Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “AMMONIUM CHLORIDE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 91 records · Page 5Linked to original sources
PubMed1989

Effect of ammonium chloride on the astrocyte benzodiazepine receptor.

We have carried out studies on the effect of ammonium chloride on the astrocyte benzodiazepine receptor. Scatchard analysis of the binding of [3H]Ro-5-4864 to homogenates prepared from primary astrocyte cultures showed a significant decrease in Kd (27% with 2 mM NH4Cl; 32% with 5 mM NH4Cl; 25% with 10 mM NH4Cl) and Bmax (14% with 10 mM NH4Cl). These findings indicate that ammonium chloride can affect the astrocyte benzodiazepine receptor, and that such receptor changes may contribute to ammonia-induced encephalopathy.

Ammonium Chloride↗
PubMed1972

The effect of steroids and ammonium chloride acidosis on phosphoenolpyruvate carboxykinase in rat kidney cortex. I. Differentiation of the inductive process and characterization of enzyme activities.

The behaviour of rat kidney cortex phosphoenolpyruvate carboxykinase has been investigated under conditions of triamcinolone administration and ammonium chloride acidosis. The concentration of phosphoenolpyruvate carboxykinase as measured by enzyme activity and immunotitration was elevated under both conditions. The mechanism of induction is different in the two cases. At doses which produce maximum stimulation, the effects of steroid and ammonium chloride were additive; only the increment in enzyme activity produced by steroid was blocked by actinomycin D. PHOSPHOENOLPYRUVATE CARBOXYKINASE ACTIVITIES IN ALL CONDITIONS INVESTIGATED SHOW SIMILAR BEHAVIOR IN DILUTE EXTRACTS: these experiments involved antibody titration, stability studies, and molecular weight determinations on sucrose gradients. The molecular weight of phosphoenolpyruvate carboxykinase was also studied in undiluted extracts prepared by high-speed centrifugation; values were determined from sedimentation data obtained with a moving-partition cell as described by Yphantis and Waugh. Under these conditions, the apparent molecular weight of phosphoenolpyruvate carboxykinase was increased from 83,000 to 128,000 by ammonium chloride acidosis. These results are discussed and a hypothesis regarding the mechanism of phosphoenolpyruvate carboxykinase regulation in kidney cortex is presented.

Acidosis↗
PubMed2003

Fetal abnormalities produced after preimplantation exposure of mouse embryos to ammonium chloride.

BACKGROUND: The aims of this study were to determine whether preimplantation exposure of mouse embryos to ammonium resulted in abnormal fetal development and to evaluate similar risks to the outcome of human assisted conception. METHODS: Mouse embryos cultured from the 1-cell stage were exposed to 0.3 mmol/l ammonium chloride for 3 days. Embryos cultured from the 2-cell stage were exposed to 0.3 or 0.6 mmol/l ammonium for 2 days. After transfer to the uteri of pseudopregnant recipient females, post-implantation development was evaluated on embryonic day 15.5 (E15.5) or E18.5. RESULTS: There was no consistent effect of preimplantation exposure to ammonium chloride on fetal or placental weights. All 101 E18.5 fetuses were normal but 5/217 E15.5 fetuses were abnormal (three exencephalic and two polydactylous), which was significantly higher than the 0/363 for the pooled groups of E15.5 control fetuses (P = 0.007). The combined E15.5 and E18.5 frequency was also significantly higher than the controls (5/318 versus 0/433; P = 0.013). CONCLUSIONS: These results support the conclusion that abnormal preimplantation culture conditions can cause fetal abnormalities in mice, but the risks may be lower than previously suggested. Further work is needed to evaluate the risk more fully but this risk should be considered when designing new strategies for human assisted conception.

Abnormalities, Drug-Induced↗
PubMed1994

Ammonium chloride exposure inhibits cytokine-mediated eosinophil survival.

To study human eosinophils, their efficient purification from peripheral blood is crucial. Although a number of purification procedures, including discontinuous Percoll and metrizamide density gradient centrifugation, have been used, it has been difficult to isolate eosinophils from normal donors with consistently high yields and purities. Recently, a new isolation technique called magnetic cell separation system (MACS) was reported. To evaluate this procedure, we isolated eosinophils from human peripheral blood using either MACS or the standard discontinuous Percoll density methods, and compared cellular viability, morphology, and response to degranulation stimuli. MACS gave a higher yield of eosinophils than Percoll density centrifugation; for example, 6.6 +/- 1.1 x 10(6) eosinophils were isolated from 20 ml of blood by MACS compared to 6.4 +/- 2.4 x 10(6) from 120 ml by Percoll density gradient. Further, the purity of eosinophils isolated by MACS was 97.1 +/- 0.5% (X +/- SEM) compared to 77.8 +/- 2.9% with Percoll. As part of the MACS protocol, erythrocytes are lysed with either 155 mM ammonium chloride or hypotonic lysis. With 155 mM ammonium chloride treatment, the eosinophils showed a striking reduction in cytokine mediated survival due to interleukin (IL)-3, IL-5 and granulocyte-macrophage colony-stimulating factor (GM-CSF), marked morphologic abnormalities and a reduced degranulation response. With hypotonic lysis, no differences were observed in survival and morphology between eosinophils purified by MACS and Percoll methods; the degranulation responses to stimuli were essentially the same between the two methods. Taken together, these observations suggest that the exposure of eosinophils to 155 mM ammonium chloride results in cellular damage. Therefore, MACS with hypotonic lysis is a useful technique to isolate eosinophils for biological study.

Ammonium Chloride↗
PubMed1994

Struvite diet in cats: effect of ammonium chloride and carbonates on acid base balance of cats.

Six healthy adult cats were fed a basal minced beef meat and rice diet (one meal per day) with varying amounts or combinations of acidifying and alkalizing additives (ammonium chloride, calcium and sodium carbonate). The base excess in the food (mmol/kg dry matter) was calculated (data on food compounds in g/kg dry matter) as follows: base excess = 49.9*Ca + 82.3*Mg + 43.5*Na + 25.6*K-64.6*P-13.4*met-16.6*cys-28.2*Cl. Base excess in the experimental diets amounted to between +305 and -1079 mmol/kg dry matter. After an adaptation period of 5 d, urine and blood pH as well as water and mineral balance were determined in the cats over a 10-15-d period. The daily mean urine pH ranged between 6.1 and 7.8. There was a highly significant correlation between the base excess in the food and the mean urine pH. The regression line was linear down to a base excess in the diet of approximately -400 to -500 mmol/kg dry matter and a pH in the urine of 6.2. The postprandial increase of urine pH was suppressed either by large amounts of ammonium chloride (> 780 mmol/kg dry matter) alone or in combination with calcium carbonate but not in combination with sodium carbonate. The relationship between the decrease of the blood pH and the amount of ammonium chloride added to the diet was more marked than the relationship between blood pH and base excess in the food.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗
PubMed1993

[Struvite calculi dietetics: 2. Effect of ammonium chloride and carbonates on the acid-base and mineral balance of cats].

Six healthy adult cats were fed a basal minced beef meat and rice diet with varying amounts or combinations of acidifying and alkalizing additives (ammonium chloride, calcium and sodium carbonate). The base excess in the food (mmol/kg dry matter) was calculated (data on food compounds in g/kg dry matter) as follows: base excess = 49.9*Ca + 82.3*Mg + 43.5*Na + 25.6*K - 64.6*P - 13.4*Met-16.6*Cystine -28.2*Cl. It amounted to between +305 and -1079 mmol/kg dry matter. Urine and blood pH as well as balance of minerals and water were determined in the cats. The mean urine pH ranged between 6.1 and 7.8. There was a highly significant correlation between the base excess in the food and the mean urine pH. The regression line was linear down to a base excess in the diet of about -400 to -500 mmol/kg dry matter and a pH in the urine of 6.2. The postprandial increase of urine pH was suppressed either by large amounts of ammonium chloride (> 780 mmol/kg dry matter) alone or in combination with calcium carbonate, but not in combination with sodium carbonate. The relationship between the decrease of the blood pH and the amount of ammonium chloride added to the diet was more marked than the relationship between blood pH and base excess in the food. In order to avoid health risks by long term application of acidifying diets it is recommended to formulate struvite diets with low base excess in such a way, that they contain as few alkalizing compounds as possible, which must be neutralized by acidifiers.

Acid-Base Equilibrium↗
PubMedDate not supplied

[Effect of ammonium chloride and urea on the activity of lactate dehydrogenase. A general model of catalysis].

The dependence of structural and functional properties of lactate dehydrogenase from the pig muscle (isoenzyme M4) on pH (6.9-8.5) on the effect of different forms of non-protein nitrogen (e.g. urea and ammonium chloride) has been investigated. It was shown that Vmax changes negligibly at pH 6.9-8.5 but K(m) increase markedly with pH elevation. At the alkali value of pH pyruvate inhibition disappeared. We have found that urea and ammonium chloride at the non-saturation concentrations inhibited the activity of lactate dehydrogenase. The inhibition constants (Ki and Ka) for urea and ammonium chloride were obtained from inhibition data. When analysing works of different authors and own results we propose the general model of catalysis of lactate dehydrogenase, which includes the formation of normal enzyme-substrate complex, abortive enzyme-NAD-pyruvate complex and the effect of different effectors, including nitrogen containing substances.

Ammonium Chloride↗
PubMed1987

Feline struvite urolithiasis: fasting reduced the effectiveness of a urinary acidifier (ammonium chloride) and increased the intake of a low magnesium diet.

In three separate experiments nine male cats were fed either a canned complete diet or a commercially available dry pelleted diet or the same dry diet containing 1.6 per cent ammonium chloride for seven days and then fasted for 20 hours. Then ad libitum feeding was continued and urine samples were taken at four-hour intervals for 12 hours and a final sample 12 hours later. Urine pH and the presence of struvite crystals in urine sediment were evaluated. The food and water intake of four of the nine cats was measured at the time of urine collection. After the fast, urine pH was raised, even after feeding the dry diet supplemented with ammonium chloride. A post prandial rise in urine pH was also seen on all three diets. After feeding the dry diet the postprandial peak pH was 7.97 and struvite occurred spontaneously. Urine pH after feeding the dry diet supplemented with ammonium chloride peaked at 7.75 then fell to 6.1 12 hours after the start of feeding. Struvite occurred spontaneously at all times until the pH reached 6.1 but when the pH of urine was raised to 7.0 the struvite crystallised. Urine pH on the canned complete diet peaked at 6.8 then fell to 5.8; struvite did not occur spontaneously but when urine pH was raised to 7.0 struvite crystallised except at the eighth and 12th hour sampling. These data show that fasting initiates a post prandial rise in urine pH and struvite crystalluria even when a normally effective urinary acidifier is used.(ABSTRACT TRUNCATED AT 250 WORDS)

Ammonium Chloride↗
PubMedDate not supplied

[Gastric emptying and metabolic acidosis. I. Study of an experimental model in rats, using an ammonium chloride solution administered through the orogastric route].

The goal of the study was get an experimental model of metabolic acidosis which was appropriated in future gastric emptying studies. For this proposal were utilized 141 female Wistar rats in three stages: in the first (n = 27) was defined the installation, manutention and spontaneous recuperation of the metabolic acidosis produced by the orogastric infusion of a two ml by 100 g of an 0.5 M ammonium chloride solution; in the second (n = 60), it was studied the gastric emptying of the same solution utilized in the first stage and in the last stage (n = 54) it was determined the gastric emptying of the water, for excluding the possibility that the acidificant solution had caused any lesion in the gastric mucosa. As control group were utilized animals fed as a sodium chloride solution in the same concentration and volume that the acidificant solution. The results showed that 6 hours after the infusion, the gastric emptying of two above mentioned meals was complete and there was still a moderate metabolic acidosis in the group with infusion of ammonium chloride solution. Further more, the metabolic acidosis persisted in moderate values until 8 hours after the infusion. Based on these data the interval between 6 and 8 hours after the infusion of the these solutions was considered the best to the further studies about metabolic acidosis and gastric emptying. Finally, the gastric emptying of water, studied in rats with acidosis and controls demonstrated no differences between them. This was interpreted as a clue that the ammonium chloride solution did not modificate the integrity of the gastric mucosa.

Acidosis↗
PubMed1996

An ultrastructure study of the in vitro effects of L-leucine methyl ester and ammonium chloride on Trypanosoma cruzi epimastigotes.

Trypanosoma cruzi epimastigotes were subjected to the lysosomotropic agents L-leucine methyl ester and ammonium chloride to determine their effects on the ultrastructure of the parasite. The lysosomotropic agents applied to epimastigotes caused a time-dependent alteration in the morphology of the cells marked by a 5-fold increase in the number of lysosomes. Continued exposure to ammonium chloride caused slight disruption of the reservosomes. The amino acid ester, however, while causing the parasite to swell after prolonged exposure (e.g., 24 h), had little effect on the reservosomes, the kinetoplast, or even the mitochondrion. A specific inhibitor of cysteine proteinases provided some protection for lysosomes from the effects of the amino acid ester. Although it is agreed that reservosomes are similar to endosomes, no lysosomal fusion with the reservosomes was observed. Acid phosphatase activity was observed only in lysosomes.

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↗
PubMed1986

Selective killing of human T-lymphotropic virus-I infected leukemic T-cells by monoclonal anti-interleukin 2 receptor antibody-ricin A chain conjugates: potentiation by ammonium chloride and monensin.

Adult T-cell leukemia is a progressive disease produced by infection of mature T-cells with the human T-lymphotropic virus-I (HTLV-I). These retrovirus infected T-cells express large numbers of receptors for interleukin 2 (or T-cell growth factor). Due to the presence of these receptors, these leukemic T-cells can be selectively killed in vitro by monoclonal anti-interleukin 2 receptor antibody covalently linked to the A chain of the plant toxin, ricin (anti-TAC-A), suggesting that such immunotoxins may be useful in the therapy of this disease. In this report we demonstrate that the lysosomotropic agent ammonium chloride and the carboxylic ionophore monensin substantially potentiate the cytotoxicity of anti-TAC-A on HUT 102 cells, a long-term cultured HTLV-I infected T-cell line. Anti-TAC-A alone produces half-maximal inhibition of protein synthesis in HUT 102 cells at a concentration of 2.2 X 10(-10) M (the 50% inhibitor, concentration). Addition of ammonium chloride or monensin augments the potency of anti-TAC-A killing 100-fold (50% inhibitory concentration = 2.5 X 10(-12) M) and 400-fold (50% inhibitory concentration = 8 X 10(-13) M), respectively; furthermore, these agents accelerate rate of anti-TAC-A intoxication and increase the specific killing of interleukin 2 receptor-bearing leukemic cells. At concentrations which cause only minor harm to colony forming hematopoietic progenitor cells (granulocyte-erythroid, monocytic, megakaryocytic colony forming unit, granulocyte-macrophage colony forming unit, macrophage colony forming unit, and granulocyte colony forming unit), anti-TAC-A alone is able to eliminate greater than 99.99% of an HTLV-I infected T-cell population. In the presence of ammonium chloride or monensin, respectively, a 3.5- and 20-fold greater cytoreduction of HTLV-I infected T-cells is achieved. Combined treatment with anti-TAC-A and monensin may offer an efficient and highly selective means of purging bone marrow of patients with adult T-cell leukemia, which may then be used for autologous marrow transplantation.

Ammonium Chloride↗
PubMed1988

Promotion of Mycoplasma pulmonis growth in rat tracheal organ cultures by ammonium chloride.

During exacerbation of respiratory mycoplasmosis in rats by environmental ammonia, numbers of Mycoplasma pulmonis organisms in the respiratory tract are increased. To test whether or not exposure of respiratory epithelium to ammonia in vitro promotes growth of the organism, rat tracheal organ cultures were treated with 50 mM ammonium chloride, inoculated with M. pulmonis, and quantitatively cultured. After 48 hours, treated tracheas harbored almost 10 times more M. pulmonis colony-forming units than control tracheas. Cellular lesions in the epithelium of treated tracheas resembled those in the nasal passages of rats exposed to gaseous ammonia. To determine whether or not growth-modifying factors were released from tracheal epithelium exposed to ammonium chloride, M. pulmonis growth was assessed in medium collected from ammonium chloride-treated and control tracheas. Growth in medium from treated tracheas was greater than that in medium from untreated tracheas.

Ammonium Chloride↗
PubMed1983

Effect of ammonium chloride treatment on human polymorphonuclear leucocyte iodination.

A discontinuous gradient of Percoll was used to remove RBCs from polymorphonuclear leucocyte (PMN) preparations. The resulting red blood cell-free preparation was used to investigate the effect of ammonium chloride on the iodination response of human PMN. Treatment of PMN with ammonium chloride for five minutes at room temperature resulted in a statistically significant increase in the iodination response of both resting and stimulated PMN.

Ammonium Chloride↗