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PubMed1986

The ontogeny of salt preference in rats.

Many mammals eat salt irrespective of need. This behavior, called salt preference or appetite, is studied primarily in adults. Little is known about its ontogeny. In these experiments, 3-18-day-old rat pups were offered saline, quinine, or ammonium chloride solutions by infusion through an anterior oral catheter, and intake was measured. At 6-18 days, pups showed the inverted U-shaped preference-aversion curve for NaCl that is characteristic of adult rats. Thus, rats express a preference for salt at a very early age. However, the curves were broader than the typical adult curve and were shifted along the concentration gradient in an age-related fashion. Consumption of quinine and ammonium chloride showed similar age-related changes. These changes may reflect the postnatal timing of the development of the rat gustatory system.

Aging↗

PubMed1976

Urine acidification capacity in renal stone formers.

A short ammonium chloride loading test was used in the investigation of renal acidification capacity of 51 patients with idiopathic recurrent renal stones containing calcium. Many of these patients had suffered from prolonged and severe stone disease. In 31% of the patients an impaired acidification with varying degrees of severity was found. Eight patients had defects suggesting distal renal tubular acidosis (RTA). One case with the complete and two cases with the incomplete form of RTA were found. A further five patients, who were all able to acidify their urine to an acid pH, had milder defects in the excretion of titratable acid and/or ammonium ions which may indicate an early stage of distal tubular acidosis. Six patients were suspected of having a proximal acidification defect, as they showed delayed responses to the ammonium chloride induced acidosis.

Acidosis↗

PubMedDate not supplied

Effects of ammonium and lactate on growth and metabolism of a recombinant Chinese hamster ovary cell culture.

A Chinese hamster ovary (CHO) cell line producing a recombinant glycoprotein was cultured in batch mode with different initial concentrations of ammonium chloride (0-10 mM), sodium lactate (0-60 mM), or sodium chloride (0-60 mM). High ammonium concentrations did not inhibit cell growth and productivity or glucose and glutamine consumption. In contrast, specific ammonia and alanine production decreased by 55% and 40%, respectively. There were also significant increases in specific aspartate and glutamate consumption in high ammonium concentrations. These observations indicated a shift in glutamine catabolic pathways in response to the effects of ammonium. The influence of lactate on growth and metabolism were the combined effects of lactate concentration and osmolarity. After "correcting" for osmolarity effects, lactate was found to inhibit growth by 25% but to increase specific productivity slightly (10%). Lactate had profound effects not only on glycolysis but also on glutaminolysis. While specific glucose and glutamine consumptions decreased by 15-20%, the effects of lactate on their metabolic products were far more significant. Lactate production was halted, and specific ammonia and alanine productions decreased by 64% and 70% at high lactate concentration. Theories on how ammonium and lactate affected the metabolic pathways of glucose and glutamine are presented.

Ammonium Chloride↗

PubMed1981

Renal tubular acidosis in primary biliary cirrhosis.

The relationship between renal tubular acidosis (RTA) and copper metabolism has been investigated in a group of 18 patients with primary biliary cirrhosis. RTA, considered when urinary pH remained above 5.4 after an oral load of ammonium chloride of 0.1 g/kg body wt, was found in 6 patients (33%). Plasma copper concentration (PCu) and urinary copper excretion (UCuV) were significantly higher in patients with RTA (PCu = 182.2 micrograms/dl, UCuV = 536.8 micrograms/24 h) than in those without (PCu = 134.2; UCuV = 170.3). Plasma copper concentration and urinary copper excretion correlated with minimal urinary pH achieved after the ammonium chloride load. A higher degree of cholestasis was present in patients with RTA than in those without, and a linear correlation was observed between PCu and UCuV and serum bilirubin. It is concluded that the increased UCuV is related to the cholestasis in primary biliary cirrhosis and that the RTA might be caused by the deposition of copper in the distal renal tubule.

Acidosis, Renal Tubular↗

PubMed2005

Endocytosis and a low-pH step are required for productive entry of equine infectious anemia virus.

Recently, it has become evident that entry of some retroviruses into host cells is dependent upon a vesicle-localized, low-pH step. The entry mechanism of equine infectious anemia virus (EIAV) has yet to be examined. Here, we demonstrate that wild-type strains of EIAV require a low-pH step for productive entry. Lysosomotropic agents that inhibit the acidification of internal vesicles inhibited productive entry of EIAV. The presence of ammonium chloride (30 mM), monensin (30 microM), or bafilomycin A (50 nM) in the medium dramatically decreased the number of EIAV antigen-positive cells. We found that a low-pH step was required for EIAV infection of tissue culture cell lines as well as primary cells, such as endothelial cells and monocyte-derived macrophages. The ammonium chloride treatment did not reduce virion stability, nor did the treatment prevent virion binding to cells. Consistent with a requirement for a low-pH step, virion infectivity was enhanced more than threefold by brief low-pH treatment following binding of viral particles to permissive cells. A superinfecting variant strain of EIAV, vMA-1c, did not require a low-pH step for productive infection of fibroblasts. However, lysosomotropic agents were inhibitory to vMA-1c infection in the other cell types that vMA-1c infected but did not superinfect, indicating that the entry pathway used by vMA-1c for superinfection abrogates the need for the low-pH step.

Ammonium Chloride↗

PubMed1994

Mitochondrial pyruvate metabolism in liver and kidney during acidosis.

Pyruvate transport and carboxylation have been determined in mitochondria from liver and kidney cortex isolated from Wistar rats with acidosis produced by three different treatments: fasting, exercise and ingestion of ammonium chloride. Fasting for 48 h or swimming for 2 h resulted in an increased rate of CO2 fixation by mitochondria from both organs incubated with pyruvate. This increase was accompanied by a rise in the rate of pyruvate transport in all cases except in mitochondria derived from the kidney of the fasted animals. Acute acidosis produced by the ingestion of ammonium chloride resulted in increases in pyruvate transport and carboxylation in kidney mitochondria, but a drop in pyruvate carboxylation was observed in mitochondria from the liver. The results are discussed in terms of the differential regulation of the mitochondria steps for gluconeogenesis from three carbon precursors in liver and kidney, taking into consideration the hormonal status of the animals and the prevailing available substrates in each condition.

Acidosis↗

PubMed1999

Acidic pH enhancement of the fusion of Newcastle disease virus with cultured cells.

Fusion of the lentogenic strain "Clone 30" of Newcastle disease virus (NDV) with the cell line COS-7 has been studied. Fusion was monitored using the octadecylrhodamine B chloride dequenching assay [Hoekstra, D., de Boer, T., Klappe, K. and Wilschut, J. (1984). Biochemistry 23, 5675-5681]. In the present work, fusion of NDV with COS-7 cells was found to occur in a time- and temperature-dependent fashion. Significant dequenching of the probe occurred at temperatures higher than 28 degrees C. A 20-fold excess of unlabeled virus inhibited fusion by about 53% compared with the control, whereas 62% inhibition of fusion was obtained after digestion of viral glycoproteins with trypsin. The data are discussed in terms of the nonfusion transfer of the probe. In addition, preincubation of cells with 50 mM ammonium chloride or 0.1% sodium azide prevented NDV from fusing with COS-7 cells by about 30% in comparison with the control. The cytopathic effect of NDV infection in cell culture in the presence of ammonium chloride was reduced compared with control. Moreover, viral preincubation at pH 5 yielded a mild inhibition of fusogenic activity. Our results suggest that NDV may use the endocytic pathway as a complementary way of entering cells by direct fusion with the plasma membrane.

Ammonium Chloride↗

PubMed1984

Effects of lysosomotropic weak bases on infection of BHK-21 cells by Sindbis virus.

The effects of the lysosomotropic weak bases chloroquine, ammonium chloride, and amantadine as well as dansylcadaverine (an inhibitor of receptor mediated endocytosis) on the replication of Sindbis virus in tissue-cultured cells was examined. Chloroquine had no effect on the expression of virus-induced homologous interference. None of these drugs significantly affected the ability of a complex of a cell and single virion to form an infectious center. Chloroquine and ammonium chloride were found to inhibit the synthesis of virus RNA in established infections when added early in infection. These drugs also inhibited the production of progeny virions when added any time after infection. These results suggest that the antiviral activity of these agents may not be due to an ability to prevent transport of the virus genome into the cell cytoplasm.

Amantadine↗

PubMed1985

Influence of nitrogen source and growth status on glutamine synthetase and glutamate synthase activity in Mycobacterium avium.

An investigation was made of the activity of glutamine synthetase and glutamate synthase from batch-cultured cells of Mycobacterium avium. The bacteria were grown in medium with ammonium chloride concentrations of 0, 0.1, 0.25, 1, 5, or 25 mumol/mL or with glutamine at 0.1 or 1 mumol/mL. The specific activity of the two enzymes was determined at 0, 22, 45, and 70 h of incubation. Regardless of the ammonia concentration in the medium, glutamate synthase specific activity was two to five times higher in extracts from elongating cells, incubated 22 h, than in those from shortened cells, incubated 45 or 70 h. In contrast, there was no apparent difference in glutamine synthetase specific activity with regard to culture age; however, glutamine synthetase specific activity varied inversely with the concentration of ammonium chloride in the medium. Cells grown in glutamine had high activity of glutamine synthetase.

Ammonium Chloride↗

PubMed1993

The frusemide test: simple screening test for renal acidification defect in urolithiasis.

Urinary pH was first labelled as a risk factor for patients with recurrent calcium stone disease of the renal tract in 1978. The standard diagnostic test for patients with a history of stones, who appear to have urinary acidification defects is the ammonium chloride test. However, the performance of this test results in significant morbidity, particularly nausea and vomiting, and as a result there is little enthusiasm for screening for such defects. We describe a screening test that may be used to determine which patients require more definitive testing. It involves an oral dose of frusemide (40 mg) followed by half-hourly urine sampling for pH. For the detection of a renal tubular acidification defect, the frusemide test had sensitivity = 100%, specificity = 82%, predictive value of a positive result = 40%, predictive value of a negative result = 100%, screening efficiency = 84%, and there was no morbidity. During the ammonium chloride test 80% of the patients vomited or felt very nauseated.

Ammonium Chloride↗

PubMed1994

Renal ammonia in autosomal dominant polycystic kidney disease.

Recent studies have suggested that defective medullary trapping of ammonia underlies the acidosis associated with renal failure and sets in motion maladaptive compensatory mechanisms that contribute to the progression of renal disease. Since a renal concentrating defect is an early functional abnormality in autosomal dominant polycystic kidney disease (ADPKD), defective medullary trapping and urinary excretion of ammonia may also occur early and have important pathophysiological consequences. The urinary pH and excretions of ammonia, titratable acid, and bicarbonate, were measured during a 24-hour baseline period and following the administration of ammonium chloride (100 mg/kg body wt) in ADPKD patients with normal glomerular filtration rate and in age- and gender-matched healthy control subjects. The distal nephron hydrogen ion secretory capacity was assessed during a bicarbonate infusion. Ammonia, sodium, pH, C3dg, and C5b-9 were measured in cyst fluid samples. The excretion rates of ammonia during the 24-hour baseline period and following the administration of ammonium chloride were significantly lower, and the relationship of ammonia excretion to urinary pH was significantly shifted downward in ADPKD. No difference in the increment of urinary pCO2 (delta pCO2) or the peripheral blood-urine pCO2 gradient (U-B pCO2) between ADPKD patients and control subjects was detected during a sodium bicarbonate infusion. Calculated concentrations of free-base ammonia in cyst fluid samples exceeded those calculated from reported concentrations of ammonia in renal venous blood of normal subjects. C3dg and C5b-9 were detected in some cyst fluids. The urinary excretion of ammonia is reduced in ADPKD patients with normal glomerular filtration rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1995

Studies on renal growth regulation by urea and ammonia in normal rat kidney cells.

The hypothesis that protein metabolites regulate renal growth has been considered for decades, and the overall objective of this work was to test this hypothesis in vitro using an established line of renal tubular epithelial cells, NRK-52E. The addition of urea to the medium of confluent cultures stimulated DNA synthesis which was dependent on the concentration of urea, but independent of the presence of serum. Urea enhanced proliferation of subconfluent cultures of NRK cells in the presence of dilute serum to a similar degree as epidermal growth factor (EGF). Either deletion of serum from the medium or allowing the cultures to achieve confluence prevented the proliferative response to urea, but not EGF. Ammonium chloride stimulated the uptake of 3H-thymidine but did not increase cell number. Ammonium chloride increased the uptake of 3H-leucine and total cellular protein/DNA, while urea had no effect on these markers of growth. The rate of hydrolysis of urea to ammonia in vitro was not altered by the presence of NRK cells. These results suggest that urea and ammonia may regulate renal mass, and that their actions are separate and different.

Ammonia↗

PubMed1999

Lipopolysaccharide of Escherichia coli, polyamines, and acetic acid stimulate cell proliferation in intestinal epithelial cells.

Our aim was to examine whether lipopolysaccharide of Escherichia coli, polyamines of dietetic and/or bacterial origin, and products of the bacterial metabolism influence cell proliferation in epithelial cells from the colon and small intestine. Lipopolysaccharide of Escherichia coli 0111:B4 was incubated with cultures from human colonic mucosa. The mitoses were arrested with Vincristine and the total number of metaphases per crypt was counted. In addition, lipopolysaccharide was incubated with a human colonic epithelial cell line from adenocarcinoma (LS-123 cells) and with a nontransformed small intestinal cell line from germ-free rats (IEC-6 cells) for 24 h. In the last 4 h, the cells were labeled with tritiated thymidine. The cells were incubated with putrescine, cadaverine, and spermidine at 10(-11)-10(-3) M and with acetic acid (10(-5)-10(-1) M), acetaldehyde (10(-10)-10(-4) M) and ammonium chloride (1-20 mM). Lipopolysaccharide of Escherichia coli increased the number of arrested metaphases in human colonic crypts and DNA synthesis in L-123 and IEC-6 cells (P < 0.001). All polyamines increased DNA synthesis in the colonic and small intestinal cell lines, the effects being more marked for putrescine (P < 0.001). The higher concentrations of acetic acid increased DNA synthesis in both epithelial cell lines (P < 0.001). Acetaldehyde slightly decreased DNA synthesis in LS-123 cells at cytotoxic concentrations. Ammonium chloride did not significantly affect DNA synthesis. The final concentration of nonionized ammonia was less than 3%. It is concluded that lipopolysaccharides of Escherichia coli and intraluminal factors derived from microorganisms increase cell proliferation in human colonic crypts and intestinal epithelial cell lines.

Acetaldehyde↗

PubMed1984

An abnormality in intracellular protein degradation in fibroblasts from patients with I-cell disease.

Degradation of endogenous proteins in five normal and five I-cell (mucolipidosis II) storage disease human fibroblasts was compared. In growing cultures (low density) long half-life proteins were degraded normally in each group of cells. However, the enhancement of proteolysis when confluence is reached, which we have characterised previously as being a lysosomal function, was less in the I-cell fibroblasts. The lysosomotropic agents ammonium chloride, pepstatin and Z-Phe-Ala-diazomethylketone, inhibited similarly proteolysis in growing and confluent cultures of both cell types. Leupeptin depressed proteolysis in both growth states for both cell types, but, whereas it failed to abolish the enhancement of degradation in confluent normal cells, surprisingly it depressed degradation in confluent I-cell fibroblasts to a lower rate than in growing I-cell fibroblasts. In spite of this, the inhibitory effects of ammonium chloride and leupeptin were not additive in either normal or I-cell fibroblasts, indicating that they act upon the same proteolytic mechanism(s). Non-lysosomal mechanisms may degrade short half-life proteins, and it seemed that turnover of such proteins was slower in I-cell fibroblasts. It is suggested that mutual regulation of participating proteolytic pathways may be responsible for the dysfunction of intracellular protein degradation in I-cell fibroblasts.

Ammonium Chloride↗

PubMedDate not supplied

Treating severe metabolic alkalosis.

The pathophysiology, symptomatology, and treatment of metabolic alkalosis are reviewed, with emphasis on treatment with intravenous hydrochloric acid. Three buffering systems are used by the body to correct an arterial pH above 7.45--tissue, respiratory, and renal systems. The kidneys have the primary responsibility for correcting a severe metabolic alkalosis, but several conditions (e.g., severe volume contraction) can interfere with the renal mechanisms. No unique symptoms are associated with metabolic alkalosis. Conventional conservative treatment of metabolic alkalosis involves meeting the patient's fluid and electrolyte needs and allowing the body to correct the alkalosis through its own mechanisms. However, when more rapid resolution of the alkalosis is needed or the patient cannot tolerate fluid and electrolyte therapy, mineral acids may be administered. Ammonium chloride and arginine monohydrochloride infusions may both be used; since both require hepatic conversion for full activity, patients with hepatic dysfunction may require alternative therapy. Dilute hydrochloric acid (0.1-0.2 N) may be given intravenously to these patients through a central-venous catheter. Dosage guidelines and formulation procedures are described in the paper, as are other possible therapeutic alternatives (dialysis, acetazolamide, cimetidine). Most cases of metabolic alkalosis can be managed with fluid and electrolyte therapy. When metabolic alkalosis needs to be resolved quickly or when conventional therapy cannot be tolerated, mineral acid administration should be instituted. The primary drug of choice for these patients is intravenous ammonium chloride; patients with hepatic or severe renal dysfunction should receive dilute hydrochloric acid via a central-venous catheter.

Acetazolamide↗

PubMedDate not supplied

Effect of chloroquine on the formation of tight junctions in cultured immature rat Sertoli cells.

Adjoining immature Sertoli cells in the seminiferous epithelium form a tight junctional complex leading to the development of the blood-testis barrier. Protease and antiprotease activities have been implicated in the process of formation of tight junctions. Here, we report the effect of chloroquine, an antimalarial drug with antiprotease activity, on the development of intercellular tight junctions in cultured immature rat Sertoli cells. For positive control, the classical lysosomotropic agent ammonium chloride was used. Sertoli cells were seeded in serum-free defined medium at a density of 3 x 10(6) cells/0.64-cm2 well on Matrigel-covered Millicell-HA filters. Chloroquine at concentrations ranging from 25 to 100 microM was added to the outer chamber of the bicameral system on either day 1 or 7 of the culture. The formation of the tight junction was monitored by the measurement of the transepithelial resistance (TER) at 24-hour intervals using an impedance meter. TER in untreated controls was 50 ohms/cm2 on day 1; it increased progressively to 80 ohms/cm2 by day 7 and plateaued until day 12. The cells treated from day 1 with chloroquine also showed a dose-dependent progressive increase in TER until day 9, reaching 225 ohms/cm2 in cells treated with the 100 microM concentration. In comparison to controls, the increase in TER was significantly higher. In cells treated with chloroquine starting from day 7 of culture onwards, there was no observable difference in TER from the untreated control. These observations demonstrate that chloroquine and ammonium chloride increase the TER of immature Sertoli cells in the bicameral chamber.

Amines↗

PubMed1993

Amphetamine and other weak bases act to promote reverse transport of dopamine in ventral midbrain neurons.

Amphetamine-like psychostimulants are thought to produce rewarding effects by increasing dopamine levels at mesolimbic synapses. Paradoxically, dopamine uptake blockers, which generally increase extracellular dopamine, inhibit amphetamine-induced dopamine overflow. This effect could be due to either inhibition of amphetamine uptake or inhibition of dopamine efflux through the transporter (reverse transport). We used weak bases and dopamine uptake blockers in ventral midbrain neuron cultures to separate the effects on blockade of amphetamine uptake from reverse transport of dopamine. Amphetamine, ammonium chloride, tributylamine, and monensin, at concentrations that produce similar reductions in acidic pH gradients, increased dopamine release. This effect was inhibited by uptake blockers. Although in the case of amphetamine the inhibition of release could have been due to blockade of amphetamine uptake, inhibition also occurred with weak bases that are not transporter substrates. This suggests that reduction of vesicular pH gradients increases cytoplasmic dopamine which in turn promotes reverse transport. Consistent with this model, extracellular 3,4-dihydroxyphenylacetic acid was increased by ammonium chloride and monensin, as would be expected with elevated cytoplasmic dopamine levels. These findings extend the weak base mechanism of amphetamine action, in which amphetamine reduces vesicular pH gradients resulting in increased cytoplasmic dopamine that promotes reverse transport.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1998

Urinary net charge in hyperchloremic metabolic acidosis.

OBJECTIVE: (i) To examine the usefulness of urinary net charge (UNa + UK - UCl) in the evaluation of hyperchloremic metabolic acidosis secondary to diarrhea, distal RTA and proximal RTA and (ii) To characterize the type of distal RTA on the basis of the underlying defect. SETTING: Pediatrics division of a tertiary referral center. SUBJECTS: Thirty four children with hyperchloremic metabolic acidosis secondary to diarrhea (n = 16), distal RTA (n = 11) and proximal RTA (n = 7). Ten normal children with ammonium chloride induced acidosis were also studied. METHODS: All subjects underwent urine collection of 30-60 minutes duration for measurement of Na, K, Cl, pH and pCO2. The measurements were also made on the blood samples collected at the midpoint of urine collection. The urinary net charge was calculated by subtracting Cl values from the sum of the Na and K. RESULTS: Patients with proximal and distal RTA had a positive urine net charge. Patients with diarrhea and ammonium chloride induced acidosis showed negative urine net charge. Patients with diarrhea with extremely low urine sodium levels showed an inappropriately high urine pH despite persistent metabolic acidosis. All patients with distal RTA were found to have a secretory type of defect. CONCLUSION: Measurement of urine net charge is helpful in the initial evaluation of a patient with hyperchloremic metabolic acidosis.

Acidosis↗