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At least 19 recordsLinked to original sources
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↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
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↗
PubMed1975

Studies in osteoporosis: the long-term effect of oophorectomy and of ammonium chloride ingestion on the bone of mature rats.

Adult female rats were subjected to a prolonged period of observation after oophorectomy. The oophorectomized animals and their controls were given a regular diet ad lib and water or ammonium chloride as their drinking fluid. Oophorectomy did not result in reduced bone density, fat free weight, total ash weight, or calcium content of the bone, thus failing to produce the changes of osteoporosis. Ammonium chloride ingestion caused significant decreases in the same parameters equally in normal and oophorectomized rats. Thus, oophorectomy neither leads to changes of osteoporosis, nor increases the sensitivity of the bone to ammonium chloride-induced osteoporosis.

Ammonium Chloride↗
PubMed1978

[Acid-excreting activity of the kidneys in dogs administered ammonium chloride into the carotid artery].

Injection of 0.5 mM of ammonium chloride into the dog carotid artery caused no changes in the blood acid-base balance, but distinctly increased the urinary excretion of both titratable acids and active hydrogen ions. The rate of glomerular filtration was slightly increased. The amount of sodium reabsorbed in the tubules was also risen. The role of humoral factors stimulating the renal acid-excreting activity, is discussed.

Acid-Base Equilibrium↗
PubMed1977

Evaluation of the effect of ammonium chloride treatment on the activity of human effector cells in antibody-dependent and spontaneous cell-mediated cytotoxicity.

The effect of ammonium chloride treatment, used to eliminate contaminating red blood cells from lymphoid cell preparations, on the cytotoxic activity of human effector cells in antibody-dependent and spontaneous cell-mediated cytotoxicity was quantitatively determined. No significant difference between the cytotoxic efficiency of treated and untreated cell preparations was observed.

Ammonium Chloride↗
PubMed1978

Antibody-dependent cellular cytotoxicity and natural cytotoxicity: effect of pre-treatment of human lymphocytes with deionised water and ammonium chloride.

Deionised water is an efficient red blood cell lytic agent with no demonstrable deleterious effects on ADCC and natural cytotoxicity (blood and tonsil). Treatment with isotonic ammonium chloride, however, produces a significant reduction of both ADCC and natural cytotoxicity. This reduction is less pronounced if the treatment is carried out at 4 degrees C and is temporary, recovery occurring over a 24 h period of incubation at 37 degrees C.

Ammonium Chloride↗
PubMed1975

The effect of gibberellic acid alone and when combined with [2-chloroethyl]-trimethyl ammonium chloride on the growth and alkaloid content of Solanum laciniatum aiton.

Solanum laciniatum Aiton treated with Gibberellic acid (GA3), [2-chloroethyl]-trimethyl ammonium chloride (CCC), and their combinations at early and late stages of growth showed that early application of 2000 ppm CCC produced the greatest stem, leaves, and whole plant dry weight, followed by the combination of early application of 1000 ppm CCC and late application of 100 ppm GA3; whereas all GA3 treatments decreased the dry weight production compared with the controls. Regarding the glyco-alkaloids, the highest percentage was obtained from the whole plant by early applications of both strengths of GA3 compared with other treatments or the controls. On the other hand, early application of 1000 ppm CCC and also late application of 50 ppm GA3 when combined with early application of either 1000 ppm or 2000 ppm CCC produced greater alkaloid percentage yields in stem, leaves, and whole plants more than other treatments or the controls. However, early application of 2000 ppm CCC produced the highest content of alkaloids in leaves and whole plants; this was followed by yields from early application of 2000 ppm CCC and 50 ppm GA3; yields from early application of 100 ppm GA3 and 1000 ppm CCC; and yields from early application of 1000 ppm CCC +50 ppm GA3.

Alkaloids↗
PubMed1978

Effect of C.C.C. [2-(chloroethyl)] trimethyl ammonium chloride on growth and sporulation in Fusarium oxysporum f. udum (butl.) Sn. et H.

In Fusarium oxysporum f. udum sporulation of macroconidia was completely inhibited due to the influence of C.C.C. [2-(Chloroethyl)] trimethyl ammonium chloride). Microconidial proliferation, on the other hand, was adversely affected and with increase in concentration of this compound a parallel and proportional decrease in the amount of microconidia was found. Size of microconidia, too, showed a concomitant decline. Although the size of the chlamydospores was also reduced, a tremendous increase in its population was evident, showing a positive response in favour of C.C.C. addition. Fungal mat accumulation, another important aspect of growth, did not evince any inhibitory pattern, compared to the progressive increase in C.C.C. amoung in younger cultures. In older cultures (15-day old), an initial depressing shock of C.C.C. addition could be seen. However, after stepwise and gradual adjustment to the new environment the same positive response of mycelial growth was discernible, although in a less degree than that of the young cultures.

Fusarium↗