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)

Recent studies of rabbit colon have indicated the presence of a vanadate-sensitive K+-dependent proton pump, suggesting the existence of an H+-K+-ATPase. The participation of such a mechanism for colonic K+ absorption in the rat has not been determined. To this purpose, we attempted to detect the presence of pH-linked mechanisms for K+ absorption in rat distal colon using 86Rb as a marker for K+. We found that Rb+ absorption in Na-Ringer directly correlated with the in vitro partial pressure of CO2 (PCO2) in aldosterone-stimulated but not in control rats. Similar studies performed using Na-free Ringer demonstrated that PCO2 markedly augmented Rb+ absorption in both control and aldosterone-stimulated rat colon. Rb+ absorption was inhibited by orthovanadate, SCH28080, and mucosal ouabain in Na-free Ringer, but there was no effect of omeprazole, furosemide, or bumetanide. Barium applied to the serosa was also effective in inhibiting Rb+ absorption, suggesting that Rb+ exit from the cell was conductive. These findings are consistent with the presence of an active K+ pump that is activated by pretreatment with aldosterone and increased in vitro PCO2 and that is inhibited by orthovanadate, SCH28080, and mucosal ouabain. The constellation of findings suggests that participation of an ATPase that is not typical of either Na+-K+-ATPase or H+-K+-ATPase.
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PMID:Aldosterone and PCO2 enhance rubidium absorption in rat distal colon. 296 41

Hypoxia was induced by exposing rats to an atmosphere of 93% N2, 7% O2 for 4-48 hr. The animals became hypoxic as indicated by a decreased blood PaO2 (mean +/- SEM: 48 +/- 10 mm Hg). Hypoxia was accompanied by metabolic acidosis (pH 7.22 +/- 0.02) and decreased serum bicarbonate levels (9.0 +/- 4.0 meq/liter). Hypoxic rats also showed evidence of tissue hypoxia; liver tryptophan oxygenase levels were increased to 21 +/- 2 nmole/min/mg protein. In the hypoxic animals there was decreased jejunal mucosal (Na+-K+)-ATPase activity and an inhibition of active intestinal transport of sodium, glucose, 3-O-methylglucose, galactose, tyrosine, phenylalanine, and glycine as determined by in vivo perfusion studies. Jejunal fructose transport, which has a large passive component, was unaffected by hypoxia. The electrolyte, carbohydrate, and amino acid transport alterations produced by hypoxia were seen in the absence of an effect on jejunal cell number, DNA synthesis, or cell turnover. There was also no evidence of histological or ultrastructural damage. Furthermore, studies with a luminal macromolecular tracer, horseradish peroxidase, indicated that the jejunal lumen-to-blood barrier to macromolecules was also unaltered in these hypoxic animals. In vitro local oxygenation of the jejunum, by bubbling of 95% O2:5% CO2, markedly improved sodium and glucose (but not 3-O-methylglucose) absorption in hypoxic rats and control rats. The (Na+-K+)-ATPase activity of the jejunal mucosa of hypoxic rats was significantly enhanced by the local bubbling of 95% O2:5% CO2. Overall, our data indicate that during relatively mild conditions of hypoxia there is an inhibition of jejunal (Na+-K+)-ATPase activity and related transport processes that is prevented by in situ oxygenation.
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PMID:Alterations in jejunal transport and (Na+-K+)-ATPase in an experimental model of hypoxia in rats. 300 54

To evaluate the relative contributions of three possible mechanisms that can be advanced to explain the observation that hyperoxia decreases serotonin uptake by endothelial cells, we examined the effect of high O2 tensions on Na+-K+-ATPase activity, ATP content, and plasma membrane fluidity in cultured endothelial cells. Confluent monolayers of pulmonary artery and aortic endothelial cells were exposed to 95% O2 (hyperoxia) or 20% O2 (controls) in 5% CO2 at 1 ATA for 4-42 h. Exposure to high O2 tensions had no effect on Na+-K+-ATPase activity or ATP content in pulmonary artery or aortic endothelial cells in culture. However, hyperoxia decreased the fluidity of the plasma membrane of pulmonary artery and aortic endothelial cells in culture, and the time course for the decrease in fluidity parallels that of the hyperoxic inhibition of serotonin transport. These results indicate that hyperoxia decreases fluidity in the hydrophobic core of the plasma membranes of cultured endothelial cells. Such decreases in plasma membrane fluidity may be responsible for hyperoxia-induced alterations in membrane function including decreases in transmembrane transport of amines.
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PMID:Hyperoxia reduces plasma membrane fluidity: a mechanism for endothelial cell dysfunction. 300 28

The metabolic activation of the carcinogens N-nitrosobis(2-oxopropyl)amine (BOP) and N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine (HPOP) by Fischer rat and Syrian hamster hepatocytes was investigated in order to determine the existence of species differences in the induction of cell mutation. The conversion of BOP and HPOP into forms mutagenic to V79 cells was studied by using the hepatocyte-mediated mutagenicity assay. Mutations at the hypoxanthine:guanine phosphoribosyltransferase locus and the Na-K-ATPase locus were scored by the induction of 6-thioguanine resistance (TGr) or ouabain resistance (Ouar), respectively. Hepatocytes of both species were capable of converting BOP and HPOP to mutagens for V79 cells in a dose-dependent manner. Metabolism of BOP by rat hepatocytes resulted in higher mutation frequencies than that by hamster hepatocytes. At a BOP concentration of 240 microM, rat hepatocyte metabolism yielded 90.7 TGr mutants and 19.5 Ouar mutants per 10(5) V79 cells. At the same concentration, hamster hepatocyte metabolism of BOP yielded 54.1 TGr mutants and 13.0 Ouar mutants per 10(5) V79 cells. These results did not correlate with the known carcinogenic potency of BOP in the hamster as compared to the rat. Hamster hepatocytes carried out the catabolism of BOP to CO2 at faster rates than rat hepatocytes; therefore, the species difference in mutagenic activation was not due to a defect in BOP uptake or metabolism by hamster hepatocytes. In contrast, metabolism of HPOP by hamster hepatocytes resulted in significantly higher mutation frequencies than that by rat hepatocytes. At an HPOP concentration of 240 microM, hamster hepatocyte metabolism yielded 83.5 TGr mutants per 10(5) V79 cells; rat hepatocyte metabolism yielded only 19.8 TGr mutants per 10(5) V79 cells. This species difference in mutagenic activation correlated well with the known potency of HPOP as a carcinogen for the hamster as compared to the rat. Since hamster pancreatic cells and subcellular fractions are known to have very limited capacity to perform the metabolic activation of HPOP, the results of this study imply that liver metabolism plays an important role in the conversion of HPOP to an agent(s) which subsequently affects the hamster pancreas. The mutagenic potency of BOP versus HPOP was compared after metabolism by hepatocytes from both species. Following their metabolism by hamster hepatocytes, the two compounds were nearly equivalent in mutagenic potency. After metabolism by rat hepatocytes, BOP was significantly more potent mutagen than HPOP.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Species specificity in the metabolism of N-nitrosobis(2-oxopropyl)amine and N-nitroso(2-hydroxypropyl)(2-oxopropyl)amine to mutagens by isolated rat and hamster hepatocytes. 311 24

The possibility of a specific CO2 concentrating mechanism present in chloroplasts of C3 plants is analyzed. Proton gradient between thylakoids and the stroma is assumed to be the driving force for this process. The possible CO2 concentrating mechanisms are: 1. HCO3- permeation into thylakoids, its dehydration there and diffusion of CO2 formed into the stroma; 2. Dehydration of HCO3- present in the stroma at the thylakoid surface in a reaction with H+ leaving the thylakoids through: a) channels of membrane-bound carbonic anhydrase; b) channels of the ATPase complex. A system of equations describing CO3- and CO2 diffusion as well as CO2 assimilation and formation was used. The increase in photosynthesis rate, upon CO2 diffusion being facilitated in the presence of carbonic anhydrase, and due to the action of CO2 concentrating mechanisms, was numerically estimated. The CO2 concentrating mechanism was shown to function effectively only with the entire chloroplast being the CO2 concentrating zone. This is the case when the bulk of stromal carbonic anhydrase is localized near the inner chloroplast envelope. The existence of CO2 concentrating mechanisms around a single granum or around thylakoids is hardly possible. Approaches enabling the detection of similar concentrating mechanisms are discussed.
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PMID:Possible CO2 concentrating mechanism in chloroplasts of C3 plants. Role of carbonic anhydrase. 312 71

An inducible O-demethylating enzyme system was characterized from Clostridium thermoaceticum cultivated at the expense of syringate. Glucose and methanol, but not CO, partially repressed its expression. Induced whole cells catalyzed the carbon monoxide (CO)-dependent O demethylation of methoxylated aromatic compounds with the concomitant formation of acetate. Pyruvate and, to a lesser extent, H2-CO2 could replace CO in these reactions. KCN inhibited pyruvate-dependent activity but not the CO-dependent activity. The ATPase inhibitor N,N'-dicyclohexylcarbodiimide, the protonophore carbonyl cyanide m-chlorophenylhydrazone, and methyl viologen did not appreciably inhibit O demethylation by induced cells, whereas Triton X-100 was inhibitory. The enzyme system appeared to convert syringate sequentially to 5-hydroxyvanillate and gallate. The proposed overall reaction stoichiometry was as follows: syringate + 2CO + 2H2O----gallate + 2 acetates. Growth-supportive methoxylated aromatic compounds were O demethylated by syringate-cultivated cells and inhibitory to syringate O demethylation.
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PMID:Characterization of a CO-dependent O-demethylating enzyme system from the acetogen Clostridium thermoaceticum. 319 14

To study HCO3- secretion in rat distal colon, we utilized a technique that permits control of electrical and chemical transepithelial gradients. With symmetrical solutions (pH 7.4, [HCO3-] 25 mM, and CO2 tension 40 mmHg) bathing both tissue surfaces and under short-circuit conditions, HCO3- secretion remained stable for greater than 4 h at 1 mueq. h-1.cm-2. As the mucosal solution was alkalinized, the serosal solution was acidified at 3.1 mueq.h-1.cm-2. Ninety-four percent of serosal acidification was accounted for by the rate of metabolic lactic acid generation and transepithelial HCO3- secretion. Clamping transepithelial voltage reversibly affected net HCO3- secretion, and a linear relationship existed between clamped mucosal voltage and net HCO3- flux (r = 0.99); mucosal voltage of -68 mV completely inhibited net secretion. The apparent permeability coefficient of the colon to HCO3- is 2.8 X 10(-6) cm/s. One millimolar ouabain completely inhibited net HCO3- secretion. Acetazolamide (10(-4) M) inhibited secretion by approximately 50%, whereas a 10(-3) M concentration inhibited secretion by 90%. These data demonstrate that net colonic HCO3- secretion can be measured without imposed electrical and chemical gradients and that this flux is voltage sensitive and depends on carbonic anhydrase and Na+-K+-ATPase activities.
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PMID:Bicarbonate secretion in rat distal colon in vitro: a measurement technique. 334 82

1. A mechanical tissue chopper was used to obtain 35-75 mg explants from 21- to 28-day-old chick liver to determine assay conditions (substrates, buffers, time), regulators (metals and hormones) and points of endogenous regulation of de novo lipogenesis (ATPase, reductive potential and protein phosphorylation). High- and low-bicarbonate-based buffers (Earl's balance salts, EBSS and Hanks' balanced salts, HBSS; respectively) were used in conjunction with sources and types of bovine serum albumin (BSA), divalent cations (Mg2+ or Ca2+), substrate (glucose or acetate) and hormones (insulin and catecholamines). 2. Neither EBSS nor HBSS changed in vitro lipogenesis, CO2 or glucose production when 20 mM HEPES was added to these salts. 3. Neither the presence nor the source of BSA (Sigma or Armour) affected metabolism. In contrast, reducing the vessel reaction surface area (5.1 vs 10.5 cm2) decreased metabolic rates. 4. Acetate was more readily utilized than glucose as an in vitro fatty acid precursor. Use of glucose was complicated by production of glucose from endogenous precursors and by label recycling. Divalent cations (Mg2+ or Ca2+) had little affect upon lipogenesis. 5. Chicken insulin (50 ng/ml) did not affect lipogenesis; however, incorporation of acetate into fatty acids was decreased by dibutyryl cyclic AMP. A catecholamine-induced decrease in vitro lipogenesis indicates that major points of regulation are under control of phosphorylation-dephosphorylation steps.
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PMID:Measurement of glucose and lipid metabolism in avian liver explants. 342 27

The purpose of this study was to determine if the metabolic response to obesity and to pair feeding of obese Zucker rats to lean Zucker rats was similar across skeletal muscles. Oxidation of glucose, palmitate and isoleucine was studied in muscle strips in vitro using appropriate 14- carbon substrates as tracers. The plantaris muscle was subjected to histochemical analyses using an alkaline actomyosin ATPase, NADH-tetrazolium reductase and an oil red 0 stain. Soleus muscles from both ad libitum and pair fed obese rats oxidized less glucose to CO2, but released similar amounts of lactate when compared to the soleus muscles of lean rats. Oxidation of glucose was similar in the extensor digitorum longus (EDL) muscle of ad libitum fed obese rats, but lower when pair fed to the intake of lean rats. No differences were apparent in palmitate oxidation to CO2 or in incorporation into lipid (both soleus and EDL muscles), except in the EDL muscle of pair-fed obese rats which exhibited a higher rate for palmitate metabolism when compared with lean rats. Isoleucine oxidation to CO2 was higher in the EDL and plantaris muscles, but similar in the soleus muscle of ad libitum-fed obese rats when compared with lean rats. The magnitude of the difference in isoleucine oxidation was similar when the obese rats were pair fed. No differences in the percentage of plantaris muscle fibers sensitive to alkaline ATPase staining were observed. The plantaris muscle of obese rats, contained a higher proportion of oxidative fibers. These results indicate the great risk in generalizing about metabolic activity of the whole skeletal muscle mass based on observations made on one, or even two, distinct muscles in this animal model. Also, pair feeding of obese to lean Zucker rats did not result in uniform changes in metabolism between muscles of the obese rats.
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PMID:Metabolic characteristics of skeletal muscle from lean and obese Zucker rats. 345 May 49

Intracellular chloride activity (acCl) and serosal as well as mucosal membrane potentials (Vcs and Vcm) were recorded in surface epithelial cells (SEC) of frog gastric mucosa during the resting state (cimetidine, 10(-4) mol/l) or during stimulation with histamine (10(-4) mol/l). Stimulation leads to a fall in acCl from 18.7 SD +/- 5.9 mmol/l (n = 26) to 13.3 SD +/- 4.9 mmol/l (n = 33). Simultaneously both cell membranes hyperpolarize, Vcs from -56.0 SD +/- 4.8 (n = 42) to -62.8 +/- 7.6 (n = 43) and Vcm from -39.6 SD +/- 5.8 (n = 42) to -47.9 +/- 7.6 (n = 43), so that intracellular chloride remains elevated above electrochemical equilibrium at both cell membranes. Reduction or omission of chloride in the lumen perfusate does not affect acCl, suggesting that the luminal cell membrane is virtually tight for chloride ions. Current induced hyperpolarization of the serosal cell membrane potential which simulates the electrical effects of stimulation, does not affect acCl either; however, inhibition of gastric acid secretion by a benzimidazol derivative which is known to block the H+/K+ ATPase prevents the fall in acCl in response to histamine. The same holds if the experimental solutions are gassed with 25% CO2 which does not interfere with acid secretion but may block cell to cell communication via gap junctions.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Histamine reduces Cl- activity in surface epithelial cells of frog gastric mucosa. Suggestive evidence for ionic coupling between surface epithelial and oxyntic cells. 348 90


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