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Effects of prior exercise or ammonium chloride ingestion on muscular strength and endurance.

Previous studies linked muscular fatigue with a decrease in blood pH. This study investigated if the means of altering pH affected the extent of muscular fatigue. Drug-induced and exercise-induced acidosis were compared to test the hypothesis that exercise-induced acidosis impairs subsequent muscular performance more than chemically induced acidosis. In eight male subjects acidosis was induced by ingesting 0.3 g.kg-1 ammonium chloride (AC) for one trial, by upper body exercise (UBE) for another trial, and after placebo (PL) treatment. They then completed a performance test (PT) of 50 maximal, bilateral isokinetic knee extensions. Whole blood pH before (pHpre) and after (pHpost) the PT was 7.412, 7.264, and 7.261 for PL, UBE, and AC, respectively; both AC and UBE decreased pH similarly compared with PL. Peak torque and total work during the PT were similar for PL and AC, and were significantly greater than after UBE. Six subjects performed a fourth trial after combined AC and UBE treatments causing a pHpre of 7.081, but there was no greater performance impairment than that caused by UBE alone. The results dissociate the extent of the impairment from the magnitude of the disruption in blood pH.

Acid-Base Equilibrium↗

The effects of quaternary ammonium chloride (alpha C12 DME AHCl) on enamel hardness and mineral loss under intra oral cariogenicity test conditions.

The effects of a quaternary ammonium compound; 2-hydroxy-ethyl-2-hydroxydodecyl-dimethyl-ammonium chloride (alpha C12 DMEAHCl) on enamel hardness and mineral loss in enamel slabs were studied under intra-oral cariogenicity test conditions. The quaternary ammonium compound without fluoride reduced enamel softening as well as the mineral loss from enamel significantly up to a depth of 100 microns from the surface. Moreover the Ca/P molar ratio of the treated enamel was comparable to untreated enamel controls. These findings suggest that the quaternary ammonium compound itself inhibits mainly demineralisation rather than remineralization under intra-oral cariogenicity test conditions.

Animals↗

Effect of drinking water containing ammonium chloride or sodium bicarbonate on Mycoplasma gallisepticum isolation in experimentally infected broiler chickens.

In each of three trials, 150 day-old broiler chicks were eyedrop inoculated with 0.04 ml of high-passage F strain Mycoplasma gallisepticum (MG) and housed in biological isolation units at 10 chicks per unit. At 4 wk of age, 50 chickens were designated as controls and remained on tap water (pH 7.30), 50 chickens were provided tap water containing 0.63% ammonium chloride (NH4Cl, pH 6.91), and 50 chickens were provided tap water containing 1.26% sodium bicarbonate (NaHCO3, pH 8.17). Fluids were supplied for ad libitum consumption. At 5 wk of age, all chickens were swabbed from the choanal cleft for MG isolation and bled from the left cutanea ulnea vein for pH determination. As a percent of total swabs obtained, significantly fewer chickens that consumed water containing NH4Cl (38.3%) were positive for MG by culture compared with either the NaHCO3 group (61.3%) or the control group (67.6%). Nonmycoplasmal swab contamination was significantly higher for chickens that consumed water containing NH4Cl (59.7%) compared with either controls (31.8%) or NaHCO3-treated chickens (38.7%). When contaminated cultures were discarded, MG isolations from the tap water group were not significantly different from MG isolations from either the NH4Cl or NaHCO3 group. However, MG isolations from the NH4Cl group (95%) were significantly less compared with the NaHCO3 group (100%). Mortality was significantly higher in chickens that consumed water containing NaHCO3 (8.7%) compared with either controls (1.3%) or the NH4Cl-treated chickens (0.7%). Blood pH values were lower for the NH4Cl group (7.927), higher for the NaHCO3 group (8.093), and intermediate for controls (8.035). Results of this study suggest that water containing NH4Cl hinders the bacteriological recovery of MG from the choanal cleft.

Ammonium Chloride↗

Effects of infusions of lysine, leucine and ammonium chloride into the hepatic portal vein of chickens on voluntary food intake.

1. Adolescent cockerels of a laying strain were prepared with catheters whose tip lay in the hepatic portal vein, to study the effect of 3-h infusions of nutrients on food intake. 2. Lysine, infused into the hepatic portal vein at rates of 150-450 mg/3 h reduced 3-h food intake by up to 58%, for a period of 6 h in previously starved birds, but had no effect on birds allowed free access to food. Infusions made into the jugular vein had no effect, suggesting a role for the liver in monitoring lysine levels. 3. Portal infusion of leucine had a delayed effect while ammonium chloride, infused at isosmolar rates to those of the lysine infusions, had very little effect on intake. 4. The results support the concept of liver sensitivity to amino acids, but the mode of action is not clear; it appears not to be via the effects of ammonia.

Ammonium Chloride↗

Mast cell exocytosis can be triggered by ammonium chloride with just a cytosolic alkalinization and no calcium increase.

A human mast cell line (HMC-1) has been used to study the effect of cytosolic alkaline pH in exocytosis. Compound 48/80, concanavalin A, and thapsigargin do not induce histamine release in HMC-1 cells. Although thapsigargin does not activate histamine release, it does show a large increase in cytosolic Ca(2+), and no change in cytosolic pH. However, when HMC-1 cells were activated with ionomycin, a significant histamine release takes place, and this effect is higher in the presence of thapsigargin. Both drugs show an additive effect on cytosolic Ca(2+) levels. Ammonium chloride (NH(4)Cl) does activate cytosolic alkalinization and histamine release, with no increase in cytosolic Ca(2+). NH(4)Cl does block the release of internal Ca(2+) by thapsigargin, not by ionomycin, and decreases Ca(2+) influx stimulated by these drugs. Under conditions in which the alkalinization induced by NH(4)Cl is blocked by acidification with sodium propionate, histamine release is inhibited. The release of histamine is also observed when NH(4)Cl is added after propionate addition, regardless of the final pH value attained. Our results show that a shift in pH alkaline values, even with final pH below 7.2 is enough to activate histamine release. A shift to less acidic values is a sufficient signal to activate the cells.

Ammonium Chloride↗

Removal and inactivation of Cryptosporidium and microbial indicators by a quaternary ammonium chloride (QAC)-treated zeolite in pilot filters.

A set of pilot filters packed with Zeolite filter media treated with a quaternary ammonium chloride (QAC) were evaluated to verify the proof of concept of their combined antimicrobial capabilities. Escherichia coli was removed and inactivated the most (2.83 log), followed by MS-2 (2.75 log), Klebsiella terriena (2.21 log), PRD-1 (1.95 log), Chlorella vulgaris (1.92 log), and Cryptosporidium parvum oocysts (1.78 log). Especially, inactivation of C. parvum oocysts (1.19 log) was higher than physical removal (0.54 log). The data suggest that QAC-treated Zeolite in the pilot filters has microbial inactivation capabilities and may have useful applications in other types of filter media.

Animals↗

Routine flow cytometric immuno-staining of T-cell perforin is preserved using diethylene glycol for erythrocyte-lysis but lost by the use of ammonium chloride.

The system of perforin-containing lytic granules of cytotoxic lymphocytes plays an important role in the immune defense machinery. Investigating the capacity and efficacy of this system in and ex vivo is helpful to understand immune responses and their modulation by therapeutic interventions. With regard to its pathophysiological function, we recently demonstrated a substantial increase of perforin-positive CD8+ T cells in the peripheral blood of patients with acute exacerbated psoriasis and severe generalized drug reactions, and, in marked contrast, a highly significant perforin-depletion and a perforin-hyperreleasability in atopic dermatitis (AD). To streamline the perforin staining procedure, isolation of peripheral blood mononuclear cells (PBMC) by Ficoll density centrifugation was to be replaced by lysis of erythrocytes. Ammonium chloride lysis, however, reduced the perforin content of CD8+ T cells substantially (up to 75-100%) as compared with Ficoll isolation of PMC. Incubation of cells in concanamycin A, a selective inhibitor of H+-ATPases, resulted in a similar loss of perforin staining pointing to the critical influence of lysosomal pH. Using diethylene glycol-mediated erythrocyte lysis, perforin was well preserved to be readily detectable by immuno flow cytometry. Representative examples of the application of this optimized perforin staining procedure as well as accumulated data are given for various dermatological disorders (psoriasis, atopic dermatitis, cutaneous drug reactions, graft-versus-host disease (GVHD) with strong involvement of the cytotoxic T-cell population. Our findings may help to explain recent conflicting reports about a widely varying range of the portion of perforin-positive cells in healthy individuals as a reflection of such artificial methodological influences.

Adenosine Triphosphatases↗

Chloroquine and ammonium chloride prevent terminal glycosylation of immunoglobulins in plasma cells without affecting secretion.

The generation of an acidic pH in intracellular organelles is required for several membrane and protein recycling processes. For instance, the internalization of ligands by receptor-mediated endocytosis is followed by the development of an acidic pH inside endosomes; this allows dissociation of the ligand, which is then transported to the lysosomes, from the receptor, which is recycled to the cell surface. There is evidence that part of this recycling process involves the distal region of the Golgi complex, where terminal glycosylation occurs: when the plasma membrane transferrin receptor is desialylated by neuraminidase treatment, it acquires new sialic acid molecules after endocytosis and before cell-surface re-expression. Golgi membranes have been shown to contain a proton pump and the distal Golgi cisternae appear to have an acidic content. Here, we have studied the effects of chloroquine and ammonium chloride, which raise the pH of acidic intracellular compartments, on the processing and secretion of immunoglobulins by plasma cells. Sialic acid transfer to terminal galactose residues, a reaction known to occur in the distal Golgi shortly before secretion, is completely and rapidly inhibited in the presence of these drugs, without significant modification of the secretion rate. This effect is accompanied by a dilatation of the Golgi cisternae and is not rapidly reversible.

Ammonium Chloride↗

The uncoating and infectivity of the flavivirus West Nile on interaction with cells: effects of pH and ammonium chloride.

Infectivity of the West Nile virus (WNV; Flaviviridae) was inactivated on exposure for brief periods (90 s) to pH 6.6 and below. This inactivation was not due to decreased interaction between cells and acid-treated virus. The RNA of [3H]uridine-labelled virus particles prebound to the cell surface before acidic pH treatment underwent rapid uncoating within 1 min at 37 degrees C at the same pH values that inactivated virus particles. The uncoating of [3H]uridine-labelled virus particles was also studied over longer time periods after synchronized internalization by P388D1 cells. At pH 7.6 uncoating occurred rapidly after a reproducible time lag of 1 min on warming to 37 degrees C and was essentially complete by 15 to 30 min after the start of internalization, leaving uncoated RNA in an infectious form. In contrast, at pH 6.2 viral uncoating occurred rapidly without any time lag and the uncoated RNA appeared to be far less infectious than that uncoated at pH 7.6. Ammonium chloride could almost totally inhibit both the infectivity and uncoating of virus particles on synchronized internalization into P388D1 cells, with a pH optimum of 8.0. These results suggest that the uncoating of virus particles is dependent on an acidic pH, although the location of uncoating (prelysosomal endosome or plasma membrane) decides whether the uncoated RNA will be infectious or not. Essentially the same results were obtained when infections were carried out in the presence of enhancing antibody.

Ammonium Chloride↗

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↗

Effects of sodium bicarbonate and ammonium chloride on the incidence of furosemide-induced fetal skeletal anomaly, wavy rib, in rats.

Furosemide produces fetal wavy ribs when administered to pregnant rats during late gestation. The compound is also known to produce metabolic alkalosis in laboratory animals and man. In order to evaluate the effect of furosemide on maternal blood pH, Crj:CD(SD) female rats received an oral administration of 150 or 200 mg/kg of furosemide by gavage on day 16 of gestation and were bled at 4 hr post-dose. Compared to an average pH of 7.39 in control females, there was a significant elevation in blood pH in these furosemide-treated females (average pH of 7.44 to 7.48). When 2% sodium bicarbonate was provided in the drinking water for females treated with 150 mg/kg of furosemide, there was a further rise in maternal blood pH (7.52) compared to females treated with furosemide alone. Associated with this elevation in maternal blood pH was a marked increase in the incidence of fetal wavy ribs (87.6% compared to 27.6%). When females treated with 200 mg/kg of furosemide were provided with 0.5% ammonium chloride, furosemide-induced maternal alkalosis was corrected (pH decreased to 7.35) and there was a reduction in the incidence of fetal wavy ribs (7.0% compared to 37.2%). In addition, maternal blood pH among individual females was positively correlated with the incidence of fetal wavy ribs (r = 0.714). These results suggest that maternal metabolic alkalosis is involved in the pathogenesis of furosemide-induced wavy ribs.

Alkalosis↗