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Comparative effects of added sodium chloride, ammonium chloride, or potassium bicarbonate in the drinking water of broilers, and feed restriction, on the development of the ascites syndrome.

A hypothesis that the ionic composition of drinking water might affect development of the ascites syndrome in broilers was investigated in two trials. The first trial comprised four groups of 650 male chicks. A control treatment was normal tap water and the other three treatments comprised the addition to the tap water of 1,000 mg/L sodium as NaCl, 5,000 mg/L NH4Cl, or 5,000 mg/L KHCO3, supplied from age 2 to 47 d. At Day 28, equally sized subsets of these groups were moved to individual cages, where they received a severe exposure to ambient cold. The development of the ascites syndrome was monitored by measurements of hematocrit and arterial blood oxygen saturation (PaO2) by oximetry, body weight, and examination of dead birds for cause of death. Mortality from ascites in cold-exposed birds from Days 28 to 47 was 28, 48, 40, and 16% in the tap water, NaCl, NH4Cl, and KHCO3 groups, respectively; only the NaCl mortality was significantly different from the tap water mortality. The KHCO3 treatment increased PaO2 (compared with tap water treatment) at Day 28 by 5.5% and at Day 35 by 10.5%, but not at Day 42. The KHCO3 caused a reduction in body weight, which was 13% less than the tap water group at Day 42, probably due to a chronic toxicity. The second trial specifically examined the same parameters with lower water levels of KHCO3 (3,000 and 1,000 mg/L), in comparison to a 10% feed restriction protocol, in order to clarify whether the increased PaO2 was due to a specific effect of the KHCO3 or was a metabolic manifestation of a reduced growth rate. The 3,000 mg/L KHCO3 treatment had no effect on PaO2, but the 1,000 mg/L treatment augmented PaO2 by 5.3% at Day 35 (but not at Days 28 or 42), without reducing the final body weight. The feed restriction group showed an elevated PaO2 of 5.4% at Day 35 (but not at Days 28 or 42), with no reduction in the final body weight. The inclusion of 1,000 mg/L of KHCO3 into the drinking water of broilers or a temporary 10% feed restriction may be means to augment PaO2.

Ammonium Chloride↗

Attenuation of murine coronavirus infection by ammonium chloride.

Ammonium chloride at a concentration of 20 mM delayed by 4-5 hr the production of virus progeny in mouse L-2 cells infected at high multiplicity with mouse hepatitis virus (MHV). This delay was seen in the production of both intracellular and extracellular virus. However, the final titers were similar to those produced by MHV-infected cells maintained in normal medium. The manifestation of virus-induced cell fusion was similarly found to be delayed, but not otherwise decreased in severity, when ammonium chloride was present in the culture medium. Ammonium chloride caused similar delays in production of virus-specific, positive-sense RNAs and of viral polypeptides. The relative proportions and apparent molecular weights of viral RNAs and polypeptides were similar to those found in MHV-infected cells cultured in normal medium. In vitro translation of endogenously produced viral RNAs in cell extracts, prepared from MHV-infected cells, was not inhibited by ammonium chloride. Thus, ammonium chloride has no specific, inhibitory effect on viral protein synthesis. Ammonium chloride did not reduce the number of virus-infected cells in culture, as monitored by infectious center assay. Analysis of early events in MHV infection showed that ammonium chloride did not affect adsorption or internalization of MHV by L-2 cells. However, the subsequent eclipse phase, as monitored by decline in infectivity of internalized virus inoculum proceeded less efficiently in the presence of ammonium chloride. On the basis of the known inhibitory effects of ammonium chloride on lysosomal/endosomal functions, the results suggest an endosomal mechanism of MHV uncoating. Thus the primary effect of ammonium chloride on MHV infection of L-2 cells is to attenuate virus uncoating, thereby chronologically displacing all subsequent virus-encoded functions.

Ammonium Chloride↗

Inhibition of some spontaneous secretory processes in macrophages and fibroblasts by ammonium chloride.

Ammonium chloride inhibits the spontaneous secretion of lysozyme by mouse macrophages and the murine macrophage-like cell line P388D1 and the spontaneous secretion of lysosomal enzymes by P388D1 cells, normal human fibroblasts and the hypersecretory mucolipidosis II (I-cell) fibroblasts. NH4Cl can also inhibit protein synthesis, but this is shown to occur mainly at higher concentrations, or after longer periods of exposure, than are needed for the inhibition of the spontaneous secretory processes. It is confirmed that this amine can also interfere with the continuous endocytosis of fluid in the murine cell types. The nature of the inhibitions is discussed.

Ammonium Chloride↗

Trabecular bone remodeling and bone mineral density in the adult cat during chronic dietary acidification with ammonium chloride.

Ammonium chloride (NH4Cl) is used as a urinary acidifier in the treatment and prevention of feline urologic syndrome. It is reported to cause alterations in calcium and bone metabolism in humans, dogs, and rats. Adult cats with normal renal function were fed 1.5% NH4Cl for 6 months to study the effects of chronic dietary acidification on trabecular bone remodeling of the iliac crest and bone mineral density (BMD) of lumbar vertebral trabecular bone and femoral cortex. Histomorphometric analyses of iliac crest biopsies were performed before and after treatment. Static and dynamic parameters of bone resorption and formation were determined. Single-energy quantitative computed tomography (SEQCT) was used to measure lumbar trabecular and femoral cortical BMD. There were no significant treatment effects in iliac crest trabecular bone remodeling or BMD of the vertebrae and femora. Bone remodeling activity decreased with time in both acidotic and control cats. Vertebral BMD increased with time in both groups of cats, whereas no change was seen in the femora. Thus, chronic dietary acidification for 6 months with therapeutic levels of NH4Cl produced no significant changes in trabecular bone remodeling or bone mineral density in adult cats.

Acidosis↗

Occupational asthma due to soft corrosive soldering fluxes containing zinc chloride and ammonium chloride.

Two cases of occupational asthma due to soft corrosive soldering fluxes used in metal jointing are described in which the diagnosis was based on work related deterioration in daily peak expiratory flow rate and positive responses in bronchial provocation tests. Both fluxes contained ammonium chloride and zinc chloride. Occupational asthma provoked by these agents has not previously been reported.

Adolescent↗

Ammonium chloride and ammonium sulfate for prevention of parturient paresis in dairy cows.

Forty-eight Holstein cows with two or more previous lactations and no history of parturient paresis were randomly assigned to one of four prepartum diets in a 2 x 2 factorial design to determine the effect of dietary supplementation with ammonium salts and Ca intake on serum Ca concentrations at calving. Four diets provided either 53 g total dietary Ca/d or 105 g Ca/d and were either supplemented with ammonium salts [100 g/d each of NH4Cl and (NH4)2SO4] or unsupplemented. Anion-cation balance of the diets, calculated as milliequivalents (Na + K)--(Cl + S), was -75 meq/kg DM with ammonium salts and +189 meq/kg DM without ammonium salts. Experimental diets were fed from 21 d prior to expected parturition until calving. Calcium intake during the feeding period did not affect the incidence of parturient paresis or serum concentrations of ionized Ca at calving. The incidence of parturient paresis was 4% with and 17% without the ammonium salts. Cows fed diets containing ammonium salts had higher serum ionized and total Ca concentrations at parturition. Serum concentrations of Mg, P, Na, K, and Cl on the day of parturition were unaffected by dietary treatment.

Ammonium Chloride↗

Investigation of the ammonium chloride and ammonium acetate inhibition of oxygen evolution by Photosystem II.

Using EPR and EXAFS spectroscopies we show that high concentrations of ammonium cations at alkaline pH are required for (1) inhibition of oxygen evolution: (2) an alteration of the EPR properties of the oxygen evolving complex: (3) the ability to detect YZ; and (4) the slow reduction of the Mn complex leading to the appearance of EPR detectable Mn2+. The inhibition of S state cycling, slowing of YZ reduction, appearance of Mn2+ and the yield of a Hpp < 10 mT S3 type EPR signal are decreased by calcium addition. This indicates that these effects were probably associated with calcium depletion arising from the high concentration of ammonium cation. The ammonia-induced changes to the S2 multiline EPR signal are not affected by calcium addition. The appearance of Mn2+ is shown to be reversible on illumination, suggesting that the Mn reduced from the native state is located at or near the native site. Simulations of the interaction which give rise to the S3 EPR signal are also presented and discussed. These indicate that lineshape differences occur through small changes in the exchange component of the interaction between the manganese complex and organic radical, probably through minor structural changes between the variously treated samples.

Acetates↗

Inhibition of human NK cell-mediated cytotoxicity by exposure to ammonium chloride.

Ammonium-chloride-containing solutions (AC) are routinely used to lyse red blood cells during preparation of PBMC. Although exposure to AC has been described to affect the ultrastructural appearance of large granular lymphocytes and to temporarily inhibit cytolytic activity of PBMC preparations, the cellular basis of this phenomenon has not been studied. Here, the inhibitory effect of AC on human CTL and NK-mediated cytotoxicity has been analyzed in 4-h 51Cr-release assays. The results show that NK killing of K562 leukemia cells and xenogeneic endothelial cells is inhibited by AC exposure. The effect is dose-dependent and reversible, because recovery of cytotoxicity is observed within 15 h of re-culturing. AC does not reduce the viability of NK cells and the inhibitory effect is not mediated by the exhaustive release of granzymes upon AC treatment. In contrast, antigen-specific CTL killing of EBV-transformed B-lymphoblastoid cell lines and xenogeneic PHA lymphoblasts was less sensitive to AC and data are presented suggesting that FasL-induced apoptosis is not inhibited by AC. In conclusion, perforin-mediated NK killing is AC-sensitive whereas CTL killing and FasL-mediated killing appear to be AC-resistant. Therefore, AC represents a powerful tool to study different mechanisms of cell-mediated cytotoxicity and may be helpful in assessing antigen-specific CTL cytotoxicity without the influence of NK cell-mediated background killing.

Ammonium Chloride↗

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↗

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↗