PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “AMMONIUM CHLORIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 793 records · Page 44Linked to original sources
PubMed1981

Renal net acid excretion in the adrenalectomized rat.

Although adrenalectomy is usually associated with an impairment of ammonium and/or titratable acid excretion by the kidney, it is uncertain whether rates of renal net acid excretion are also reduced. Further, it is unclear whether the absence of the adrenal gland itself or other factors of adrenal insufficiency mediate such changes in renal acidification parameters. For example, dramatic increases in ammonium excretion can accompany correction of the hyperkalemia seen in adrenal insufficiency. There is also evidence that reduced rates of acid excretion can result from changes in food intake, urine flow rate, urine pH or distal sodium delivery rates. With these considerations in mind, we undertook studies to isolate the chronic effects of adrenalectomy on renal net acid excretion rates in the unanaesthetized rat. To avoid supranormal potassium stores, we gave the adrenalectomized animals potassium-restricted diets. In balance studies, urine flow rates, urine pH, food intake, and distal sodium delivery rates were all successfully controlled for 13 days by pair feeding and by appropriately changing the sodium and potassium contents of diets. Adrenalectomized rats excreted less net acid than did control animals with or without ammonium chloride loading. Further, the severe metabolic acidosis associated with ammonium chloride loading was clearly mitigated by steroid replacement. Accordingly, we conclude that the adrenal gland is essential for normal renal net acid excretion.

Acid-Base Equilibrium↗
PubMed2003

Improving titrimetric techniques by modelling pH change in activated sludge systems.

Existing titrimetric techniques rely on a well defined hydrogen ion production rate. In particular, they are only suitable in circumstances in which constant background pH influencing reactions take place. This is rarely the case due to the presence of the carbonate acid/base system. In this paper, a model, which describes the influence of the nitrification process on pH and accounts for the action of the carbonate system, is presented. The validity of the model is tested by comparison of model predictions for the important state variables with that of experimental data from a batch oxidation of ammonium nitrogen. The two cases studied are the responses of an endogenously respiring nitrifying sludge to: an ammonium chloride pulse and a pulse of both bicarbonate and ammonium chloride. The results are most encouraging as the dynamic HPR response is mirrored by the model simulation. Furthermore, using the model for data interpretation, the initial nitrogen substrate levels are recovered. It is shown that this could not have been achieved in either case using existing titrimetric techniques.

Bioreactors↗
PubMedDate not supplied

Determination of volatile bases in seafood using the ammonia ion selective electrode: collaborative study.

Nine collaborating laboratories tested a combination of 23 seafood samples for volatile bases using an ammonia ion selective electrode. Results were reported as mg NH3/100 g fish, but the method reflected levels of both ammonia and trimethylamine, which permeated the ammonia membrane. The 23 samples were broken down into 8 blind duplicate pairs, 2 Youden matched pairs, and 3 single samples covering fresh to spoiled product ranging from 8 to 82 mg NH3/100 g. Seven species were evaluated: Atlantic cod, squid, Atlantic halibut, gray sole, monkfish, dogfish, and Atlantic mackerel. The ammonia electrode assay was performed on an aqueous homogenate consisting of 95 mL distilled water and 5.0 g sample tissue. Alkaline ion strength adjusting solution (2 mL) was added to the homogenate to liberate ammonia that was sensed by the ion specific electrode and measured on a precalibrated portable meter. Repeatability standard deviations (RSDr) ranged from 4.2 to 17%; reproducibility standard deviations (RSDR) ranged from 8.8 to 21%. A standard ammonium chloride solution was provided to all laboratories to spike 3 different samples at 10 mg NH3/100 g. Recoveries of added ammonia as ammonium chloride for fresh, borderline, and spoiled samples were 88.6, 107, and 128%, respectively.

Ammonia↗
PubMed1994

Latency of cathepsin B secreted by human colon carcinoma cells is not linked to secretion of cystatin C and is relieved by neutrophil elastase.

The lysosomal cysteine proteinase cathepsin B is shown to be secreted by ten human colon carcinoma cell lines and to accumulate in culture media as a latent enzyme. The cell lines also secrete a physiological inhibitor of cathepsin B, cystatin C. A significant correlation was found between secretion of the latent enzyme and the inhibitor (r = 0.755, P < 0.01). The aim of the present study was to modulate the respective secretion of the two antagonists to test whether or not latency of cathepsin B was due to the concomitant secretion of the inhibitor. SW480 colon carcinoma cells were treated with the acidotropic agent ammonium chloride, phorbol 12-myristate 13-acetate, and the inflammatory cytokines TGF-beta, TNF-alpha, and IL-1 beta. Ammonium chloride significantly increased latent cathepsin B levels without affecting the constitutive secretion of cystatin C. Phorbol 12-myristate 13-acetate induced a 4- to 5-fold increase in secreted latent cathepsin B, but did not alter significantly the accumulation of cystatin C in media. The cytokines, TGF-beta, TNF-alpha, and IL-1 beta, had no major effect on the expression of these two antagonists. Latent cathepsin B released from human carcinoma cells could be efficiently activated by neutrophil elastase at neutral pH. It is concluded that latent cathepsin B is a true proenzyme rather than an enzyme-inhibitor complex. In addition, our data from neutrophil elastase activation experiments indicate that a proteolytic system for activation of the tumor cell-secreted latent enzyme may exist in vivo.

Adenocarcinoma↗
PubMed1994

Urinary acidification and urinary excretion of calcium and citrate in women with bilateral medullary sponge kidney.

Urinary acidification ability, acid-base status and urinary excretion of calcium and citrate were evaluated in 10 women with bilateral medullary sponge kidney (MSK) and in 10 healthy women. Patients with MSK had higher fasting urine pH compared to normal controls (p < 0.01). Four patients had incomplete renal tubular acidiosis (iRTA), 3 had hypercalciuria, and 5 patients had hypocitraturia. The 24-hour urinary excretion of calcium was increased in the females with MSK (5.23 +/- 0.78 mmol) compared to the healthy females (3.49 +/- 0.29 mmol) (p < 0.02), and increased in MSK patients with iRTA (7.32 +/- 1.45 mmol) compared to patients with normal urinary acidification (3.83 +/- 0.12 mmol) (p < 0.01). The patients with iRTA had reduced levels of plasma standard bicarbonate (20.5 +/- 1.0) after fasting compared to patients with normal urinary acidification (23.8 +/- 0.8) and healthy women (22.7 +/- 0.6) (p < 0.01), and reduced levels of 24-hour urinary excretion of citrate (0.93 +/- 0.25 mmol) compared to patients with normal urinary acidification (3.58 +/- 0.51) and healthy women (2.78 +/- 0.49) (p < 0.005). A positive correlation was found between the degree of acidosis during ammonium chloride loading and urinary excretion of calcium (r = 0.71, p = 0.02), and a negative correlation between the degree of acidosis during ammonium chloride loading and urinary citrate excretion (r = 0.87, p = 0.001). The results suggest that defective urinary acidification might play an important role in the mechanism of hypercalciuria and hypocitraturia in patients with medullary sponge kidney.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Renal Tubular↗
PubMed1987

Hyperammonemia causes altered protein phosphorylation in astrocytes.

Treatment of primary astrocyte cultures with ammonium chloride for one day prior to phosphoprotein labeling resulted in a reduction in phosphate incorporation in a 66-kDa protein. Increasing ammonium chloride concentrations (2, 5, and 10 mM) led to greater reductions in phosphate incorporation in this band. The specificity of the effect was indicated by the lack of change in phosphate incorporation in 7 other protein bands. These results indicate that protein phosphorylation can be affected by pathophysiological concentrations of ammonia and suggest that altered protein phosphorylation may be related to the pathogenesis of disorders such as hepatic encephalopathy and Reye's syndrome where ammonia has been implicated as an important etiological factor.

Ammonia↗
PubMed1975

The influence of phentolamine on the hyperglycaemic and lipolytic effects of ammonia in sheep.

Intravenous infusion over 30 min of ammonium chloride [10-1 g/kg b.w.] caused a significant increase of blood glucose and free fatty acids levels, and a similar effect was observed with adrenaline. Phentolamine [1 mg/kg b.w.] abolished the hyperglycaemic action of ammonium chloride but only slightly diminished the lipolytic effect. It is concluded that the ammonium ion influences carbohydrate metabolism chiefly by way of catecholamines and stimulation of alpha-adrenergic receptors, while tissue lipids are mobilized by ammonia by another route, possibley directly.

Ammonia↗
PubMed1987

The role of lysosomal enzymes in killing of mammalian cells by the lysosomotropic detergent N-dodecylimidazole.

The sensitivity of cultured human and hamster fibroblast cells to killing by the lysosomotropic detergent N-dodecylimidazole (C12-Im) was investigated as a function of cellular levels of general lysosomal hydrolase activity, and specifically of cysteine cathepsin activity. Fibroblasts from patients with mucolipidosis II (I-cell disease) lack mannose-6-phosphate-containing proteins, and therefore possess only 10-15% of the normal level of most lysosomal hydrolases. I-cell fibroblasts are about one-half as sensitive to killing by C12-Im as are normal human fibroblasts. Overall lysosomal enzyme levels of CHO cells were experimentally manipulated in several ways without affecting cell viability: Growth in the presence of 10 mM ammonium chloride resulted in a gradual decrease in lysosomal enzyme content to 10-20% of control values within 3 d. Subsequent removal of ammonium chloride from the growth medium resulted in an increase in lysosomal enzymes, to approximately 125% of control values within 24 h. Treatment with 80 mM sucrose caused extensive vacuolization within 2 h; lysosomal enzyme levels remained at control levels for at least 6 h, but increased 15-fold after 24 h of treatment. Treatment with concanavalin A (50 micrograms/ml) also caused rapid (within 2 h) vacuolation with a sevenfold rise in lysosomal enzyme levels occurring only after 24 h. The sensitivity of these experimentally manipulated cells to killing by C12-Im always paralleled the measured intracellular lysosomal enzyme levels: lower levels were associated with decreased sensitivity while higher levels were associated with increased sensitivity, regardless of the degree of vacuolization of the cells. The cytotoxicity of the cysteine proteases (chiefly cathepsin L in our cells) was tested by inactivating them with the irreversible inhibitor E-64 (100 micrograms/ml). Cell viability, protein levels, and other lysosomal enzymes were unaffected, but cysteine cathepsin activity was reduced to less than 20% of control values. E-64-treated cells were almost completely resistant to C12-Im treatment, although lysosomal disruption appeared normal by fluorescent visualization of Lucifer Yellow CH-loaded cells. It is concluded that cysteine cathepsins are the major or sole cytotoxic agents released from lysosomes by C12-Im. These observations also confirm the previous conclusions that C12-Im kills cells as a consequence of lysosomal disruption.

Ammonium Chloride↗
PubMed1990

Ammonium effects on streptonigrin biosynthesis by Streptomyces flocculus.

A defined medium containing glucose and ammonium as the sole carbon and nitrogen sources was developed to support growth and streptonigrin production. In this defined medium, increased initial levels of ammonium resulted in increased growth suggesting that nitrogen is the growth limiting nutrient. In some cases, increased initial ammonium levels resulted in decreased specific streptonigrin productivity, suggesting that nitrogen regulatory mechanisms may adversely affect streptonigrin biosynthesis. This suggestion that nitrogen regulation adversely affects antibiotic biosynthesis is further supported by results from two studies in which the ammonium supply to the cells was controlled. In the first study, streptonigrin productivity and final titer were enhanced by the addition of an ammonium trapping agent. In the second experiment, when ammonium chloride was fed slowly throughout the course of cultivation, the production phase was lengthened and the maximum antibiotic concentration was enhanced compared to the batch controls containing either the same initial or the same total ammonium chloride levels. Although our results indicate streptonigrin production may be subject to nitrogen regulatory mechanisms, the effect of nitrogen on streptonigrin production cannot be strictly correlated to the extracellular ammonium concentration. In fact, we observed that when ammonium was depleted from the medium, streptonigrin production ceased.

Ammonium Chloride↗
PubMed1979

[The effects of non-protein-nitrogen additives on lipid and carbohydrate metabolisms in sheep (author's transl)].

The effects of NPN administration on lipid and carbohydrate metabolisms were investigated in 14 sheep. Blood non-esterified fatty acids (NEFA) are increased by intra-ruminal dosage with urea (10 g), 1 p. 1000 ammonia solution (1 l) or ammonium chloride (17.6 g). Peak values are recorded 3 to 4 hours after the injection. An early rise of NEFA and hyperglycemia are observed when ammonium chloride is injected intra-venously. The time-course of the variations of the different blood constituents (ammonia, glucose, NEFA, urea) as well as the lack of any action following intra-venous urea injections suggest that lipid mobilization is induced by the increased level of blood ammonia. The involvement of a strenghened activity of the sympathetic-adrenal system is evidenced by the increased elimination of urinary catecholamines.

Ammonia↗
PubMedDate not supplied

[Lysosomotropic compounds inhibiting the multiplication of Junin virus].

A number of lysosomotropic compounds of diverse chemical structure, ammonium chloride, procaine and chlorpheniramine, were found to inhibit the infection of Vero cells by Junín virus. Viral replication was almost totally inhibited by 15 mM ammonium chloride, when added either before or within the first hour of infection and a significant inhibition (97.8%) was observed when it was added 8 hours after infection. These results agree with a model which postulates that arenavirus entry occurs by receptor-mediated endocytosis.

Ammonium Chloride↗
PubMed1989

The effect of adrenal denervation on the metabolic effects of hyperammonemia in sheep.

The metabolic effect of intravenous infusion of ammonium chloride (60 mumol/(kg body weight.min] was compared in five sheep before and after adrenal denervation. Adrenal denervation completely abolished the hyperglycemic effect of ammonium chloride, diminished the rise of pyruvate and lactate concentration, and failed to influence the lipolytic effect of NH4Cl. It is suggested that the metabolic effects of ammonia are in a different degree related to the action of ammonia on the central nervous system and (i) the hyperammonemic effect of ammonia completely depends on the neurogenic increase of adrenal medullary hormones; (ii) the rise of blood lactate and pyruvate level observed during hyperammonemia is only partially mediated by adrenaline; and (iii) the lipolytic effect of ammonia ion does not depend on the nerve-controlled secretion of adrenal medullary hormones.

Adrenal Glands↗
PubMed1980

Hippocampal glutamate release after porta cava anastomosis: reduced sensitivity to ammonia inhibition.

In vitro measurements of basal efflux and evoked release of exogenous and endogenous glutamate from rat hippocampus showed that exposition of the tissue to pathophysiological concentrations of ammonium chloride (3 mM) for 40--60 min abolished the KCl-induced release of endogenous glutamate. Basal efflux of endogenous glutamate was elevated by ammonium chloride with a delay of 30--40 min. In an attempt to link these observations to the pathogenesis of hepatic coma, rats were subjected to porta-cava anastomosis, and the hippocampal tissue was tested for ammonia sensitivity 3--4 weeks after the operation. The results showed that ammonia perfusion of the tissue was without effect effect on either basal or KCl-evoked release of endogenous glutamate. In addition, the utilization of glutamine for glutamate formation was influenced in hippocampal but not cortical tissue form porta-cava anastomized rats. The results suggest that ammonia is an important factor for the disturbed metabolism of the neurotransmitter pool of glutamate in hepatic failure.

Ammonia↗
PubMed2001

Acute metabolic acidosis decreases muscle protein synthesis but not albumin synthesis in humans.

Chronic metabolic acidosis induces negative nitrogen balance by either increased protein breakdown or decreased protein synthesis. Few data exist regarding effects of acute metabolic acidosis on protein synthesis. We investigated fractional synthesis rates (FSRs) of muscle protein and albumin, plasma concentrations of insulin-like growth factor-I (IGF-I), thyroid-stimulating hormone (TSH), and thyroid hormones (free thyroxin [fT(4)] and triiodothyronine [fT(3)]) in seven healthy human volunteers after a stable controlled metabolic period of 5 days and again 48 hours later after inducing metabolic acidosis by oral ammonium chloride intake (4.2 mmol/kg/d divided in six daily doses). Muscle and albumin FSRs were obtained by the [(2)H(5)ring]phenylalanine flooding technique. Ammonium chloride induced a significant decrease in pH (7.43 +/- 0.02 versus 7.32 +/- 0.04; P < 0.0001) and bicarbonate concentration (24.6 +/- 1.6 versus 16.0 +/- 2.7 mmol/L; P < 0.0001) within 48 hours. Nitrogen balance decreased significantly on the second day of acidosis. The FSR of muscle protein decreased (1.94 +/- 0.25 versus 1.30 +/- 0.39; P < 0.02), whereas the FSR of albumin remained constant. TSH levels increased significantly (1.1 +/- 0.5 versus 1.9 +/- 1.1 mU/L; P = 0.03), whereas IGF-I, fT(4), and fT(3) levels showed no significant change. We conclude that acute metabolic acidosis for 48 hours in humans induces a decrease in muscle protein synthesis, which contributes substantially to a negative nitrogen balance. In contrast to prolonged metabolic acidosis of 7 days, a short period of acidosis in the present study did not downregulate albumin synthesis.

Acidosis↗
PubMed1988

Fibroblasts maintain a complete endocytic pathway in the presence of lysosomotropic amines.

We have investigated the effects of the lysosomotropic amines, ammonium chloride and chloroquine, on the delivery of fluid-phase pinocytic tracers to lysosomes in Chinese hamster ovary (CHO) cells. In preliminary experiments, 15 mM ammonium chloride and 0.1 mM chloroquine were found to be sufficient to give maximal protection of endocytosed material from digestion in a lysosome. In the presence of either amine at these concentrations, the generation time of CHO cells was depressed by less than 30% even though selective depletion of lysosomal hydrolases was observed. For cells treated with either amine for 1 or 6 days the amount of horseradish peroxidase (HRP) internalized in a 1-h pulse was approximately 50-70% of that of control. By cell fractionation, cells treated with amine for 2 or 6 days were found to accumulate fluorescein-dextran or HRP in lysosomes. HRP accumulation in lysosomes in amine-treated cells was also observed by electron microscopy. Little exocytosis of lysosomal HRP into the media was observed under any condition. We conclude that in long-term amine-treated CHO cells endocytic vesicle traffic is maintained.

Ammonium Chloride↗
PubMed1983

Alkalinizing the intralysosomal pH inhibits degranulation of human neutrophils.

Degranulation of lysosomes is one of the consequences of neutrophil activation. Regulatory mechanisms of lysosomal secretion are thought to be localized largely in the plasma membrane and cytosol, with the lysosome playing a passive role in secretion. Recent evidence indicates that the intralysosomal pH is highly acidic (pH congruent to 5.5) and is maintained by active transport of H+. We investigated whether changes in the intralysosomal pH altered the availability of lysosomes for exocytosis. Intralysosomal pH in intact neutrophils was monitored with the weakly basic fluorescent probe, 9-aminoacridine (9AA). The weak bases, methylamine, chloroquine, clindamycin, propanolol, and ammonium chloride (0.1-50 mM), caused an alkalinization of the intralysosomal pH as determined by reversal of quenching of 9AA fluorescence. Similarly, each of the weak bases, including ammonium chloride, methylamine, chloroquine, ethylamine, propylamine, propanolol, clindamycin, and dansylcadaverine, inhibited neutrophil degranulation in response to the calcium ionophore A23187, phorbol myristate acetate, or the chemotactic peptide, formyl-methionine-leucine-phenylalanine plus cytochalasin B. These studies indicate that an acid intralysosomal pH is important to the neutrophil secretory response and suggest that the lysosome may play an active part in control of degranulation.

Adult↗
PubMed1979

Effect of levulinic acid on pigment biosynthesis in Agmenellum quadruplicatum.

When levulinic acid was added to a growing culture of the cyanobacterium (blue-green alga) Agmenellum quadruplicatum PR-6, delta-aminoelevulinic acid accumulated in the medium and chlorophyll a synthesis and cell growth were inhibited, but there was a small amount of c-phycocyanin synthesis. The amount of delta-aminolevulinic acid produced in the treated culture did not fully account for the amount of pigment synthesized in the untreated control. Levulinic acid and either sodium nitrate or ammonium chloride were added to nitrogen-starved cultures of PR-6, and delta-aminolevulinic acid production and chlorophyll a and c-phycocyanin content were monitored. When ammonium chloride was added as a nitrogen source after nitrogen starvation, the cells recovered more rapidly than when sodium nitrate was added as a nitrogen source. In cultures recovering from nitrogen starvation, synthesis of c-phycocyanin occurred before synthesis of chlorophyll a.

Aminolevulinic Acid↗