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Results for “AMMONIUM CHLORIDE”

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PubMed1987

Gastrocystoplasty and colocystoplasty in canines: the metabolic consequences of acute saline and acid loading.

An experimental canine model was developed to quantitate the net transmural ion flux of colon and gastric segments used for augmentation cystoplasty. Gastrocystoplasty (4) or colocystoplasty (4) was constructed in 8 female mongrels. Acute intravenous saline and acid loading experiments were performed 2 to 4 weeks after cystoplasty. The mean solute excretion rates for sodium, chloride, phosphorus and ammonia exhibited opposite trends during acute saline and acid loading in this experimental model. The net flux of chloride, ammonia, phosphorus and sodium ions in the colocystoplasty animals was from the mucosa/urine surface to the serum (reabsorption). The opposite trend was true for the gastrocystoplasty. By not reabsorbing ammonium chloride, the gastrocystoplasty preserved an important renal mechanism for systemic acid elimination. This may help to prevent the hyperchloremic metabolic acidosis that can develop when urine comes in contact with small or large bowel segments.

Acid-Base Equilibrium↗

PubMed1976

Uptake of diphtheria toxin and its fragment A moiety by mammalian cells in culture.

Evidence suggesting that diphtheria toxin reaches the cytoplasm of susceptible mammalian cells by two independent mechanisms is presented. A schematic model describing the two processes of toxin entry into the cell is developed. One process of toxin uptake considered to by physiologically significant is passage of the protein toxin through the plasma membrane. This most likely happens by binding of fragment B to receptors on the membrane and by subsequent toxin-membrane interaction so that ultimately fragment A, the enzymatically active moiety, is transported tothe cell interior. This process, which ultimately leads to cessation of protein synthesis and cell death, involves a comparatively small number of toxin molecules. A second mechanism of toxin uptake is by classical pinocytosis. The majority of toxin taken into the cell is accomplished by this process. The fate of toxin taken into HEp-2 cells via pinocytosis is proteolysis by lysosomal enzymes. Thus, such vesicle-bound toxin is ordinarily not expressed biologically. Evidence suggesting that ammonium chloride provides total protection to diphtheria toxin-susceptible cells by preventing entry of toxin by the specific receptor-associated process is also provided; data showing that the ammonium salt immobilizes bound toxin on the plasma membrane of HEp-2 cells are presented. Finally, it is suggested that actively endocytic cells such as guinea pig macrophages interact with toxin in a significantly different manner than do nonphagocytic cells.

Ammonium Chloride↗

PubMed1976

Oxygen requirement for acetylene reduction by pure cultures of rhizobia.

The oxygen and nutritional requirements for acetylene reduction by Rhizobium japonicum and Rhizobium sp. in liquid culture are described. The optimal oxygen concentration was about 0.1% in the gas phase, which is lower than that of any other known aerobic nitrogen-fixing microorganism. these organisms are also unique in that nitrogenase synthesis is not repressed in the presence of ammonium chloride under certain cultural conditions, in contrast to other wild-type bacteria.

Acetylene↗

PubMedDate not supplied

[Evaluation of the arterial share of portal flow using a scintigraphic technique in patients with liver cirrhosis. Correlations with other parameters of portal hypertension].

This study aimed to measure in semiquantitative terms the arterial-venous ratio of the portal flow using a scintigraphic technique, by means of a simple intravenous injection of a 99mTcDiethylHIDA bolus, a method which was found to be extremely simple and non-invasive, with a good degree of repeatibility. The percentage of arterialisation of the portal flow was found to be higher in cirrhotic patients compared to non-hepatopathic subjects, and among cirrhotic patients it was correlated with the severity of disease, the presence and degree of esophageal varices, and the presence of porto-systemic shunts, assessed using the ammonium chloride test.

Adult↗

PubMed1981

Chromatography of human leukocyte interferon on controlled pore glass.

Human leukocyte interferon (HuIFN-alpha ) was adsorbed on controlled pore glass (CPG) beads in 0.01 M potassium phosphate, pH 7.2. Partial recovery fo HuIFN-alpha from CPG, ranging from 50% to 75%, was obtained with ethylene glycol (6.8 M), ammonium chloride (1.0 M) and Tris.HCl (1.0 M). A near complete recovery (90%) was obtained with potassium phosphate (1 M), but there was no selectivity in the elution vis á vis other proteins. An efficient elution of HuIFN-alpha was accomplished with tetramethyl-, and tetraethylammonium chlorides: the recovery of HuIFN-alpha was complete at low concentrations (0.25 M to 0.50 M) of these salts at pH 8.0 and the elution of interferon was more selective than with other eluants.

Ammonium Chloride↗

PubMed1992

Newly synthesized class II MHC chains are required for VSV G presentation to CTL clones.

Mechanisms of antigen processing and presentation to thymus-derived lymphocytes have been under intense study for several years, focusing on both Class I-restricted antigen presentation and Class II-MHC restricted responses. The studies described here examine the processing and presentation of exogenously provided soluble glycoprotein of the vesicular stomatitis virus and as well as newly synthesized viral glycoprotein. Evidence is provided that newly synthesized Class II MHC chains are required for cell surface expression of processed glycoprotein determinants irrespective of the origin of the viral antigen. Inhibitors of distinct cellular processes, including ammonium chloride, emetine, and Brefeldin A, have been used to dissect the pathways utilized.

Ammonium Chloride↗

PubMed1982

Methylamine uptake in Pseudomonas species strain MA: utilization of methylamine as the sole nitrogen source.

The uptake of methylamine as the sole nitrogen, but not carbon, source by Pseudomonas sp. strain MA was investigated. Under these growth conditions, a high-affinity, low-capacity uptake system was present having a Km of 16 microM and Vmax of 2 nmol.min-.mg (dry weight) of cells that was competitively inhibited by ammonium chloride. The transport system was induced by growth on succinate with methylamine as the sole nitrogen source.

Ammonium Chloride↗

PubMed2006

Vanadium recovery from oil fly ash by leaching, precipitation and solvent extraction processes.

In order to reduce the environmental impact due to land disposal of oil fly ash from power plants and to valorize this waste material, the removal of vanadium was investigated using leaching processes (acidic and alkaline treatments), followed by a second step of metal recovery from leachates involving either solvent extraction or selective precipitation. Despite a lower leaching efficiency (compared to sulfuric acid), sodium hydroxide was selected for vanadium leaching since it is more selective for vanadium (versus other transition metals). Precipitation was preferred to solvent extraction for the second step in the treatment since: (a) it is more selective; enabling complete recovery of vanadate from the leachate in the form of pure ammonium vanadate; and (b) stripping of the loaded organic phase (in the solvent extraction process) was not efficient. Precipitation was performed in a two-step procedure: (a) aluminum was first precipitated at pH 8; (b) then ammonium chloride was added at pH 5 to bring about vanadium precipitation.

Aluminum↗

PubMedDate not supplied

[Gastric emptying and metabolic acidosis. III. Study of gastric retention of a sodium citrate solution using an experimental model of metabolic acidosis in rats].

The gastric emptying of sodium citrate solution 0.25 mEq/ml was studied in rats with metabolic acidosis induced by orogastric infusion of 0.5 M ammonium chloride solution. Two control groups were used: one infused with 0.5 M sodium chloride and the other with water. The 3 solutions content was 2 ml/100 g weight of the animal. Six hours after the infusion, there was a moderate metabolic acidosis in the group with ammonium citrate. This 6 hour interval marked the beginning of the gastric emptying study. The test meal (sodium citrate 0.25 mEq/ml) was utilized containing 6 mg% red fenol as a marker. The gastric emptying of sodium citrate was studied at 5, 10, 20 and 30 minutes after the infusion, and the results showed no differences between the 3 groups. The data suggest that the duodenal receptors to pH were more effective do determine the pattern of gastric response than the acidosis.

Acid-Base Equilibrium↗

PubMed1982

Pulmonary oxygen toxicity: possible role of ammonia in desorbing lung surfactant.

A porous membrane has been synthesized from a fine-weave cotton fabric carboxylated to simulate the fixed negative charges in the alveolar wall. When this membrane is treated with pulmonary surfactant in physiological concentrations, especially DPL, it loses its fluid permeability and can support a pressure of physiological saline of over 272 torr without bursting through. When the saline is replaced by isotonic ammonium chloride solution, the average penetration pressure is reduced to 187 torr. This is discussed in relation to the known production of ammonia upon hyperbaric exposure (1) and the competition of the resulting positive ammonium ions for the negative sites on the alveolar wall previously occupied by the positive quaternary ammonium ions of the effectively cationic lung surfactant. Successful replacement must then promote edema formation. This is put forward as a possible mechanism for the indirect (blood-borne) effect of oxygen upon the lung. It offers possible explanations for the potentiation of pulmonary oxygen poisoning by higher partial pressures or higher molecular weights of the inert gases present and the finding that increased permeability of epithelium precedes edema formation (18).

Ammonium Chloride↗

PubMed1999

Adenovirus cellular receptor site recirculation of HeLa cells upon receptor-mediated endocytosis is not low pH-dependent.

HeLa cells were depleted of 75% of the available adenovirus type 2 specific cellular receptor sites (CRSs) by controlled attachment of viruses at a high multiplicity of infection. Upon removal of unattached viruses and further incubation, the cells were able to recycle the CRSs to 75% of the level of uninfected control cells within 5 h. The rate of virus receptor recycling was approx. 1 CRS x min-1 x cell-1. The existence of receptor recycling further strengthens the involvement of a total process of receptor-mediated endocytosis in adenovirus internalization. The recirculation process was neither affected by the lysosomotropic agents ammonium chloride and amantadine-HCl, nor by the ionophore monensin or the multifunctional weak-base amine chloroquine.

Adenoviruses, Human↗

PubMed1997

pH-dependent perforation of macrophage phagosomes by listeriolysin O from Listeria monocytogenes.

The pore-forming toxin listeriolysin O (LLO) is a major virulence factor implicated in escape of Listeria monocytogenes from phagocytic vacuoles. Here we describe the pH-dependence of vacuolar perforation by LLO, using the membrane-impermeant fluorophore 8-hydroxypyrene-1,3,6-trisulfonic acid (HPTS) to monitor the pH and integrity of vacuoles in mouse bone marrow-derived macrophages. Perforation was observed when acidic vacuoles containing wild-type L. monocytogenes displayed sudden increases in pH and release of HPTS into the cytosol. These changes were not seen with LLO-deficient mutants. Perforation occurred at acidic vacuolar pH (4.9-6.7) and was reduced in frequency or prevented completely when macrophages were treated with the lysosomotropic agents ammonium chloride or bafilomycin A1. We conclude that acidic pH facilitates LLO activity in vivo.

Ammonium Chloride↗

PubMed1992

Stimulation of monooxygenation and conjugation after liver transplantation in the rat: involvement of Kupffer cells.

The success rate of liver transplantation has improved markedly during the last few years and, although this patient population receives multiple drug therapies, the effect of liver transplantation on drug metabolism has been studied very little. Therefore, the purpose of this study was to assess the metabolism of model drug substrates after liver transplantation in the rat. Rat livers were stored for 4 hr in cold Euro-Collins solution, transplanted orthotopically, and then perfused 2 hr later with oxygenated Krebs-Henseleit buffer, using a nonrecirculating system. Rates of monooxygenation of the model compound p-nitroanisole, conjugation of p-nitrophenol, and uptake of oxygen were measured. All parameters studied were elevated significantly, by nearly 2-fold, by transplantation. Specifically, monooxygenation was increased from 2.9 +/- 0.2 to 5.1 +/- 0.4 mumol/g/hr, conjugation was elevated from 3.3 +/- 0.6 to 7.7 +/- 0.1 mumol/g/hr, and O2 uptake was stimulated from basal values of 114 to 197 mumol/g/hr. Transplantation did not, however, alter rates of monooxygenation and conjugation in isolated microsomes supplemented with excess cofactor. When donor rats were pretreated with the Kupffer cell toxicant gadolinium chloride (10 mg/kg, intravenously) 30 hr before liver storage, the elevation after transplantation in all parameters studied was prevented. Depletion of carbohydrate reserves by fasting of donor rats did not prevent stimulation of monooxygenation and conjugation. On the other hand, urea synthesis from ammonium chloride, a process dependent on mitochondrial NADPH, was increased and monooxygenation was diminished after transplantation, suggesting the involvement of mitochondria in this phenomenon. Indeed, mitochondria isolated 2 hr postoperatively exhibited significantly elevated respiratory control ratios and higher state 3 rates of respiration. Taken together, these data support the hypothesis that Kupffer cells, activated by transplantation, release mediators that stimulate mitochondria in parenchymal cells and enhance drug metabolism by increasing cofactor supply (e.g., NADPH for monooxygenation and UDP-glucuronic acid for glucuronidation).

Ammonium Chloride↗

PubMed1990

Internalization of the cytotoxic molecules of T101 F(ab')2-(ricin-A-chain) immunotoxin into human T-leukemic cells.

We have investigated the internalization step of an immunotoxin and its relationship with cytotoxicity, with the F(ab')2-T101(ricin-A-chain) immunotoxin, directed against the CD5 antigen expressed on leukemic CEM cells. We first demonstrated that the biological action of the conjugate was related to its entry into the cell by an energy-dependent endocytotic process. We also found that during the first hours of cell intoxication, internalization is not the rate-limiting step of immunotoxin cytotoxicity. Internalization becomes limiting in cell intoxication only when the entry rate is low. Lastly we show that ammonium chloride, which strongly enhances immunotoxin potency, acts on internalized molecules for a very short time, suggesting that this enhancer affects an early intracellular step.

Ammonium Chloride↗

PubMed1984

Comparative studies on the oxidative processes during phagocytosis measured by luminol-dependent chemiluminescence.

Four different methods, using luminol-enhanced chemiluminescence, are described for assessment of the oxidative processes associated with the phagocytosis of opsonized zymosan by granulocytes. The techniques described in the literature using whole blood as a substrate gave unreliable results due to quench effects of contaminating red blood cells, unpredictable serum interferences, or varying ratios of granulocytes and zymosan. In order to avoid these side effects, rapid and simple methods for the isolation of the granulocytes were applied, e.g. lysis of erythrocytes by ammonium chloride, or the isolation of granulocytes on a percoll gradient. The latter procedure proved to be reliable, simple and sufficiently quick for a routine application.

Ammonium Chloride↗

PubMed1987

Benylin dependence, metabolic acidosis and hyperglycaemia.

We describe a patient who had consumed large quantities of a proprietary cough mixture containing diphenhydramine, ammonium chloride and sodium citrate (Benylin expectorant) daily for several months and subsequently presented with confusion, marked metabolic acidosis and non-ketotic hyperglycaemia.

Acidosis↗

PubMedDate not supplied

[Gastric emptying and metabolic acidosis. II. Study, in an experimental model in rats, of gastric retention of a sodium bicarbonate solution].

The gastric emptying of a 0.25 M sodium bicarbonate solution was studied in rats with metabolic acidosis induced by a previous (6 hours) orogastric infusion of a 0.5 M ammonium chloride solution. Two control groups were used: one previously infused with 0.5 M sodium chloride and the other with water, in the same volume that further solutions. Every animal was fed with 2 ml/100 g of its weight of these solutions. The test meal (bicarbonate solution) was utilized containing 6 mg% red fenol as a marker. The gastric retentions were determined 6 hours after those first meals at 5, 10, 20 and 30 minutes. The results demonstrated that the gastric retentions of the bicarbonate solution were significantly lower in the acidotic group than that one of water group (at 20 minutes) and that one of the sodium chloride (at 10, 20 and 30 minutes). The data here presented suggest that metabolic acidosis accelerates the gastric emptying of a sodium bicarbonate solution.

Acidosis↗

PubMed1986

Loading tests for diagnosis of metabolic anomalies in urinary stone formers.

Four per cent of the population in the industrialized countries of Europe suffer once or several times from urinary calculus in the course of their lives. The high number of recurrences (50 to 60%) necessitates specific prophylaxis. Depending on the precise stone composition, a specific metabolic investigation should be undertaken in cases with recurrent urinary calculus. Within a special laboratory diagnostic program, all major anomalies can be diagnosed by means of loading tests. With the ammonium chloride loading test, renal tubular acidosis is diagnosed; the calcium loading test differentiates the types of hypercalciuria and the purine loading test verifies "latent hyperuricaemia".

Acidosis, Renal Tubular↗