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PubMed1990

Prolonged storage of red cells with ammonium chloride and mannitol.

Recently, a new preservation medium consisting of ammonium chloride added to adenine, glucose, mannitol, citrate, and potassium phosphate, was described. Unexpectedly, the predominant effect on red cell storage was an initial elevation of ATP levels, followed by remarkable maintenance of these levels at 12 to 18 weeks with acceptable 24-hour survival. The aim of the study reported here was to investigate the reasons for the advantageous effects of the different constituents. With the new preservation medium, ATP content was maintained at acceptable levels for at least 8 weeks with low spontaneous hemolysis. However, similarly high ATP levels were also maintained in the absence of ammonium chloride. Comparable results were obtained on substituting sodium for potassium salts in the new medium. When the main cation in the preservation medium was replaced by sodium, the addition of ammonium or rubidium chloride did not provide an advantage. Therefore, ammonium chloride was not essential for this medium, whereas mannitol does seem to be essential in a solution whose content of nonpermeant solutes is hypotonic.

2,3-Diphosphoglycerate↗
PubMed1994

Effect of ammonium chloride on multiplication of rinderpest virus in Vero cells.

Ammonium chloride, a lysosomotropic weak base, inhibited replication of rinderpest virus in Vero cells. The inhibition of replication was dose-dependent and the minimum effective dose of ammonium chloride was determined as 5-10 mmol/l. The fusion efficiency and the yield of both cell-free and cell-associated virus were reduced in the presence of the inhibitor. Western blot analysis of rinderpest virus-infected Vero cells revealed that synthesis of two virus-induced polypeptides were affected by the presence of ammonium chloride.

Animals↗
PubMed2006

N-Chlorotaurine and ammonium chloride: an antiseptic preparation with strong bactericidal activity.

The bactericidal activity of the endogenous antiseptic N-chlorotaurine (NCT) is significantly enhanced in the presence of ammonium chloride which induces the formation of monochloramine (NH(2)Cl) whose strong bactericidal activity is well known. In this study the properties of NCT plus ammonium chloride have been investigated. The reaction of active chlorine compounds like chloramine-T (N-chlorotoluene-sulfonamide sodium), chloroisocyanuric acid derivatives, hypochlorites (NaOCl, CaOCl(2)) with ammonium chloride did not stop at the stage of monochloramine, and the pungent smelling by-products di- and trichloramine, NHCl(2) and NCl(3), were also formed. This was not the case with NCT where only monochloramine was generated. The equilibrium constant of the reaction of NCT with ammonium was found to be [Formula: see text] , which allows to estimate the equilibrium concentration of monochloramine in aqueous solutions of NCT and ammonium chloride. At concentrations each ranging between 0.01% and 1.0% it comes to [NH(2)Cl]=3.5-254 ppm. As an unexpected result the monochloramine containing formulation turned out to be most stable in plain water without buffer additives. Quantitative killing assays revealed complete inactivation of 10(6) to 10(7)CFU/mL of seven bacterial strains by 0.1% NCT plus 0.1% ammonium chloride within 5 min, while with plain 0.1% NCT an incubation time of 2-4h was needed to achieve the same effect. The highly significant increase of bactericidal activity (200-300-fold) could be assigned to the presence of monochloramine which could be isolated by vacuum distillation. Aqueous solutions of NCT and ammonium chloride provide a highly effective and well tolerable antiseptic preparation appropriate to a treatment cycle of at least 1 month if stored in the refrigerator.

Ammonium Chloride↗
PubMed1994

Endotoxin-induced nitric oxide synthesis in the perfused rat liver: effects of L-arginine and ammonium chloride.

We used the single-pass-perfused rat liver model to study short-term regulation of endotoxin-inducible nitric oxide synthesis by following the release of nitrite and nitrate, the oxidation products of nitric oxide, into the effluent perfusate. In endotoxin-pretreated livers, the basal nitrite+nitrate release was 5.3 +/- 1.2 nmol.gm liver-1.min-1. Nitrite and nitrate release was stimulated by L-arginine in a dose-dependent and saturable fashion. Maximal nitrite+nitrate release with 1 mmol/L L-arginine infused to the influent perfusate was 10.2 +/- 1.1 nmol.gm liver-1.min-1, with a half-maximal effect at 53 mumol/L L-arginine. In the absence of molecular oxygen, nitric oxide synthesis was inhibited. Ammonium chloride infusion also stimulated nitrite and nitrate release to a maximal rate of 9.2 +/- 0.8 nmol.gm liver-1.min-1 with half-maximal effects at 60 mumol/L ammonium chloride. Ammonium chloride-stimulated nitrite and nitrate release was abolished when urea synthesis was inhibited by bicarbonate-free liver perfusion. Citrulline and ornithine (200 mumol/L each) were without effect on nitrite and nitrate release. L-Nitroarginine methyl ester inhibited both, L-arginine-and ammonium chloride-induced nitrite and nitrate release. Stimulation of nitric oxide synthesis by L-arginine and ammonium chloride addition (1 mmol/L each) was accompanied by a threefold-to-fourfold increase of cyclic GMP release into the effluent perfusate. In livers of endotoxin-pretreated rats the urea production from L-arginine was higher than that in untreated livers, suggesting induction of an L-arginine transport system in hepatocytes by endotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonium Chloride↗
PubMed1989

Ammonium chloride alters secretory protein sorting within the maturing exocrine storage compartment.

Addition of 20 mM ammonium chloride during in vitro chase incubation of [35S]methionine pulse-labeled parotid tissue does not perturb the magnitude or radiochemical composition of secretion stimulated by isoproterenol. An apparent inhibition of stimulated output of radiolabeled secretory proteins that was observed when ammonium chloride was added immediately postpulse (but not at later time points prior to stimulation) could be accounted for by slowdown in Golgi transit of exocrine secretory protein at a stage prior to completion of terminal glycosylation. Thus, ammonium chloride does not block entry of newly synthesized secretory proteins into the secretagogue-releasable storage granule compartment. By contrast, ammonium chloride increases the output and substantially alters the relative composition of newly synthesized protein in unstimulated secretion. The latter effects could be assigned to stages of intracellular transport that normally occur at chase times greater than 60 min postpulse and thus are focused within the maturing acinar storage granule. Notably, the compositional alterations cannot reflect the preferential exocytosis of immature granules. Taken together, these results suggest that the sorting of exocrine secretory proteins into the secretagogue-regulated pathway may not involve positive selection by a pH-based process initiated in a pregranule compartment. Rather, unstimulated secretion may arise by a negative sorting (or exclusion) process that occurs during compaction of proteins for storage within maturing granules and that is perturbed by weak base addition. Sorted (or excluded) proteins would appear to follow the vesicular (nongranular) secretory pathway that originates in maturing granules (von Zastrow, M., and Castle, J.D. (1987) J. Cell Biol. 105, 2675-2684).

Ammonium Chloride↗
PubMed1983

Susceptibility of the expression of parallel tubular structures in lymphocytes to the exposure to ammonium chloride buffer.

In isolation procedures for lymphocytes, isotonic ammonium chloride buffers are frequently used to lyse erythrocytes. In addition to evidence for an effect on lymphocyte function we now report a morphological alteration after treatment of lymphocytes with ammonium chloride buffer. Expression of parallel tubular structures was lost and only amorphous, electron-dense granules could be observed.

Ammonium Chloride↗
PubMedDate not supplied

[Effect of ammonium chloride on NDP(P)+-dependent glutamate dehydrogenase from bovine liver].

It was shown that NAD(P)(+)-dependent glutamate dehydrogenase from bovine liver (EC 1.4.1.3) was activated under the action of ammonium chloride in concentration which corresponded to the level of ammonium in normal blood (2-10 mM). Ammonium chloride increases the activity of glutamate dehydrogenase 1.8 times. Having enhanced the level of ammonium chloride to the amount which corresponds to the level of ammonium ions in blood during the pathology (10-25 mM), this substance inhibited the enzyme activity of glutamate dehydrogenase. Influence of 20 mM ammonium chloride on IR-spectra of NAD(P)(+)-dependent glutamate dehydrogenase in the deuterium oxide solution leads to the widening of the absorption line at 3300 cm-1 toward the higher energy. It is supposed that inhibition action of ammonium ions on the activity of glutamate dehydrogenase is connected with partial destruction of stereoregular hydrogen bonds in the enzyme molecule.

Ammonium Chloride↗
PubMed1978

The effect of ammonium chloride and glucagon on the metabolism of glutamine in isolated liver cells from starved rats.

1. Glucagon stimulated gluconeogenesis from glutamine in isolated liver cells to a far greater extent than that from any other amino-acid precursor. 2. Low concentrations of ammonium chloride (less than 1 mM) stimulated glucose production from glutamine. Glucagon further stimulated this glucose production, even in the presence of saturating concentrations of ammonium chloride. 3. In agreement with previous reports, glutamine hydrolysis by isolated mitochondria was found to be stimulated by ammonium chloride. It was found that ammonium chloride activated mitochondrial glutamine hydrolysis at the same concentrations at whict it stimulated glucose production from glutamine in liver cells. The effective activation of glutamine hydrolysis by ammonimum chloride in intact mitochondria was partially inhibited by rotenone and was abolished by uncoupling agents. 4. The addition of glucagon to hepatocytes metabolising glutamine led to a decrease in the intracellular concentration of glutamine and an increase in the intracellular concentration of glutamate. 5. It is likely that glucagon stimulates gluconeogenesis from glutamine by mechanisms which are additional to those that may operate in the stimulation of gluconeogenesis from other amino-acid precursors. It is suggested that both ammonium chloride and glucagon exert their effects on glutamine metabolism by increasing the effective activity of mitochondrial glutaminase (EC 3.5.1.2.).

Amino Acids↗
PubMed1993

[The morphologic changes of rat astrocytes treated with ammonium chloride in vitro].

Primarily cultured astrocytes were treated with ammonium chloride in various concentrations, namely 5mM, 10mM and 15mM. The changes were does-and time-dependent. After 1 to 4 days of treatment, there were mild vacuolization, eosinophilic granulation, hypertrophy and hyperplasia with increasing mitotic figures and enhanced GFAP reactivity. The number of cells and mitoses were four and five times more than those of the normal controls respectively (P < 0.01). The cells displayed an increase in number and width of the processes. The mean area, perimeter as well as the form factors were significantly increased as compared with those of the control (P < 0.01). While in the later stage (7-10 days after NH4Cl treatment), lamellation and fragmentation of the cellular processes, remarkable vacuolization and granulation as well as appearance of eosinophilic bodies in the cytoplasm were obtained accompanied with vacuolated or pyknotic nuclei. The GFAP reactivity became weak even negative. The results indicated that to the administration of ammonium chloride, the astrocytes had a dynamic plasticity.

Ammonium Chloride↗
PubMed1975

The effect of chronic ammonium chloride ingestion on parathyroid hormone function.

The purpose of this study was to examine the effect of ammonium chloride ingestion on the hypercalcemic effect of parathyroid hormone in vivo. Thyroparathyroidectomized rats were given 1.5% ammonium chloride for 5-6 days. Ingestion of ammonium chloride increased serum calcium, but also significantly enhanced the calcium elevating effect of injected parathyroid extract. This result is compatible with a proposed hypothesis that the calcium mobilizing function of the parathyroid hormone may be enhanced by the hormone's own influence on systemic hydrogen ion concentration.

Administration, Oral↗
PubMed1991

Effects of dietary ammonium chloride and variations in calcium to phosphorus ratio on silica urolithiasis in sheep.

Ammonium chloride was added to diets varying in Ca content to evaluate its potential in preventing silica urolith formation in sheep. A 2 x 2 factorial experiment involved wether lambs with ad libitum access to a diet of 50% grass hay and 50% ground oats plus supplement. The basal diet contained on a DM basis 3.3% SiO2, .31% Ca, .22% P, 11.6% CP, and 26% ADF. Treatments (38 to 39 lambs/treatment) consisted of a control (C), limestone to increase dietary calcium to .6% (L), 1% ammonium chloride (A), and L + A (LA). After a 118-d experimental period, siliceous kidney deposits were found only in C and L, with silica making up 93% to 95% of the urolithic ash. Urolith incidences were 13% (C) and 18% (L), respectively. The lack of urolith development in lambs fed A and LA (ammonium chloride effect, P less than .01) and a trend toward a lower urolith incidence in C vs L (P less than .02) support the hypothesis that acid-forming effects of the diet and a reduction in the dietary Ca to P ratio reduce silica urolith formation.

Ammonium Chloride↗
PubMed1975

Glutamine production by the isolated perfused rat heart during ammonium chloride perfusion.

Myocardial levels of ammonia, glutamate, and glutamine and the release of glutamate and glutamine were studied in the isolated perfused rat heart during perfusion with ammonium chloride, epinephrine, and conditions of anoxia or ischaemia. Perfusion for 15 min with effective ammonium chloride concentrations of 0.53, 0.71, and 2.06 mmol/l resulted in glutamine production of 1.34, 0.95, and 4.41 mmol with 15 min-1/200 dry weight compatible with the presence of glutamine synthetase in rat myocardium. Myocardial ammonium content was unchanged by perfusion with 0.53 and 0.71 mmol/l ammonium chloride, but was increased by 1.36 mumol with 15 min-1/200 mg dry weight by perfusion with 2.06 mmol/l ammonium chloride. Increased myocardial contents of ammonia and glutamine were not accompanied by depression of left ventricular pressure. Perfusion with epinephrine (0.20 mug/ml) resulted in an increased myocardial content of glutamine. Anoxia or ischaemia resulted in no changes in ammonia content, and no changes in glutamine or glutamate production. The net release of glutamine into the perfusate was about 10 times the net release of glutamate.

Ammonia↗
PubMed1983

Percutaneous absorption of an antimicrobial organosilicon quarternary ammonium chloride in rabbits.

The percutaneous absorption of an organosilicon quaternary ammonium chloride (14C)-3-(trimethoxysilyl)-propyldimethyloctadecyl ammonium chloride (14C-Si-QAC) was studied in rabbits. Aqueous solution of 14C-Si-QAC was either applied to the intact, clipped back of animals for 10 days or administered by a single intravenous dose. Urine and feces were collected at 24-h intervals and tissue concentration of radioactivity was determined at the end of the 10-day study period. Elimination of 14C-Si-QAC after parenteral administration was slow and occurred by both urine and feces (13.5% in urine and 20% in feces). No radioactivity was found in the urine of dermally treated animals. Tissue concentrations of 14C were highest in the liver, lung and kidneys after i.v. administration. None was detected in tissues of dermally treated animals. The results showed that the absorption of 14C-Si-QAC through the skin of the rabbit was essentially zero. The potential absorption hazard of the use of this antimicrobial agent in contact with the skin is therefore considered to be insignificant.

Animals↗
PubMed2001

Long-term ammonium chloride or sodium bicarbonate treatment in two models of polycystic kidney disease.

Administration of ammonium chloride aggravates, while short-term administration of sodium or potassium bicarbonate lessens the development of polycystic kidney disease in Han:SPRD rats. We have conducted studies to determine whether the protection afforded by the administration of sodium bicarbonate is sustained and prevents development of uremia during chronic administration and whether the effects of the administration of ammonium chloride and sodium bicarbonate are also observed in a different model of polycystic kidney disease, the CD1-pcy/pcy mouse. We found that chronic administration of 200 mM sodium bicarbonate to Han:SPRD rats inhibited cystic enlargement and prevented the subsequent development of interstitial inflammation, chronic fibrosis, and uremia. We also found that, while the administration of ammonium chloride has similar effects in Han:SPRD rats and CD1-pcy/pcy mice, the administration of sodium bicarbonate is only protective in the Han:SPRD rats. This probably reflects differences in these models (predominately involvement of proximal tubules in Han:SPRD rats and of collecting ducts and distal tubules in pcy/pcy mice) and the different location and nature of the renal metabolic responses to the administration of acid or alkaline load.

Ammonia↗
PubMed1975

Xenopus laevis cement gland as an experimental model for embryonic differentiation. I. In vitro stimulation of differentiation by ammonium chloride.

Ectoblastic cells explanted from the animal pole of young Xenopus laevis gastrulae have been cultured in vitro. When these cells were cultured for five days in standard salt solutions they formed atypical epidermis. When they were first submitted for 6 h to Holtfreter solution containing ammonium chloride and then transferred for five days in standard Barth's solution they underwent differentiation into typical cement gland tissue. The optimum concentration of ammonium chloride was 10 mM. Below and above this concentration the resulting cement glands had a smaller volume. The optimum duration for the initial stimulation with 10 mM ammonium chloride in Holtfreter solution was 6 h. Shorter stimulation times produced only small cement glands. Longer initial incubations in ammonium chloride resulted in progressive dissociation of the explants. To obtain the best differentiation into cement gland it appeared that the pH of the ammonium chloride solution should be between 7-5 and 7-7. When the stimulation is performed under these optimum conditions the cement gland measured after five days of culture accounts for 80-90 percent of the explanted tissue. This means that all or almost all of the competent superficial layer of the ectoblastic cells underwent differentiation into cement gland. No other differentiated tissue was observed in the explants. The cement gland is a very simple organ containing only one single cell type. The gland obtained under the described in vitro conditions is therefore proposed as an experimental model for biochemical studies on early embryonic differentiation.

Ammonium Chloride↗
PubMed2000

Ammonium chloride potentiation of streptozotocin-induced diabetes in juvenile pigs.

In preparation for direct vital microscopic evaluation of microcirculatory dynamics in the diabetic pig myocardium, we were initially unsuccessful in inducing sustained hyperglycemia in juvenile pigs using streptozotocin according to previously reported methods. Therefore, we modified the technique in a way previously unreported in an effort to improve the success rate of diabetes induction. In the first set of 9 pigs, we followed described methods of intravenous injection with 150 mg/kg streptozotocin. In the second group of 9, the technique was modified. The change was based on human studies with ammonium chloride and animal experiments with alloxan, and consisted of the addition of a period of pretreatment with ammonium chloride. Of the nine pigs not treated with ammonium chloride, only two developed sustained hyperglycemia in excess of 17 mmol/L (300 mg/dl), and only after reinjection with a full dose of streptozotocin within 7 days of the first injection. Conversely, of the ammonium chloride pretreated pigs, eight of nine developed diabetes. We conclude that the addition of ammonium chloride to produce systemic acidosis prior to streptozotocin injection improves the efficacy of the drug.

Acidosis↗
PubMed1986

Ammonium chloride slows transport of the influenza virus hemagglutinin but does not cause mis-sorting in a polarized epithelial cell line.

The effects of the weak base ammonium chloride on the intracellular transport and sorting of the influenza hemagglutinin to the apical plasma membrane of polarized epithelial cells were examined in infected Madin-Darby canine kidney cells. Ammonium chloride was found to significantly retard cell surface appearance of the hemagglutinin but to have no effect on either the initial sorting or steady-state levels of hemagglutinin on the apical domain. Based on the rate of acquisition of resistance to endo H, the timed addition of ammonium chloride, and dissociation by reduced temperature incubation of cell surface appearance of the hemagglutinin from early stages of transport and processing, it was determined that the likely site of ammonium chloride action was the trans Golgi.

Ammonium Chloride↗
PubMed1984

Effects of ammonium chloride on resorption of fetal rat bones in organ culture.

Ammonium chloride, a known inhibitor of lysosomal function, was found to be a rapid and potent inhibitor of 45Ca release from fetal rat bones in organ culture. The response to parathyroid hormone and prostaglandin E2 was inhibited in a dose-related, reversible fashion. The activity of the lysosomal enzyme beta-glucuronidase in the medium closely paralleled 45Ca release. Ammonium chloride may now be added to the list of antilysosomal agents that inhibit bone resorption in vitro.

Ammonium Chloride↗