resistance of the skeletal muscle. We investigated whether a defect of insulin-dependent glucose transporter (GLUT 4) translocation might contribute to the pathogenesis of the insulin-resistant state. fa/fa rats, lean controls (Fa/Fa) as well as normal Wistar rats were injected intraperitoneally with insulin and were killed after 2 or 20 min, respectively. Subcellular fractions were prepared from hind-limb skeletal muscle and were characterized by determination of marker-enzyme activities and immunoblotting applying antibodies against alpha 1 Na+/K+ ATPase. The relative amounts of GLUT 1 and GLUT 4 were determined in the fractions by immunoblotting with the respective antibodies. Insulin induced an approximately two-fold increase of GLUT 4 in a plasma membrane and transverse tubule enriched fraction and a decrease in the low density enriched membrane fraction in all three groups of rats. There was a high individual variation in GLUT 4 translocation efficiency within the groups. However, no statistically significant difference was noted between the groups. No effect of insulin was detectable on the distribution of GLUT 1 or alpha 1 Na+K+ ATPase. The data suggest that skeletal muscle insulin resistance of obese Zucker rats is not associated with a lack of GLUT 4 translocation.
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PMID:Insulin-induced translocation of GLUT 4 in skeletal muscle of insulin-resistant Zucker rats. 815 Feb 26

Hypertension is a complication of reflux nephropathy commonly occurring during adolescence and young adult life. We studied cellular sodium transport in an adolescent cohort with this condition as abnormal sodium transport is a feature of human hypertension. Thirty males and 52 females with reflux nephropathy, (median age 20.3 years) had erythrocyte ouabain sensitive sodium-potassium ATPase (Na/K ATPase) pump site number (Bmax) and red cell sodium concentration (RBC Na+) measured in 1988. Six years later, 55 of those had red cell sodium-lithium counter transport (LCT) measured. On both occasions, their renal function and blood pressure (BP) were determined. Bmax in the study group (median 10.3 nmol/l) was significantly less than that of controls (median 11.45 nmol/l). Nine patients who were diagnosed as having hypertension during the 6 year study period appeared to have a lower Bmax compared with that of normotensives in the group. RBC Na+ and LCT of the study group were not significantly different from that of controls. The Na/K ATPase activity is diminished, and sodium-lithium counter transport is unchanged in reflux nephropathy. Further study is needed to ascertain the link between these observations and the onset of high BP.
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PMID:Abnormalities of erythrocyte sodium transport in reflux nephropathy. 888 May 62

After massive small bowel resection, the intestine adapts to compensate. In addition to proliferation, enterocytes also undergo selective functional adaptation. In this study we examined the effect of intraperitoneal administration of epidermal growth factor (EGF) on the expression of the brush border dissacharidase sucrase, the sodium glucose cotransporter (SGLT1), and the sodium-potassium ATPase pump (NaK ATPase) by enterocytes in the remnant intestine after massive small bowel resection. Adult Lewis rats underwent either ileal transection or 70% proximal intestinal resection. These animals were subdivided into groups that received either saline or EGF intraperitoneally for 1 week. Ilea from each group were harvested 4 weeks postoperatively. Enterocytes were separated from these segments by calcium chelation. The total protein from the isolated cells was subjected to Western blot analysis. Administration of EGF to animals that underwent transection did not significantly alter the expression of sucrase, SGLT1, or NaK ATPase. After intestinal resection, the expressions of sucrase and SGLT1 were significantly increased. The combination of EGF administration and intestinal resection resulted in a further increase in SGLT1 expression. The intraperitoneal administration of EGF selectively enhanced the expression of SGLT1 by enterocytes after massive small bowel resection. Administration of EGF to sham-operated animals did not have similar effects. These results suggest that EGF augments the adaptive response and may therefore have a therapeutic role in the management of patients with short bowel syndrome.
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PMID:Epidermal growth factor selectively enhances functional enterocyte adaptation after massive small bowel resection. 907 Jan 88

The sodium-potassium ATPase (Na+/K+-ATPase or Na+/K+-pump) is an enzyme present at the surface of all eukaryotic cells, which actively extrudes Na+ from cells in exchange for K+ at a ratio of 3:2, respectively. Its activity also provides the driving force for secondary active transport of solutes such as amino acids, phosphate, vitamins and, in epithelial cells, glucose. The enzyme consists of two subunits (alpha and beta) each expressed in several isoforms. Many hormones regulate Na+/K+-ATPase activity and in this review we will focus on the effects of insulin. The possible mechanisms whereby insulin controls Na+/K+-ATPase activity are discussed. These are tissue- and isoform-specific, and include reversible covalent modification of catalytic subunits, activation by a rise in intracellular Na+ concentration, altered Na+ sensitivity and changes in subunit gene or protein expression. Given the recent escalation in knowledge of insulin-stimulated signal transduction systems, it is pertinent to ask which intracellular signalling pathways are utilized by insulin in controlling Na+/K+-ATPase activity. Evidence for and against a role for the phosphatidylinositol-3-kinase and mitogen activated protein kinase arms of the insulin-stimulated intracellular signalling networks is suggested. Finally, the clinical relevance of Na+/K+-ATPase control by insulin in diabetes and related disorders is addressed.
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PMID:Regulation of the Na+/K+-ATPase by insulin: why and how? 960 21

Cellular redox status and membrane protein activities were analyzed in kidneys from rats with ischemic acute renal failure (ARF). ARF was induced by clamping the left renal artery for 50 min. A parallel group of control animals was processed. In the ischemic group urea plasma levels were statistically increased as compared with the control group. Studies employing whole kidney homogenates revealed that ischemia produces an increment in lipid peroxidation levels and a reduction in glutathione concentration and in superoxide dismutase and glutathione peroxidase activities. Since lipid peroxidation may alter the function of membrane proteins we determined succinate cytochrome c reductase (SuccR), sodium-potassium ATPase (Na-K-ATPase), glucose-6-phosphatase (G-6-Pase) and alkaline phosphatase (ALP) activities in whole renal homogenates. Only G-6-Pase and ALP activities were modified by ischemia. Since ALP is a brush border membrane (BBM) enzyme and BBM is one of the main target structures in ARF, we assessed some parameters of BBM functionality. ALP, gamma-glutamyl transferase (gamma-GT) and 5'-nucleotidase (5'-NT) showed diminished activities in BBM from ischemic kidneys. Ischemia also modified the Vmax of paraaminohippuric acid (PAH) uptake without altering Km. An increment of lipid peroxidation and membrane fluidity in BBM was observed after the treatment. Total membrane proteins and protein recoveries in BBM were similar in both experimental groups. Sialic acid and sulfhydryl levels were similar in BBM from ischemic kidney and control ones. In summary, ARF induced by renal artery clamping for 50 min takes place with a significant increase in urea plasma levels. A decrease in the antioxidant defense system is detected. This induces lipid peroxidation in whole renal tissue, which may justify the diminished activities of some membrane enzymes such as G-6-Pase and ALP. A specific analysis of BBM function reveals a significant increment of lipid peroxidation which may be the cause of an increased membrane fluidity. This latter parameter might be, at least in part, responsible for the damaged function of apical ALP, 5'-NT, gamma-GT and PAH carrier.
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PMID:Impairment of cellular redox status and membrane protein activities in kidneys from rats with ischemic acute renal failure. 968 97

Resolution of pulmonary oedema is mediated by active absorption of liquid across the alveolar epithelium. A key component of this process is the sodium-potassium ATPase (Na+K+-ATPase) enzyme located on the basolateral surface of epithelial cells and up-regulated during oedema resolution. We hypothesised that lung liquid clearance could be further up-regulated by lipid-mediated transfer and expression of exogenous Na+K+-ATPase cDNA. We demonstrate proof of this principle in a model of high permeability pulmonary oedema induced by intraperitoneal injection of thiourea (2.5 mg/kg) in C57/BL6 mice. Pretreatment of mice (24 h before thiourea) by nasal sniffing of cationic liposome (lipid #67)-DNA complexes encoding the alpha and beta subunits of Na+K+-ATPase (160 microg per mouse), significantly (P<0.01) decreased the wet:dry weight ratios measured 2 h after thiourea injection compared with control animals, pretreated with an equivalent dose of an irrelevant gene. Whole lung Na+K+-ATPase activity was significantly (P<0.05) increased in mice pretreated with Na+K+-ATPase cDNA compared both with untreated control animals as well as animals pretreated with the irrelevant gene. Nested RT-PCR on whole lung homogenates confirmed gene transfer by detection of vector-specific mRNA in three of four mice studied 24 h after gene transfer. This demonstration of a significant reduction in pulmonary oedema following in vivo gene transfer raises the possibility of gene therapy as a novel, localised approach for pulmonary oedema in clinical settings such as ARDS and lung transplantation.
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PMID:Pretreatment with cationic lipid-mediated transfer of the Na+K+-ATPase pump in a mouse model in vivo augments resolution of high permeability pulmonary oedema. 1084 56

The protective effect of Nardostachys jatamansi (NJ) on neurobehavioral activities, thiobarbituric acid reactive substance (TBARS), reduced glutathione (GSH), thiol group, catalase and sodium-potassium ATPase activities was studied in middle cerebral artery (MCA) occlusion model of acute cerebral ischemia in rats. The right MCA of male Wistar rats was occluded for 2 h using intraluminal 4-0 monofilament and reperfusion was allowed for 22 h. MCA occlusion caused significant depletion in the contents of glutathione and thiol group and a significant elevation in the level of TBARS. The activities of Na(+)K(+) ATPase and catalase were decreased significantly by MCA occlusion. The neurobehavioral activities (spontaneous motor activity and motor coordination) were also decreased significantly in MCA occlusion group. All the alternations induced by ischemia were significantly attenuated by 15 days pretreatment of NJ (250 mg/kg po) and correlated well with histopathology by decreasing the neuronal cell death following MCA occlusion and reperfusion. The study provides first evidence of effectiveness of NJ in focal ischemia most probably by virtue of its antioxidant property.
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PMID:Protective effect of Nardostachys jatamansi in rat cerebral ischemia. 1247 70

The isoprenoid pathway produces 3 key metabolites: digoxin (membrane sodium-potassium ATPase inhibitor and regulator of neurotransmitter transport), dolichol (regulates N-glycosylation of proteins), and ubiquinone (free radical scavenger). The pathway was assessed in patients with human male infertility (oligospermia and decreased motility). It was also studied for comparison in patients with right hemispheric, left hemispheric, and bihemispheric dominance. The results of the study showed that the isoprenoid pathway was upregulated with increased digoxin synthesis in all 3 groups of patients. There was also a reduction in membrane Na(+)-K(+) ATPase activity and serum magnesium levels. There was an increase in tryptophan catabolites and a reduction in tyrosine catabolites. The dolichol and glycoconjugate levels increased and lysosomal stability was reduced with increased serum lysosomal enzymes in all 3 groups. The ubiquinone levels were low and free radicals increased. The cholesterol:phospholipid ratio increased and glycoconjugate was reduced in the membrane of these patients. This pattern correlated with those in right hemispheric dominance. The significance of these factors in the pathogenesis of human male infertility is discussed.
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PMID:Isoprenoid pathway dysfunction in human male infertility. 1262 48


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