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PubMed2003

Simulation of the bis-(penicillamine) enkephalin in ammonium chloride solution: a comparison with sodium chloride.

In order to quantify specific ion effects, a simulation study of bis(penicllamine) enkephalin, also known as DPDPE, has been performed in aqueous ammonium chloride solution and has been compared to a previous simulation of DPDPE in aqueous sodium chloride solution. Global thermodynamics have been calculated for a model system and the solution environment around DPDPE has been characterized. Associations of ions with DPDPE have been investigated. The observed differences between sodium chloride solution and ammonium chloride solution suggest that individual cations affect the solvation and peptide binding properties of a given anion.

Ammonium Chloride↗
PubMed1992

Lipophilicity determination of some monoamine oxidase inhibitors: the effect of methanol and ammonium chloride.

The lipophilicity (RM value) of seventeen monoamine oxidase inhibitory drugs was determined by reversed-phase thin-layer chromatography, and the effect of salt concentration on the reversed-phase retention was studied by adding ammonium chloride to the eluent. Each drug exhibited regular retention behaviour, its RM value linearly decreasing with increasing concentration of methanol in the eluent. Ammonium chloride decreased the retention: the effect was higher at lower salt concentrations, which indicates that the phenomenon is of saturation character. The influence of ammonium chloride depended on the concentration of methanol (on the dielectric constant of the eluent) suggesting that methanol suppresses the dissociation of ammonium chloride resulting in a modified salting-in effect.

Ammonium Chloride↗
PubMedDate not supplied

[Metabolic processes in the tissues of pregnant animals and their fetuses affected by ammonium chloride].

The acid-alkali state of blood as well as some parameters of energy, nitrogen and protein metabolism in animals at the last stage of pregnancy and in their fetuses have been studied as affected by ammonium chloride. It is shown that ammonium chloride in a dose of 0.6 g per 1 kg of the body weight that was given to duply pregnant animals per os evokes the decrease of O2 partial pressure and the increase of the amount of CO2 in the blood, stimulates the processes of ureogenesis and glycoly-sis, inhibits reactions of tissue respiration, changes redox-state of free nicotinamide coenzymes and intracellular level of inorganic phosphorus in the organism of animals at the last stage of pregnancy. Analogous changes of metabolic processes under high content of ammonium chloride in the organism are also observed in their fetuses.

Ammonium Chloride↗
PubMed1983

Ruminal infusion of ammonium chloride in lactating cows to determine effect of pH on ammonia trapping.

Milking rations containing 16 (control), 13.2, and 10.4% protein were fed to four midlactation, rumen-fistulated Holstein cows. Ammonium chloride was infused ruminally for 5 consecutive days after morning feeding when cows were fed milking rations containing 13.2 and 10.4% protein. Amount infused was equivalent to the ammonia in 1 or 2% dietary urea. Rumen and blood samples were taken prior to and following morning feedings. Intake of milking ration was the same across treatments. Initial rumen pH was higher for ammonium chloride treatments. It then declined, as did the control, to the same, lowest pH at 1.5 to 3 h postfeeding. Rumen ammonia increased rapidly for cows receiving both ammonium chloride treatments to .5 h postfeeding and then declined rapidly. Blood urea nitrogen was highest for cows fed the control ration, peaked .5 h postfeeding for cows infused with the low ammonium chloride, then dropped and peaked again 6 h postfeeding. Blood ammonia was highest among treatments for control cows and differed by sampling time only for control cows with a peak .5 h postfeeding. Because lower rumen pH traps ammonia preventing rapid absorption into blood, interpretation of high rumen ammonia must consider effect of rumen pH.

Ammonia↗
PubMed1996

Investigation into intraerythrocytic and extraerythrocytic acid-base and electrolyte changes after long-term ammonium chloride administration in dogs.

OBJECTIVES: To investigate the effect of ammonium chloride-induced urine acidification on acid-base status (ABS) of blood, plasma, and erythrocytes, and to compare the diagnostic value of acid-base analysis for erythrocytes with that for blood and plasma. DESIGN: Ammonium chloride (100 mg/kg of body weight) was administered orally every 12 hours for 8 consecutive days. The ABS was determined daily in venous blood, plasma, and lysed, packed erythrocytes (erythrolysate) and in urine. In plasma and erythrocytes, concentrations of sodium Na+) and potassium (K+) were analyzed. ANIMALS: 16 clinically normal (8 treated and 8 control dogs. PROCEDURE: The acid-base analysis (standard pH, standard bicarbonate concentration, base excess, and carbon dioxide tension) in blood, plasma, and erythrocytes was determined by use of the CO2, O2 gas equilibration method. Determination of urine ABS (pH, concentrations of acids and bases, net acid-base excretion, base-acid quotient) was performed by titration methods. Determination of concentrations of Na+ and K+ in erythrocytes was performed by flame photometry, and in plasma, by use of ion-specific electrodes. RESULTS: Ammonium chloride caused metabolic acidosis in blood and plasma, but no change of ABS in erythrocytes. The concentrations of K+ in plasma and erythrocytes did not change in treated dogs; however, the concentrations of Na+ in plasma and erythrocytes decreased significantly (P < 0.05) after ammonium chloride administration. Urinary acid excretion increased significantly (P < 0.05) in treated dogs; urine pH was between 4.51 and 5.49 at all times. CONCLUSIONS: Ammonium chloride administration (100 mg/kg, PO, q 12 h) causes substantial blood and urine acidification but does not influence erythrocyte ABS. In this study, determination of erythrocyte ABS did not provide any additional benefit in diagnosing metabolic acidosis, compared with analysis of blood.

Acid-Base Equilibrium↗
PubMed1989

Role of acidic intracellular compartments in the biosynthesis of Dictyostelium lysosomal enzymes. The weak bases ammonium chloride and chloroquine differentially affect proteolytic processing and sorting.

Radiolabel pulse-chase and subcellular fractionation procedures were used to analyze the transport, proteolytic processing, and sorting of two lysosomal enzymes in Dictyostelium discoideum cells treated with the weak bases ammonium chloride and chloroquine. Dictyostelium lacks detectable cation-independent mannose-6-phosphate receptors and represents an excellent system to investigate alternative mechanisms for lysosomal enzyme targeting. Exposure of growing cells to ammonium chloride, which increased the pH in intracellular vacuoles from 5.4 to 5.8-6.1, slowed but did not prevent the proteolytic processing and correct localization of pulse-radiolabeled precursors to the lysosomal enzymes alpha-mannosidase and beta-glucosidase. Additionally, ammonium chloride did not affect transport of the enzymes to the Golgi complex, as they acquired resistance to the enzyme endoglycosidase H at the same rate as in control cells. When the pH of lysosomal and endosomal organelles was raised to 6.4 with higher concentrations of ammonium chloride, the percentage of secreted (apparently mis-sorted) precursor polypeptides increased slightly, but proteolytic processing of intermediate forms of lysosomal enzymes to mature forms was greatly reduced. The intermediate and mature forms of alpha-mannosidase and beta-glucosidase did, however, accumulate intracellularly in vesicles similar in density to lysosomes. In contrast, in cells exposed to low concentrations of chloroquine the intravacuolar pH increased only slightly (to 5.7); however, enzymes were inefficiently processed and, instead, rapidly secreted as precursor molecules. Experiments involving the addition of chloroquine at various times during the chase of pulse-radiolabeled cells demonstrated that this weak base acted on a distal Golgi or prelysosomal compartment to prevent the normal sorting of lysosomal enzymes. These results suggest that although acidic endosomal/lysosomal compartments may be important for the complete proteolytic processing of lysosomal enzymes in Dictyostelium, low pH is not essential for the proper targeting of precursor polypeptides. Furthermore, certain amines may induce mis-sorting of these enzymes by pH-independent mechanisms.

Acetylglucosaminidase↗
PubMed1983

Effects of charcoal, sodium bicarbonate, and ammonium chloride on chlorpropamide kinetics.

The effects of activated charcoal, sodium bicarbonate, and ammonium chloride by mouth on chlorpropamide kinetics was studied in six healthy subjects. Activated charcoal, 50 gm, given immediately after 250 mg chlorpropamide reduced its absorption by 90%, but when given in repeated doses from 6 hr on (50 gm followed by 12.5 gm at 6-hr intervals) it did not shorten the chlorpropamide half-life (t 1/2). The t 1/2 of chlorpropamide was shortened from 49.7 +/- 7.4 to 12.8 +/- 1.1 hr by sodium bicarbonate and prolonged to 68.5 +/- 10.5 hr by ammonium chloride. The 72-hr urinary excretion of chlorpropamide was increased fourfold by alkalinization and decreased to 1/20 of baseline by acidification of the urine. The renal clearance of chlorpropamide correlated with urinary pH, ranging from 1 to 1000 ml/hr at the pH from 5 to 8. Urinary pH is likely to explain at least a part of great interindividual differences in the serum chlorpropamide concentrations during steady-state and variations in amount of urinary metabolites. In chlorpropamide intoxications activated charcoal can reduce absorption and alkalinization of the urine accelerates its elimination.

Adult↗
PubMed1984

Thyroparathyroidectomy exaggerates calciuric action of ammonium chloride in rats.

The effects of chronic ammonium chloride (NH4Cl) administration on urinary calcium, urinary hydroxyproline, and calcium and phosphate balances were studied in intact and thyroparathyroidectomized (TPTX) rats. NH4Cl (2 g/100 g diet) was administered for 16 days to growing rats consuming a low calcium (0.1% Ca) diet. NH4Cl increased urinary calcium and hydroxyproline. NH4Cl caused greater urinary calcium loss in TPTX than in intact rats, but hydroxyproline excretion in these groups was similar. Compensatory increases in net alimentary absorption of calcium and phosphate occurred in intact but not in TPTX rats. Urinary cAMP was depressed by thyroparathyroidectomy but was unaffected by NH4Cl. It is concluded that NH4Cl depresses renal tubular reabsorption of calcium and increases bone resorption in the presence and absence of the thyroid and parathyroid glands. However, our results suggest that parathyroid hormone plays an important calcium-sparing role, while calcitonin may act to limit the rate of bone resorption, in intact rats during chronic administration of NH4Cl.

Ammonium Chloride↗
PubMed1984

Evaluation of ammonium chloride as a urinary acidifier in the cat.

Twenty-four cats were fed a dry commercial cat food once daily for 2 weeks and then ad libitum for 2 weeks. Urine pH was measured 4 times daily the last 3 days of each feeding period. Subsequently, the cats were allotted to 2 equal groups and fed ad libitum an experimental, dry ration with or without 1.5% ammonium chloride for 11 months. During this period, urine pH was measured at 1, 3, 6, and 9 weeks, then monthly through 29 weeks, and then every 6 weeks for the duration of the study. When the cats were fed ad libitum, urine pH remained constant throughout the day, regardless of ration. In cats fed once daily, urine pH increased to 7.6 by 2 hours after feeding and remained between 6.6 and 7.6 for 9 hours. Urine pH remained constant throughout the study when cats were fed the experimental ration with or without 1.5% ammonium chloride, but was significantly different (P less than 0.01) between the 2 groups, 5.9 +/- 0.3 (n = 1,035) and 7.0 +/- 0.5 (n = 616), respectively. Ammonium chloride consumption had no effect on food and water consumption or body weight. It was concluded that ammonium chloride was an effective urinary acidifier for a prolonged time, maintained urine pH below 6.6, and did not decrease food intake when given at a concentration of 1.5% of the diet.

Ammonium Chloride↗
PubMed1981

Effects of ammonium chloride on urinary pH and cigarette smoking behavior.

We determined the effects of acidification of urinary pH on cigarette smoking behavior to assess the postulated relationships between stress, urinary pH, and cigarette smoking. Urine was acidified by short-term administration of 12.5, 25, and 50 mg/kg ammonium chloride and long-term administration of 50 mg/kg ammonium chloride. Measurements of cigarette smoking behavior included the number of cigarettes smoked as well as automated measures of puff frequency and duration. Short- and long-term administration of ammonium chloride induced decreases in urinary pH but failed to induce any substantial changes in number of cigarettes smoked, puff frequency, or puff duration.

Ammonium Chloride↗
PubMed1989

The effect of ammonium chloride on the multiplication of herpes simplex virus type 1 in Vero cells.

The multiplication of herpes simplex virus type 1 (HSV-1) in Vero cells is inhibited by ammonium chloride. The formation of infectious virus was inhibited immediately after the addition of the agent into the culture fluid and was restored by removal of the agent. Although neither viral DNA replication nor nucleocapsid formation were affected by the addition of ammonium chloride at 4 h postinfection, the agent markedly inhibited the formation of enveloped particles and completely the formation of infectious progeny virus. These results indicate that one of the effects of ammonium chloride on the multiplication of HSV-1 is the inhibition of envelopment of viral nucleocapsids. In addition, the envelopment of HSV-1 nucleocapsids was inhibited immediately after the addition of monensin into the culture fluid. These findings suggest the importance of acidic pH of an intracellular compartment in the envelopment of HSV-1.

Ammonium Chloride↗
PubMed1972

The effect of steroids and ammonium chloride acidosis on phosphoenolpyruvate carboxykinase in rat kidney cortex. II. The kinetics of enzyme induction.

The kinetics of the induction of rat kidney phosphoenolpyruvate carboxykinase activity after triamcinolone and ammonium chloride administration have been investigated with a view to the further differentiation of the two processes. The half-life of kidney phosphoenolpyruvate carboxykinase activity, as measured from the decay curve after a single doses of triamcinolone, is approximately 1.4 hr. This compares with a half-life for the enzyme from acidotic kidney of approximately 3.4 hr. Analysis of the data indicates that the induction of phosphoenolpyruvate carboxykinase activity by triamcinolone may be attributed to an increase in de novo protein synthesis. Induction by acidosis is qualitatively distinct and is partly attributed to a reduction in the rate of decay of phosphoenolpyruvate carboxykinase activity. The activities of the gluconeogenic enzymes glucose-6-phosphatase, fructose-1,6-diphosphatase, and phosphoenolpyruvate carboxykinase in both liver and kidney have been measured in animals separately treated with triamcinolone and ammonium chloride. Triamcinolone significantly increases the activities of liver phosphoenolpyruvate carboxykinase, kidney glucose-6-phosphatase, and kidney phosphoenolpyruvate carboxykinase only; ammonium chloride stimulates a 200% increase in kidney phosphoenolpyruvate carboxykinase, but has no effect on the other enzymes. The induction processes whereby triamcinolone increases phosphoenolpyruvate carboxykinase activities in liver and kidney differ quantitatively.

Acidosis↗
PubMed1980

Effect of sodium bicarbonate and ammonium chloride ingestion in experimental gentamicin nephrotoxicity in rats.

To examine the possibility that gentamicin binding to renal tubular epithelium is electrostatic, the effect of sodium bicarbonate-induced alkaline diuresis and ammonium chloride administration on the course of gentamicin nephrotoxicity in male Fischer 344 rats was examined. After 14 days of gentamicin, sodium bicarbonate drinking animals did not differ significantly from tap water drinking controls in the degree of nephrotoxicity as determined by serum creatinine, in vitro para-aminohippurate and N-methylnicotinamide uptake, histology and renal cortical gentamicin concentrations. However, 7/10 sodium bicarbonate drinking animals had extensive intratubular renal calcifications as compared to 0/29 tap water drinkers. Ammonium chloride drinking animals had more severe toxicity than tap water drinking controls. We conclude that in our model, sodium bicarbonate administration does not reduce experimental gentamicin toxicity and is associated with intratubular calcification. Ammonium chloride potentiates gentamicin nephrotoxicity.

Ammonium Chloride↗
PubMed1986

Experimental studies on therapy of metabolic alkalosis during the beginning of uremia. Influences of ammonium chloride on the intra- and extracellular acid-base status of the rat.

Metabolic alkalosis during renal failure or uremia presents a difficult problem for the clinician. In this study the effects of ammonium chloride, an agent clinically used for the correction of severe metabolic alkalosis, were studied on the extra- and intracellular acid-base balance of nephrectomized rats. While the extracellular acid-base status was determined from blood gas measurements, intracellular pH was calculated from the distribution of 5,5-dimethyl-2,4-oxazolidinedione. It was found that the administration of NH4Cl leads to a significant increase of intracellular pH though extracellular plasma pH decreases, and that ammonium chloride causes only an insignificant reduction of the intracellular bicarbonate concentration. The observed intracellular pH increase may have adverse consequences for patients and raises objections to the further use of ammonium chloride in the treatment of metabolic alkalosis, especially during renal failure or uremia.

Acid-Base Equilibrium↗