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PubMed1969

Studies on a nucleoprotein prepared from rat liver polysomes by digestion with T1 ribonuclease.

1. Treatment of rat liver polysomes in a buffer containing 2.5mm-magnesium chloride with T(1) ribonuclease at a concentration of 330units/ml. of reaction medium at 37 degrees for 2hr. leads to the production of an insoluble nucleoprotein. 2. On the bases of analysis for protein and RNA and of u.v.-absorption spectra the nucleoprotein appears to have lost approx. 60% of the structural RNA originally present in the ribosome. Degradation of (3)H-labelled polysomes (structural RNA labelled with orotic acid) with T(1) ribonuclease leads to nucleoprotein preparations retaining approx. 30% of the radioactivity originally present in the polysomes. By means of sucrose-density-gradient centrifugation it is shown that the nucleoprotein preparations are free of single 73s ribosomes and ribosomal subunits. No evidence for the presence of 28s and 18s structural RNA was obtained on examination of extracted nucleoprotein-particle RNA by means of sucrose-density-gradient centrifugation. 3. Digestion of washed polysomes carrying (14)C-labelled nascent peptide chains with T(1) ribonuclease gives a nucleoprotein particle that retains approx. 70% of the original labelled chains. Treatment of labelled nucleoprotein particles with 1mm-puromycin in the absence of transfer factors releases 20% of the labelled chains. Addition of GTP (0.48mumole) increases this release to 37%. 4. Treatment of nucleoprotein particles carrying (14)C-labelled peptide chains with either EDTA (50mm) or ammonium chloride (0.5m) brings about a small release of labelled material (approx. 15%). 5. Disruption of nucleoprotein particles carrying (14)C-labelled peptide chains with either sodium dodecyl sulphate or 2m-lithium chloride, followed by addition of transfer RNA as marker and chromatography on Sephadex G-200, show in both cases that considerable amounts of labelled peptide material move well ahead of the added transfer RNA marker. Further, if nucleoprotein particles carrying labelled peptide chains are treated with 0.3m-potassium hydroxide at 20 degrees for 24 hr., neutralized to pH7.6, and then chromatographed on Sephadex G-200, the labelled peptide material moves much closer to the added transfer RNA marker. These results suggest that a proportion of the nascent (14)C-labelled peptides on the nucleoprotein are attached to transfer RNA or large fragments of transfer RNA. 6. [(3)H]Polyuridylic acid binds to nucleoprotein particles in 1mm-magnesium chloride. The rate of binding is rapid when measured at 20 degrees .

Ammonium Chloride↗

PubMed1997

Modulation of hormone-induced calcium oscillations by intracellular pH in rat hepatocytes.

Single isolated rat hepatocytes were used to investigate the influence of intracellular pH (pHi) on hormone-induced cytosolic Ca2+ oscillations, using videofluorescence microscopy. Although pHi did not vary after alpha-adrenergic stimulation, manipulations of pHi induced pronounced alterations in the frequency of oscillations. Increasing the resting pHi with ammonium chloride (5-20 mM), trimethylammonium (2-10 mM), or triethylammonium (1.2-8 mM) reduced the frequency of oscillations. A change in pHi of > 0.25 was sufficient to reversibly inhibit oscillations. This effect could be overcome by increasing the agonist concentration or by adding 8-bromoadenosine 3',5'-cyclic monophosphate, an agent known to potentiate the alpha-adrenergic response. Cellular acidification, obtained by the ammonium prepulse method as well as by application of acetate or the ionophore nigericin, in the continuous presence of agonist was accompanied by a modest frequency increase of the oscillations, leading in some cases to an overstimulated state. This study indicates that pHi, within a range of values expected to occur in vivo (0.1-0.2 pH units), exerts a chronotropic effect on phenylephrine-induced Ca2+ oscillations. In contrast, oscillations induced by ADP or vasopressin were pHi invariant.

Adrenergic alpha-Agonists↗

PubMed1988

Drosophila cathepsin B-like proteinase: a suggested role in yolk degradation.

A cysteine, cathepsin B-like proteinase activity has been found in Drosophila embryos. It appears associated with yolk granules and its activity during embryogenesis correlates well with the degradation of these organelles. In mature oocytes, the enzyme is found in an inactive form which may be activated by limited proteolysis by a serine proteinase also present in oocytes. In early embryos, when solubilized in vitro, the cathepsin B-like proteinase is found in a form of high molecular mass (approx 1000 kDa). This decreases with development down to about 39 kDa, likely the mass of the free proteinase. The heavy form apparently results from the tight association with a yolk protein complex. The proteinase has been found in vitro to degrade readily the yolk polypeptides. The proteinase activity increases during early embryogenesis in parallel with the decrease in molecular weight of the heavy form, and decreases to low values in late embryos. We have also found that ammonium chloride can inhibit in vivo the degradation of yolk and, in parallel, the developmental inactivation of the proteinase. The results altogether suggest that the cathepsin B-like proteinase is implicated in yolk degradation in Drosophila.

Ammonium Chloride↗

PubMed1984

Mechanism of autodegradation of cell-surface macromolecules shed by human melanoma cells.

The mechanism of autodegradation of cell-surface macromolecules shed by human melanoma cells was studied by incubating radio-iodinated shed macromolecules with unlabeled sister cells and measuring the appearance of acid-soluble radioactivity. After a preliminary latent period of 1-3 h, degradation continually increased up to 24 h and was concentration-dependent. By contrast, binding to cells was very rapid reaching half-maximal value within 15 min. Autodegradation was markedly reduced (44-82%) by pharmacological agents which interfere with endocytosis or lysosomal enzyme activity, including drugs which inhibit receptor migration into coated pits (dansylcadaverine), endocytosis and intracellular transport (colchicine, cytochalasin B, and monensin), and the activity of lysosomal enzymes (chloroquine, ammonium chloride, leupeptin). Degradation was almost totally suppressed (95%) at 4 degrees C. These data suggest that surface macromolecules shed by melanoma cells are autodegraded in part by re-uptake into melanoma cells followed by degradation in lysosomes.

Ammonium Chloride↗

PubMed2006

Mutagenicity of diesel exhaust particles mediated by cell-particle interaction in mammalian cells.

Diesel exhaust particle (DEP) has been identified as a class 2A human carcinogen and closely related to the increased incidence of respiratory allergy, cardiopulmonary morbidity and mortality, and risk of lung cancer. However, the molecular mechanisms of DEP mutagenicity/carcinogenicity are still largely unknown. In the present study, we focused on the mutagenicity of DEPs in human-hamster hybrid (A(L)) cells and evaluated the role of cell-particle interaction in mediating mutagenic process. We found that DEPs formed micron-sized aggregates in the medium and located mainly in large cytoplasmic vacuoles of cells by 24h treatment. The cellular granularity was increased by DEP treatment in a dose-dependent manner. DEPs resulted in a dose-dependent increase of mutation yield at CD59 locus in A(L) cells, while inflicting minimal cytotoxicity. There was a more than two-fold increase of mutation yield at CD59 locus in A(L) cells exposed to DEPs at a dose of 50mug/ml. Such induction was significantly reduced by concurrent treatment with phagocytosis inhibitors, cytochalasin B and ammonium chloride (p<0.05). These results provided direct evidence that DEPs was mutagenic in mammalian cells and that cell-particle interaction played an essential role in the process.

Ammonium Chloride↗

PubMed1987

Toxicity of ligand and antibody-directed ricin A-chain conjugates recognizing the epidermal growth factor receptor.

Approximately equal amounts of 125I-mAb 225 (a monoclonal antibody recognizing the human epidermal growth factor receptor) and 125I-labeled epidermal growth factor (125I-EGF) were bound by HeLa cells. However, these two EGF receptor binding moieties had different fates after binding. Sixty percent of cell-associated 125I-EGF was internalized. The majority of internalized 125I was released from the cell within 2 hr. In contrast, whereas only 30% of bound 125I-mAb 225 was internalized by HeLa cells, the internalized radioactivity remained cell-associated. EGF and mAb 225 were used to construct ricin A-chain (RTA) conjugates. The two chimeric molecules, EGF-RTA and mAb 225-RTA, were equally toxic to human HeLa cells. EGF-RTA was also toxic to murine 3T3 cells. In contrast, mAb 225-RTA was not toxic to 3T3 cells, consistent with the human EGF-receptor specificity of mAb 225. Neither conjugate was cytotoxic to EGF receptor-deficient 3T3-NR6 cells. Rapidity and potency of protein synthesis inhibition of HeLa cells were equivalent for the two chimeric conjugates, as was the degree to which colony-forming ability was reduced. However, ammonium chloride enhanced the toxicity of EGF-RTA but not mAb 225-RTA, suggesting that the two toxic chimeric toxins--like the unconjugated receptor-binding moieties--are processed differently by HeLa cells.

Ammonium Chloride↗

PubMed1991

Inhibition of duck hepatitis B virus infection by lysosomotropic agents.

The early phases of hepadnaviral infection were studied in primary duck hepatocyte cultures. Incubation of duck hepatocytes in vitro with duck hepatitis B virus (DHBV) resulted in infection with high levels of viral replication. The lysosomotropic agents ammonium chloride and chloroquine effectively inhibited viral infection, indicating that DHBV infection, similar to infection with other enveloped viruses, depends on receptor-mediated endocytosis and involves membrane fusion triggered by low pH.

Ammonium Chloride↗

PubMed1998

Rapid killing of Mycobacterium terrae by N-chlorotaurine in the presence of ammonium is caused by the reaction product monochloramine.

We have studied the activity of the weak endogenous oxidant N-chlorotaurine against Mycobacterium terrae. The study revealed slow killing of more than 2h duration by 1% (55 mM) N-chlorotaurine. In the presence of ammonium chloride, however, killing times decreased to a few minutes, even by 0.1% N-chlorotaurine. This phenomenon is explained by formation of the lipophilic and therefore more bactericidal monochloramine as a result of transhalogenation of ammonia by N-chlorotaurine.

Ammonium Chloride↗

PubMed1983

[Treatment of infection stones. I. Dissolution of experimental infection stones in rats].

The in vivo solubility of struvite stones experimentally induced in rats was investigated. The struvite stones implanted into bladders of normal rats were reduced in weight; and, they were dissolved by oral administration of ammonium chloride. Cefmetazone cured pyelonephritis and dissolved the bladder stones when it was administered to rats with urinary tract infection caused by Proteus mirabilis. Normalization of urine by antibiotics and acidifying agents may dissolve struvite stones, and help treat infection stones.

Ammonium Chloride↗

PubMed1985

Microvillar elongation following parthenogenetic activation of sea urchin eggs.

Parthenogenetic activation of unfertilized sea urchin eggs with ammonium chloride at pH 8.0 resulted in a slow, but dramatic, reorganization of surface microvilli in four species of sea urchin eggs. Following NH4Cl treatment, elongation of microvilli on the egg surface was observed concomitant with the formation of microfilament bundles within the microvillar cores. A minimum of 2 h of treatment was required for elongation and microfilament bundle formation to occur. The maintenance of elongated microvilli was pH-sensitive; removal of the activating agent resulted in the retraction of extended microvilli while readdition of NH4Cl caused microvilli to elongate again. Accompanying microvillar elongation in activated eggs, there was an increased calcium uptake as measured by 45Ca uptake. Blocking calcium uptake by incubation in lanthanum chloride or zero-calcium seawater containing 2 mM EGTA prevented microvillar elongation. These results suggested that elongation of microvilli following parthenogenetic activation by NH4Cl is pH- and calcium-dependent and is similar to that observed during normal fertilization.

Ammonium Chloride↗

PubMed1989

Effect of immunotoxins against Trypanosoma cruzi.

Immunotoxins were constructed with IgG antibodies against Trypanosoma cruzi surface antigens by hybridization with abrin (ITA) and ricin (ITR) A chains. The biological activity of the hybrid macromolecules was tested on the parasite forms. Motility of parasite forms was lost in vitro after incubation with ITR. In general, killing of the parasite with ITR was more efficient than with ITA. Inhibition of protein synthesis after incubation with either ITR or ITA, measured by 3H-leucine incorporation, confirmed the parasite immobilization experiments. The lethal effect was potentiated when the immunotoxins were used in the presence of 2.5 mM ammonium chloride. T. cruzi antibodies specific to cell surface antigens are excellent drug carriers that can be delivered to the target cell. However, ITR and ITA did not reduce parasitemia or increase survival of mice infected with T. cruzi.

Abrin↗

PubMed1981

Primary antibody responses to hapten-modified syngeneic cells: exceptional immunogenicity of erythrocytes.

Intravenous injection of fluorescein isothiocyanate-modified syngeneic spleen cells (FITC-SSC) into mice induced T cell-independent, anti-hapten plaque-forming cell responses. In contrast to the high immunogenicity of FITC-coupled SSC or bone marrow cells, thymus, lymph node or peritoneal exudate cells were poorly immunogenic. Further analysis showed that FITC-syngeneic peripheral blood red cells were as immunogenic as FITC-SSC containing a similar number of red cells. The immunogenicity of the red cells was confirmed by treatment of FITC-SSC with 0.83% ammonium chloride before sensitization with FITC. This procedure almost totally abolished the immunogenicity regardless of the concentration of hapten with which they were sensitized. In addition, heat treatment or fixation with glutaraldehyde destroyed the immunogenicity of FITC-SSC.

Ammonium Chloride↗

PubMed1976

Stimulation of hepatic glycogen synthesis by amino acids.

Hepatocytes isolated from livers of fasted rats form little glycogen from glucose or lactate at concentrations below 20 mM. Glycogen is formed in substantial quantities at a glucose concentration of 60 mM. In the presence of 10 mM glucose, 20-30% as much glycogen as glucose is formed from fructose, sorbitol, or dihydroxyacetone. The addition of either glutamine, alanine, or asparagine stimulates the formation of glycogen from lactate 10- to 40-fold. The formation of glucose and glycogen is then about equal, and glycogen deposition in hepatocytes is similar to rates attained in vivo after fasted rats are refed. The amino acids stimulate 1.5- to 2-fold glycogen synthesis from fructose, and 2- to 4-fold synthesis from dihyDROXYACETONE. Ammonium chloride is about one-half as effective as amino acids in stimulating glycogen synthesis when glucose with lactate are substrates. It increased glycogen synthesis 25-50% from fructose but inhibited synthesis from dihydroxyacetone plus glucose.

Alanine↗

PubMed1981

Metabolism of asialotranscortin by hepatocytes and cortisol binding to hepatocytes.

Binding and catabolism of iodinated human transcortin and asialotranscortin were studied in isolated rat hepatocytes. Human transcortin binding to hepatocytes was very low (less than 3%) while 40-60% of the asialotranscortin bound to the hepatocytes. Asialofetuin inhibited asialotranscortin binding to hepatocytes, producing 50% inhibition of binding at 5 x 10-9M, but had no effect on transcortin binding. The lysosomal inhibitors leupeptin (0.05 mM) and ammonium chloride (10 mM) had no effect on asialotranscortin binding but prevented the latter's catabolism, suggesting lysosomal involvement in asialotranscortin degradation. Both transcortin and asialotranscortin inhibited the binding of [3H]cortisol to the hepatocytes in a dose-dependent manner.

Ammonium Chloride↗

PubMed1986

Stability and inactivation of HTLV-III/LAV under clinical and laboratory environments.

The stability of human T-cell lymphotropic virus type III/lymphadenopathy-associated virus (HTLV-III/LAV) under environmental conditions encountered in a clinical or laboratory setting and its inactivation by commonly used chemical disinfectants were investigated. Under our experimental conditions utilizing a highly concentrated viral preparation, virus with an initial infectious titer of approximately 7 log10 tissue culture infectious dose (TCID50) per milliliter can be recovered for more than a week from an aqueous environment held at room temperature (23 to 27 degrees C) or at 36 to 37 degrees C. Virus recovery is reduced at a rate of approximately 1 log10TCID50 per 20 minutes when held at 54 to 56 degrees C. Dried and held at room temperature, HTLV-III/LAV retains infectivity for more than three days with a reduction of approximately 1 log10TCID50 per nine hours. Viral infectivity is undetectable and reduced more than 7 log10TCID50 within one minute with 0.5% sodium hypochlorite, 70% alcohol, or 0.5% nonidet-P40, and within ten minutes with 0.08% quaternary ammonium chloride or with a 1:1 mixture of acetone-alcohol. These results help provide a rational basis to prevent the accidental spread of HTLV-III/LAV in the laboratory or clinical setting.

Ammonium Chloride↗

PubMed1995

The interaction of gadolinium complexes with isolated rat hepatocytes.

The lanthanide metal, gadolinium, is currently used in contrast agents for magnetic resonance imaging. We have performed a study of the interaction between isolated rat hepatocytes and 153Gd complexed to diethylene-triamine pentaacetic acid (DTPA) or to DTPA-albumin conjugates. The study shows that isolated hepatocytes are able to take up both types of 153Gd complexes. The 153Gd-DTPA-albumin complexes are apparently taken up by pinocytosis, and possibly receptor-mediated endocytosis and/or adsorptive endocytosis, whereas the uptake mechanism of 153Gd-DTPA is unknown. The 153Gd-DTPA-albumin complexes, but not the 153Gd-DTPA complex, are degraded by the cell. The degradation is inhibited by ammonium chloride. Gadolinium is slowly released back to the medium after loading of the cells with both complex types. In the experiments reported here no evidence of any adverse effects on the hepatocyte resulting from exposure to the 153Gd-complexes were observed.

Albumins↗

PubMed1989

Differing polarity of the constitutive and regulated secretory pathways for von Willebrand factor in endothelial cells.

von Willebrand factor (vWf) is secreted from endothelial cells by one of two pathways-a constitutive pathway and a regulated pathway originating from the Weibel-Palade bodies. The molecular form of vWf from each of these pathways differs, with the most biologically potent molecules being released from Weibel-Palade bodies (Loesberg, C., M. D. Gonsalves, J. Zandbergen, C. Willems, W. G. Van Aken, H. V. Stel, J. A. Van Mourik, and P. G. DeGroot. 1983. Biochim. Biophys. Acta. 763:160-168; Sporn, L. A., V. J. Marder, and D. D. Wagner. 1987. Cell. 46:185-190). We investigated the polarity of the two secretory pathways using human umbilical vein endothelial cells cultured on polycarbonate membrane filters which allowed sampling of media from both the apical and basolateral compartments. After metabolic labeling of cells, vWf (constitutively secreted during a 10-min period or released during a 10-min treatment with a secretagogue) was purified from the apical and basolateral chambers and subjected to gel analysis. Approximately equal amounts of vWf were constitutively secreted into both chambers, and therefore this secretory pathway appeared to be nonpolarized. On the contrary, an average of 90% of vWf released from Weibel-Palade bodies after treatment with the calcium ionophore A23187 or PMA appeared in the basolateral chamber, indicating that the regulated pathway of secretion is highly polarized. Thrombin, a secretagogue which promotes disruption of the endothelial monolayer, led to release of vWf from cells with no apparent polarity. The presence of microtubule-depolymerizing agents nocodazol and colchicine inhibited the polarized release of vWf. Ammonium chloride treatment did not disrupt the polarity of the regulated secretory pathway, indicating that maintenance of low pH in intracellular compartments was not required for the polarized delivery of preformed Weibel-Palade bodies to the plasma membrane.

Ammonium Chloride↗

PubMed1993

Application of the WATR technique for water suppression in 1H NMR spectroscopy in determination of the kinetics of hydrolysis of neostigmine bromide in aqueous solution.

Both ammonium chloride and guanidinium chloride were used to secure water suppression in 1H NMR spectra using the 'Water Attenuation by T2 Relaxation' (WATR) technique. The effect of phosphate buffer in the suppression was investigated over a range of pH values at 80 MHz. The spin-spin relaxation time of water protons at 80 MHz was found to reach a minimum at pH 7.3 in the presence of 0.1 M phosphate buffer and 1 M guanidinium chloride; these conditions were therefore chosen for subsequent use of the WATR technique in a study of the kinetics of hydrolysis of neostigmine bromide. The method was found to be very convenient for studies of the hydrolysis of this representative amide.

Ammonium Chloride↗