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PubMed1986

Regulation of nitrogenase activity by ammonium chloride in Azospirillum spp.

Ammonium chloride (greater than or equal to 0.05 mM) effectively and reversibly inhibited the nitrogenase activity of Azospirillum brasilense, Azospirillum lipoferum and Azospirillum amazonense. The glutamine synthetase inhibitor L-methionine-DL- sulfoximine abolished this "switch-off" in A. lipoferum and A. brasilense, but not in A. amazonense. Azaserine, an inhibitor of glutamate synthase, inhibited nitrogenase activity itself. This provides further evidence for glutamine as a metabolite of regulatory importance in the NH4+ switch-off phenomenon. In A. brasilense and A. lipoferum, a transition period before the complete inhibition of nitrogenase activity after the addition of 1 mM ammonium chloride was observed. The in vitro nitrogenase activity also was decreased after treatment with ammonium. During sodium dodecyl sulfate-polyacrylamide gel electrophoresis, a second dinitrogenase reductase (Fe protein) subunit appeared, which migrated in coincidence with the modified subunit of the inactive Fe protein of the nitrogenase of Rhodospirillum rubrum. After the addition of ammonium 32P was incorporated into this subunit of the Fe protein of A. brasilense. In A. amazonense, the inhibition of nitrogenase activity by ammonium was only partial, and no transition period could be observed. The in vitro nitrogenase activity of ammonium-treated cells was not decreased, and no evidence for a modified Fe protein subunit was found. Nitrogenase extracts of A. amazonense were active and had an Fe protein that migrated as a close double band on sodium dodecyl sulfate-polyacrylamide gel electrophoresis.

Ammonium Chloride↗
PubMed1979

Effect of ammonium chloride on osmotic behavior of red cells in nonelectrolytes.

Ammonium chloride, demonstrated to be a permeating electrolyte for human red cells in water or sodium chloride solutions, has been shown to act as if it contributes osmotic support in the presence of sucrose. The additional protection provided by ammonium chloride against hemolysis in hypotonic sucrose was found to approximate the milliosmolar concentration of the added salt. In view of previous suggestions that potassium loss was responsible for the increased protection observed with hypotonic nonelectrolyte alone, it was considered reasonable that the further protection afforded by ammonium chloride might reflect a comparable mechanism. Such a relationship was not observed. When added to isosmotic sucrose, ammonium chloride was found to be as effective as sodium chloride in preventing rather than augmenting potassium loss, in accord with the observations of others. Under hypotonic conditions, however, the addition of ammonium chloride had no effect on potassium loss beyond that observed in hypotonic sucrose alone. Equivalent additions of sodium chloride eliminated the potassium loss entirely. It was concluded that sucrose, and possibly other nonelectrolytes, acted to modify the red cell's permeability to ammonium chloride. It is this conversion of ammonium chloride to an impermeant molecule that is considered to be responsible for the observed osmotic support as well as for the markedly disparate findings in sodium chloride solutions.

Ammonium Chloride↗
PubMed2006

Effects of dioctadecyl dimethyl ammonium chloride on the rheological behavior of behenyl trimethyl ammonium chloride/1-hexadecanol/water ternary system.

The effects of dioctadecyl dimethyl ammonium chloride (DODAC) on the rheological properties of ternary systems consisting of behenyl trimethyl ammonium chloride (C22TAC), 1-hexadecanol (C16OH), and water are studied to improve the long-term stability and to establish the preparation method of cosmetic products. The basic ternary systems behave as solids at low stresses, due to the formation of lamella liquid crystals called alpha gel. The additions of DODAC to ternary systems cause the rupture of alpha gel structures and transformation to vesicles. The structures of molecular assemblies are confirmed through particle size distribution, differential scanning calorimetry, and freeze fracture electron microscopy. The vesicle structures formed in coexistence of single-chain surfactant and double-chain surfactant are highly stable. Because the quaternary systems are considered to be constructed by the mixtures of alpha gel and vesicles at the appropriate concentrations of DODAC, the rheology can be controlled by the structural balance between them.

Fatty Alcohols↗
PubMed1979

Balance of net base in the rat. V. Effects of oral ammonium chloride loading.

The physiology of oral ammonium chloride loading was studied in four groups of male weanling rats weighing about 100 g and fed either standard ground Rostock rat food (containing 317 mmol net base/kg) or ground barley (containing only 20 mmol net base/kg). One group of animals on the Rostock diet received oral supplements of ammonium chloride (approximately 32 mmol . kg-1 . day-1) sufficient to provide a net zero rate of oral net base intake. In this group, ongoing fecal net base excretion caused net acid to be absorbed at an average rate of 15 mmol . kg-1 . day-1. The mean rate of renal net acid excretion rose markedly (by 29.4 mmol . kg-1 . day-1); and over an 8-day balance period the animals were able to maintain near-normal balances of net base. During a subsequent 8-day recovery the pattern of mineral turnover returned to normal. Even in the barley-fed rats, gastrointestinal net acid absorption was observed. These animals suffered a 61% reduction in the rate of body growth, but the overall rate of net base retention, per kilogram of mass gain, was close to the reference value. Finally, the combination of barley and ammonium chloride led to weight loss, positive net acid balances (8.5 mmol . kg-1 . day-1), and a maximal rate of renal net acid excretion (50.8 mmol . kg-1 . day-1). Some implications for the metabolism of organic acids are discussed.

Acid-Base Equilibrium↗
PubMedDate not supplied

Synthesis and anti-microbial activities of choline-like quaternary ammonium chlorides.

New choline-like quaternary ammonium chlorides were obtained. The work-up procedure of synthesis was quick and efficient. The obtained chlorides showed anti-microbial activities. Quaternary ammonium chlorides derivatives of deanol esters exhibited strong activity and wide anti-bacterial spectra, similar to the activity of benzalkonium chloride. The relationship between chemical structure and anti-microbial activity was analyzed by the QSAR method.

Ammonium Chloride↗
PubMed1986

Modification of behavioral effects and biodisposition of phencyclidine in rats by ammonium chloride.

The ability of ammonium chloride (NH4Cl) treatment to alter the pharmacological effects and biodisposition of phencyclidine (PCP) was investigated in rats. Either a single gavage of NH4Cl (2.5 mEq/kg) or six hourly gavages with either 2.5 or 5.0 mEq/kg of NH4Cl decreased urinary pH to approximately 5.5 at the 7-hr time point. A single gavage with NH4Cl (2.5 mEq/kg) failed to alter the time course of rotarod performance in rats that had been treated 45 min earlier with either 10, 25 or 50 mg of PCP per kg (p.o.). A treatment regimen of six hourly gavages of NH4Cl (5.0 mEq/kg) proved to be highly toxic, whereas gavages with 2.5 mEq/kg did not produce overt effects. Six hourly treatments with the lower dose of NH4Cl did not alter motor impairment induced by oral doses of 10 and 25 mg/kg of PCP but did diminish that produced by 50 mg/kg. This treatment regimen also produced a slight reduction in the time course of motor dysfunction in rats receiving an i.v. injection of either 5, 10 or 15 mg/kg of PCP. The biodisposition of orally administered [3H]PCP (50 mg/kg) was altered by six hourly gavages of 2.5 mEq/kg of NH4Cl in that urinary excretion of [3H]PCP was increased whereas concentrations in kidney, lung and brain were significantly decreased at selected times. However, the brain concentrations of [3H]PCP, as measured by area under the curve, were not altered significantly by NH4Cl treatments.

Administration, Oral↗
PubMed1983

Ammonium chloride and methylamine hydrochloride antagonize clostridial neurotoxins.

Ammonium chloride (1-8 mM) and methylamine hydrochloride (1-16 mM) produce concentration-dependent antagonism of the onset of neuromuscular blockade caused by botulinum toxin types A, B and C (all at 1 X 10(-11) M) and by tetanus toxin (3 X 10(-10) M). Neither drug antagonizes the onset of paralysis caused by beta-bungarotoxin (1 X 10(-7) M) or by taipoxin (1 X 10(-8) M). At concentrations that produce antagonism of clostridial neurotoxins, ammonium chloride and methylamine hydrochloride (8-10 mM) do not inactivate toxin molecules, nor do they produce irreversible changes in tissue function. When studied under conditions that impose partial synchrony on the mechanism of clostridial neurotoxin action, ammonium chloride and methylamine hydrochloride do not inhibit ligand binding and do not reverse neuromuscular blockade. The drugs act solely to antagonize internalization of toxins by cholinergic nerve endings. As a result of inhibiting the process of internalization, the drugs trap the toxins at an antitoxin sensitive site.

Ammonium Chloride↗
PubMed1987

Reevaluation, using marker enzymes, of the ability of saponin and ammonium chloride to free Plasmodium from infected erythrocytes.

Saponin and ammonium chloride lysis have been applied for some time to the separation of erythrocyte membranes from malarial-infected erythrocytes, allowing easy isolation of the parasites. We present a reevaluation of the use of saponin and ammonium chloride as tools for isolating Plasmodium (knowlesi or falciparum) parasites. Acetylcholine esterase (EC 3.1.1.7) was used as an erythrocyte membrane marker and CDP-choline: 1,2-diacylglycerol cholinephosphotransferase (EC 2.7.8.2) as a parasite membrane marker to monitor fractionation by these agents. Both saponin and ammonium chloride produced hemolysis of uninfected and infected erythrocytes, but failed to separate host erythrocyte membrane from the parasite, regardless of its stage. Thus, saponin and ammonium chloride can be used to isolate whole infected erythrocytes, depleted of hemoglobin, by selective disruption of uninfected cells.

Acetylcholinesterase↗
PubMed1997

Seromuscular colocystoplasty lined with urothelium protects dogs from acidosis during ammonium chloride loading.

PURPOSE: We compared the metabolism of intravesical ammonium chloride in dogs in which the bladder had been enlarged by seromuscular colocystoplasty lined with urothelium, dogs that had undergone conventional colocystoplasty and control dogs. MATERIALS AND METHODS: Eight adult female mongrel dogs were divided into control (2), colocystoplasty (3) and seromuscular colocystoplasty (3) groups. Serum creatinine, bicarbonate, sodium, chloride, and potassium levels were measured every 2 weeks during the 6-week recovery period. Six weeks after augmentation the dogs were placed under general anesthesia, the bladder was instilled with a hyperosmolar solution of 400 mmol/l. ammonium chloride, the femoral artery and portal vein were cannulated to obtain blood samples and the ureters were divided with the proximal ends diverted to allow serial urine measurements. Blood and urine electrolyte analysis was performed at 0, 60, 120, 180 and 240 minutes after the intravesical instillation of ammonium chloride. RESULTS: During acid loading dogs that had undergone conventional colocystoplasty had a progressive decrease in serum carbon dioxide and arterial pH as well as increased levels of serum chloride and a significant increase in plasma ammonia concentration in the portal vein compared to controls and dogs that had undergone seromuscular colocystoplasty. In contrast, there were no differences in seromuscular colocystoplasty compared to control animals. CONCLUSIONS: Increased ammonia in the portal vein and hyperchloremic acidosis in dogs that underwent conventional colocystoplasty suggest intravesical absorption of ammonium chloride. Dogs that underwent augmentation with seromuscular colocystoplasty lined with urothelium seemed to respond to acute intravesical ammonium in a way similar to that of control dogs and they are protected from these metabolic anomalies.

Acidosis↗
PubMed1979

Inhibition of murine natural killer cell-mediated cytotoxicity by pretreatment with ammonium chloride.

In the present study the effect of ammonium chloride on murine natural killer (NK) cell-mediated cytotoxicity to T cell lymphoma, YAC-1 was studied. It was found that ammonium chloride treatment significantly reduced the cytotoxicity of splenic NK cells without any detectable change in cell viability. It is, therefore, suggested to avoid ammonium chloride treatment in order to obtain the realistic reflection of murine NK cell activities.

Ammonium Chloride↗
PubMed1995

Use of peritoneal dialysis, continuous arteriovenous hemofiltration, and continuous arteriovenous hemodiafiltration for removal of ammonium chloride and glutamine in rabbits.

OBJECTIVE: We compared the ability of peritoneal dialysis, hemofiltration, and continuous hemodiafiltration to remove infused ammonium chloride. STUDY DESIGN: Anesthetized adult rabbits received an intravenous infusion of ammonium chloride. Two methods of removal of ammonium chloride were performed in each animal and compared. In group 1 (n = 6), peritoneal dialysis (dialysate = 75 ml.kg-1) and continuous arteriovenous hemofiltration (CAVH) with a polysulfone 800 cm2 hemofilter (Minifilter Plus; Amicon Division, W. R. Grace & Co., Danvers, Mass.) were simultaneously performed for 40 minutes. In group 2 (n = 6), peritoneal dialysis and continuous arteriovenous hemodiafiltration (CAVHD) (dialysate flow = 1000 ml.hr-1) were simultaneous performed for 40 minutes. In group 3 (n = 6), CAVH and CAVHD were performed successively in random order for 30 minutes each. RESULTS: Animals had high and stable ammonium chloride and glutamine plasma levels during the experimental procedure. No significant difference in ammonium chloride clearance was observed between PD and CAVH (group 1). In comparison with PD or CAVH, CAVHD resulted in significantly higher clearances of ammonium chloride (40% +/- 10% vs 96% +/- 34%, respectively) and of glutamine (195% +/- 17% vs 77% +/- 25%, respectively). CONCLUSION: The overall results indicate that CAVHD should be considered for hyperammonemia when peritoneal dialysis is indicated but unfeasible or inefficient.

Ammonium Chloride↗
PubMed1994

Inhibitory effect of ammonium chloride on acetylcholine-induced relaxation.

We designed the present study to clarify whether the intracellular pH change by ammonium chloride influences endothelium-dependent relaxation in thoracic aorta of 9-week-old Sprague-Dawley rats. Intracellular alkalinization with 3 mmol/L ammonium chloride, which did not affect resting vascular tone, attenuated acetylcholine-induced relaxation but not nitroglycerin vasodilation. Acetylcholine relaxation was more inhibited by a shorter duration of treatment. Thus, change in intracellular pH may be important in the effect because the alkalinizing effect of ammonium chloride disappears gradually. In support of this, the proton ionophore nigericin abolished the effect. Also, amiloride shortened the effect of ammonium chloride, suggesting that intracellular pH plays a role: sodium-proton antiport antagonizes the disappearance of ammonium chloride-induced intracellular alkalinization. The synthesis of vasoconstrictor prostaglandins, such as thromboxane A2, may be stimulated during acetylcholine treatment, resulting in the attenuation of acetylcholine relaxation, because the relaxation was abolished by treatment with the phospholipase A2 inhibitor quinacrine, cyclooxygenase inhibitor indomethacin, prostaglandin H2/thromboxane A2 receptor antagonist S1452, and thromboxane A2 synthase inhibitor dazmegrel. Phospholipase A2 may contribute to the effect of intracellular alkalinization, which is compatible with the fact that the optimal pH of phospholipase A2 is neutral to alkaline. In addition, superoxide dismutase attenuated the effect of ammonium chloride. In conclusion, intracellular alkalinization by ammonium chloride attenuated acetylcholine-induced relaxation, possibly through the interrelated production of both thromboxane A2 and superoxide radicals.

Acetylcholine↗
PubMed1965

Mode of inhibition of diphtheria toxin by ammonium chloride.

Kim, K. (University of Washington, Seattle), and N. B. Groman. Mode of inhibition of diphtheria toxin by ammonium chloride. J. Bacteriol. 90:1557-1562. 1965.-The inhibition of diphtheria toxin by ammonium salts was independent of toxin concentration over a 100-fold range of toxin. Inhibition by minimal concentrations of ammonium chloride was abolished by lowering the pH, indicating that free ammonia is the active form of inhibitor. A single addition of ammonium chloride inhibited toxin for a limited period of time, but periodic readdition of the ammonium salt was required to sustain inhibition indefinitely in the absence of antitoxin. Toxin was not destroyed and its adsorption occurred equally well in the presence or absence of ammonium chloride. Preadsorbed toxin was also effectively inhibited by the addition of ammonium chloride. Inhibited toxin remained accessible to antitoxin neutralization. Attempts to reverse ammonia inhibition by the addition of succinate or reduced nicotinamide adenine dinucleotide were unsuccessful. Attempts to inhibit toxin by interfering with active transport were also unsuccessful.

Adsorption↗
PubMed1979

Treatment of alkalosis with ammonium chloride: a case report.

Coma due to ammonium chloride used in the treatment of severe metabolic alkalosis is reported in a patient with normal hepatic and renal function. All symptoms resolved following discontinuance. Ammonium chloride should be abandoned as a treatment for metabolic alkalosis.

Alkalosis↗
PubMed2004

Dip-pen nanolithography with poly(diallyl dimethyl ammonium) chloride.

Poly(diallyl dimethyl ammonium) chloride (PDAC), a high molecular weight cationic polyelectrolyte, was used as ink for dip-pen nanolithography. Line patterns were generated on bare silicon wafers directly with PDAC-coated tips. Widths and heights of lines increased with decreasing scan rates. At the same scan rate, widths and heights of patterning decreased with increasing PDAC molecular weight. The dependence of line width on inverse writing speed was found to be consistent with a modified diffusion model.

Computer Simulation↗
PubMed2001

Fetal exencephaly arising as a result of preimplantation exposure to ammonium chloride.

OBJECTIVES: To investigate the effect of preimplantation exposure to 0.6 mM ammonium chloride on both preimplantation and postimplantation development of (F1 x F1) strain mouse embryos. METHOD: Two-cell stage mouse embryos were randomly allocated to culture in either M16 medium or M16 added with 0.6 mM ammonium chloride for 2 days before being transferred to 2.5 day pseudopregnant recipients. Embryo morphology was assessed after 1 and 2 days of culture. The recipient females were sacrificed on day 15.5 of gestation. The number of implantation sites, fetuses, moles and any gross abnormalities found were noted. RESULTS: There was no significant difference in the number of embryos reaching morula stage after two days of culture between the two groups (chi2=0.86, P>0.05). Implantation and pregnancy loss rates between the two groups were within comparable ranges. Crown-rump length was significantly higher in the group of embryos exposed to ammonium chloride (t=2.46, P<0.05). There was one gross abnormality, exencephaly, detected in the experimental group (4.35% per fetus obtained). CONCLUSIONS: Besides the abnormal increase in fetal size, preimplantation exposure to ammonium chloride also resulted in gross abnormality, exencephaly. If such effects occurred in the course of human in vitro fertilization, it could be devastating. Further study in this aspect is, therefore, clinically very important in preventing unwanted abnormalities that could arise from human in vitro fertilization.

Ammonium Chloride↗
PubMed1976

Temporary inhibition of antibody-dependent, cell-mediated cytotoxicity by pretreatment of human attacking cells with ammonium chloride.

Treatment of lymphoid cell preparations with ammonium chloride buffers to remove contaminating erythroid cells markedly reduced the ability of these cells to function as attacking cells in antibody dependent cell mediated cytotoxicity tests (ADCC). The lymphoid cells, however, retained their ability to adhere to antibody-coated target cells. Recovery of function 20 hr after exposure to ammonium chloride suggests a metabolic rather than receptor effect of these salts on the ADCC function of lymphocytes.

Ammonium Chloride↗