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)

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

The mechanism of nickel transport by Clostridium pasteurianum was investigated by using 63NiCl2 and a microfiltration transport assay. Nickel transport was energy dependent, requiring either glucose or sucrose; xylose and o-methyl glucose did not support growth, butyrogenesis, or transport. Transport was optimum at pH 7 and 37 degrees C, and early-stationary-phase cells had the highest propensity for nickel transport. The apparent Km and Vmax for nickel transport approximated 85 microM Ni and 1,400 pmol of Ni transported per min per mg (dry weight) of cells, respectively. On the basis of metal specificity, nickel appears to be transported primarily by a magnesium transporter, although an alternative nickel transporter may also be involved. ATPase inhibitors (N,N'-dicyclohexylcarbodiimide, tributyltin chloride, 7-chloro-4-nitrobenz-2-oxa-1,3-diazole, and quercetin), protonophores (carbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophenol, and gramicidin D), metal ionophores (valinomycin, monensin, and nigericin), benzyl viologen, carbon monoxide, and oxygen inhibited nickel transport. Nickel transport was coupled indirectly to butyrogenesis and was dependent on the energy state of the cell.
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PMID:Energy-dependent transport of nickel by Clostridium pasteurianum. 333 82

Methane formation from acetate by resting cells of Methanosarcina barkeri was accompanied by an increase in the intracellular ATP content from 0.9 to 4.0 nmol/mg of protein. Correspondingly, the proton motive force increased to a steady-state level of -120 mV. The transmembrane pH gradient however, was reversed under these conditions and amounted to +20 mV. The addition of the protonophore 3,5,3',4'-tetrachlorosalicylanilide led to a drastic decrease in the proton motive force and in the intracellular ATP content and to an inhibition of methane formation. The ATPase inhibitor N,N'-dicyclohexylcarbodiimide stopped methanogenesis, and the intracellular ATP content decreased. The proton motive force decreased also under these conditions, indicating that the proton motive force could not be generated from acetate without ATP. The overall process of methane formation from acetate was dependent on the presence of sodium ions; upon addition of acetate to cell suspensions of M. barkeri, a transmembrane Na+ gradient in the range of 4:1 (Na+ out/Na+ in) was established. Possible sites of involvement of the Na+ gradient in the conversion of acetate to methane and carbon dioxide are discussed. Na+ is not involved in the CO dehydrogenase reaction.
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PMID:Bioenergetics of methanogenesis from acetate by Methanosarcina barkeri. 334 22

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

An open circuit kinetic model was developed to calculate the time course of proximal tubule cell pH, solute concentrations, and volume in response to induced perturbations in luminal or peritubular fluid composition. Solute fluxes were calculated from electrokinetic equations containing terms for known carrier saturabilities, allosteric dependences, and ion coupling ratios. Apical and basolateral membrane potentials were determined iteratively from the requirements of cell electroneutrality and equal opposing transcellular and paracellular currents. The model converged to membrane potentials accurate to 0.05% in one to four iterations. Model variables included cell concentrations of Na, K, HCO3, glucose, pH (uniform CO2), volume, and apical and basolateral membrane potentials. The basic model contained passive apical membrane transport of Na/H, Na/glucose, H and K, basolateral transport of Na/3HCO3, K, H, and glucose, and paracellular transport of Na, K, Cl, and HCO3; apical H and basolateral 3Na/2K-ATPases were present. Apical Na/H and basolateral K transport were regulated allosterically by pH. Apical Na/H transport, basolateral Na/3HCO3 transport, and the 3Na/2K-ATPase were saturable. Model parameters were chosen from data in the rat proximal tubule. Model predictions for the magnitude and time course of cell pH, Na, and membrane potential in response to rapid changes in apical and peritubular Na and HCO3 were in excellent agreement with experiment. In addition, the model requires that there exist an apical H-ATPase, basolateral Na/3HCO3 transport saturable with HCO3, and electroneutral basolateral K transport.
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PMID:Kinetic transport model for cellular regulation of pH and solute concentration in the renal proximal tubule. 358 Apr 82


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