PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “AMMONIUM CHLORIDE”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

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

At least 181 records · Page 10Linked to original sources
PubMed1999

Ammonium-chloride-induced prostatic hypertrophy in vitro: urinary ammonia as a potential risk factor for benign prostatic hyperplasia.

To test the possibility that urinary ammonia could be a risk factor for benign prostatic hyperplasia (BPH), we explored the cellular effects of ammonium chloride (NH(4)Cl) on prostatic cancer cells used as an experimental model. Following treatment of human prostatic cancer DU-145 cells with the varying concentrations of NH(4)Cl for 3 days, cell growth was inhibited by approximately 50% at 5 mM NH(4)Cl and almost completely inhibited at 10 mM NH(4)Cl. However, the individual cell size in these treated cells became approximately 2-fold larger and cellular protein content was also up to 2.5-fold greater than in untreated cells. This protein increase appeared to result from the reduced protein degradation, verified by metabolic labeling with [(14)C]valine. Western blot analysis further suggested that such reduced protein turnover could in part be due to the inactivation of a lysosomal acid protease, cathepsin D. Taken together, these studies demonstrate NH(4)Cl-induced hypertrophy in prostatic cancer cells, as evidenced by the growth inhibition, cell enlargement, and cellular protein increase. Therefore, ammonia is not an inert metabolic product; instead, its chronic effects on the prostate may ultimately lead to significant cellular and biochemical alterations of the prostate such as BPH.

Ammonia↗
PubMed1992

Leupeptin and ammonium chloride inhibit intrinsic factor mediated transcytosis of [57Co]cobalamin across polarized renal epithelial cells.

The [125I] intrinsic factor (IF) mediated transcytosis of [57Co]Cyanocobalamin (Cbl) by polarized opossum kidney cells was inhibited (greater than 80%) by preincubation of the cells with lysosomotropic agents leupeptin or ammonium chloride. Inhibition of Cbl transcytosis resulted in the intracellular accumulation of both [125I]IF (48 kDa) and [57Co]Cbl. Intracellular degradation of [125I]IF occurred during normal cellular transcytosis of [57Co]Cbl and in one h following internalization the major intracellular degradation products of IF were two polypeptides of Mr 29 kDa and 19 kDa. The size of the major degradation product of IF in the basolateral media was 10 kDa. Based on these results, we suggest that IF is internalized by the renal epithelial cells and is degraded by leupeptin-sensitive acid proteases during Cbl transcytosis.

Ammonium Chloride↗
PubMed1987

Effect of ammonium chloride ingestion on Eimeria acervulina-infected chicks fed excess copper.

Four experiments were conducted with broiler chicks to investigate the effect of dietary NH4Cl on gain, feed efficiency, duodenal pH, and liver Cu concentration of Eimeria acervulina-infected chicks. Experimental coccidial infection reduced chick gain, feed efficiency, and duodenal pH, but it increased liver Cu concentration in chicks fed excess Cu. Ammonium chloride had no effect on gain, feed efficiency, liver Cu concentration, or on duodenal pH.

Ammonium Chloride↗
PubMed2006

Reovirus variants selected for resistance to ammonium chloride have mutations in viral outer-capsid protein sigma3.

Mammalian reoviruses are internalized into cells by receptor-mediated endocytosis. Within the endocytic compartment, the viral outer capsid undergoes acid-dependent proteolysis resulting in removal of the sigma3 protein and proteolytic cleavage of the mu1/mu1C protein. Ammonium chloride (AC) is a weak base that blocks disassembly of reovirus virions by inhibiting acidification of intracellular vacuoles. To identify domains in reovirus proteins that influence pH-sensitive steps in viral disassembly, we adapted strain type 3 Dearing (T3D) to growth in murine L929 cells treated with AC. In comparison to wild-type (wt) T3D, AC-adapted (ACA-D) variant viruses exhibited increased yields in AC-treated cells. AC resistance of reassortant viruses generated from a cross of wt type 1 Lang and ACA-D variant ACA-D1 segregated with the sigma3-encoding S4 gene. The deduced sigma3 amino acid sequences of six independently derived ACA-D variants contain one or two mutations each, affecting a total of six residues. Four of these mutations, I180T, A246G, I347S, and Y354H, cluster in the virion-distal lobe of sigma3. Linkage of these mutations to AC resistance was confirmed in experiments using reovirus disassembly intermediates recoated with wt or mutant sigma3 proteins. In comparison to wt virions, ACA-D viruses displayed enhanced susceptibility to proteolysis by endocytic protease cathepsin L. Image reconstructions of cryoelectron micrographs of three ACA-D viruses that each contain a single mutation in the virion-distal lobe of sigma3 demonstrated native capsid protein organization and minimal alterations in sigma3 structure. These results suggest that mutations in sigma3 that confer resistance to inhibitors of vacuolar acidification identify a specific domain that regulates proteolytic disassembly.

Adaptation, Physiological↗
PubMed1985

Effects of ammonium chloride on synaptic transmission in the rat hippocampal slice.

Effects of ammonia on excitatory synaptic transmission were studied in the rat hippocampal slice preparation. Population spikes, elicited by orthodromic or antidromic stimulation, were recorded in the cell body layer of the CA1, CA3 and dentate regions. Perfusion with 5 mM ammonium chloride induced a profound and reversible depression of orthodromically evoked population spikes in all three regions. Antidromic population spikes were not depressed in any of the regions, indicating that neither axonal conduction nor electrical excitability were affected by ammonia. The paired-pulse test revealed a transient disinhibition during the early phase of perfusion. Iontophoretic application of glutamate evoked unit firing even when the synaptically evoked responses were reduced by ammonia, indicating that the postsynaptic sensitivity to the putative transmitter was not depressed. Depression of release of the excitatory transmitter, probably because of depletion following the block of transmitter synthesis, is the likely explanation of these findings. It is suggested that ammonia-induced depression of excitatory transmission may account for coma and other symptoms of central nervous system depression encountered in hyperammonemic states.

Ammonium Chloride↗
PubMed1992

Miniature endplate potentials induced by ammonium chloride, hypertonic shock, and botulinum toxin.

Intracellular recordings were made at the neuromuscular junction (NMJ) of the mouse diaphragm to study alteration of miniature endplate potential (MEPP) amplitude and rise time after different treatments. Following either hyperosmotic shock or 3 to 5 min of incubation in 10 to 50 mM ammonium chloride (NH4Cl) (replacing NaCl, a treatment which is known to raise intracellular pH) MEPP frequencies increased and the amplitudes of MEPPs decreased. These treatments as well as type A botulinum toxin (BoTx) gradually prolonged the rising phase of some MEPPs, which increased their time-to-peak (slow-MEPPs; Vautrin and Kriebel: Neuroscience 41:71-88, 1991) and increased eventually their amplitude. Fasciculation after hyperosmotic shock or during NH4Cl challenge was blocked by D-tubocurarine and was due to large slow-MEPPs that reached threshold for the muscle fiber action potential. The development of fasciculation provided the time course for the development of giant-MEPPs. Increased frequency of giant MEPP is accompanied by a block of the nerve-evoked muscle contraction. Effects of BoTx on spontaneous release were functionally antagonized either by NH4Cl or hyperosmotic shock. NH4Cl delayed BoTx blockage of bell-MEPPs. Data suggest that BoTx alters the formation of transmitter packets gradually but similarly to other treatments which increase incidence of skew-MEPPs.

Action Potentials↗
PubMed1996

Synthesis and antimicrobial activity of new quaternary ammonium chlorides.

Decyldimethylamine reacts readily with chloromethylalkyl ethers of sulfides, chloromethylbenzyl ethers or sulfides and chloromethylcycloalkyl ethers to give quaternary ammonium chlorides in very good yields. All the chlorides studied showed antimicrobial activity. The relationship between the chemical structure and antimicrobial activity was analyzed by rough sets.

Bacteria↗