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At least 19 recordsLinked to original sources
PubMed1979

[Toxicity of ammonium acetate in rats with acute and subacute galactosamine-induced hepatitis (author's transl)].

Ammonia toxicity and the protective effect of arginine thereon were investigated in rats after single and repeated doses of galactosamine. Urea cycle enzymes and ornithine-oxo-acid transaminase activities were measured in rat liver homogenates. Ammonium acetate proved to be less toxic in rats treated with single or repeated doses of galactosamine than in untreated animals. Urea cycle enzyme activities of galactosamine-treated rats were clearly lowered. The protective effect of arginine against lethal ammonia intoxication was found in animals that had been treated with galactosamine as well as in untreated rats. Since the toxicity of ammonium acetate is lower in rats with galactosamine hepatitis, in which the activities of the liver urea cycle enzymes are reduced, it seems likely that ammonia detoxication in galactosamine-poisoned rat liver partly bypasses the urea cycle.

Acetates↗
PubMed2026

Proteomic analysis of ammonia-induced stress in Chinese hamster ovary (CHO) cell cultures.

Ammonia (NH₃) and its ionic form ammonium (NH₄+) are both metabolic waste products and essential nitrogen sources within Chinese hamster ovary (CHO) cell cultures. Although necessary for amino acid synthesis, excessive accumulation in the extracellular environment can exert stress, reducing cell proliferation and impairing the efficiency of recombinant protein production. Proper endoplasmic reticulum (ER) function is critical for CHO cells as biotherapeutic producers. Previous work has linked elevated ammonia concentrations to reduced productivity via altered N-glycosylation pathways, but its broader effects on ER biology remain unclear. In this study, we applied high-resolution mass spectrometry to perform a comprehensive analysis of changes in the ER proteome in CHO cells exposed to two ammonia concentrations, 10 mM and 30 mM, 48 and 120 h after supplementation. Both conditions suppressed cell growth and reduced product titre; however, the 10 mM supplementation resulted in a minor increase in specific cell productivity. Gene Ontology analysis revealed that ammonia strongly affected the tricarboxylic acid cycle, as well as key metabolic, catabolic and biogenetic processes. Several ER membrane proteins, including HMGCR and PREB, were consistently downregulated. In extended cultures, transmembrane proteins linked to Golgi-transport were upregulated, while vesicle transport associated proteins were downregulated, indicating altered intracellular trafficking. SIGNIFICANCE: This study provides a novel perspective on CHO cell biology under environmental stress by investigating the impact of ammonia accumulation in culture. Despite its presence in CHO culture, ammonia has been relatively under-investigated, compared to other culture conditions. Using high-throughput mass spectrometry for comprehensive proteomic profiling, we characterise the cellular response to ammonia build-up with a level of depth not previously applied to the study of this biological stressor. By specifically analysing proteins localised to the ER, we identify candidate pathways and molecular mechanisms that contribute to reduced CHO cell growth and productivity, offering insights directly relevant to industrial bioprocessing conditions. The link between ammonia concentration and a decrease in productivity has previously been linked to genes involved in N-glycosylation of the recombinant biotherapeutic, but the full extent of ammonia stress on ER function has not yet been investigated. These methods were applied to two IgG producing CHO cell lines to allow for comparison of cell line specific stress adaptations, as well as comparing the short- and long-term effects of excess ammonia.

Proteomics↗
PubMed1975

Chemical modulation of diphtheria toxin action on cultured mammalian cells.

Ammonium chloride (4 times 10-3 M) rendered HEp-2 monolayers completely insensitive to the action of diphtheria toxin, as measured by de novo protein synthesis. Total protection was observed even with large amounts of toxin (400 minimum lethal doses/ml). Ammonium chloride did not reduce toxicity by direct action on the protein, nor did it prevent the adsorption of toxin to the cell membrane. Although the ammonium salt did not block the initial interaction between cell and toxin, it did maintain the toxin at a site amenable to neutralization with antitoxin. Surface-adsorbed toxin was inactivated by cellular enzymes or alternatively was desorbed from the membrane during a 12-h incubation in the presence of ammonium chloride. In addition, ammonium chloride provided protection to both toxin-sensitive guinea pig peritoneal macrophages and a partially toxin-resistant strain of HEp-2 cells. Sodium arsenite was effective in protecting cell monolayers from the action of diphtheria toxin; unlike ammonium chloride, its action was not dependent upon continued incubation with cells during exposure to toxin. Inhibitors of energy metabolism abolished toxin action either totally (sodium fluoride) or partially (dinitrophenol and sodium cyanide). Inhibitors of cellular proteases, on the other hand, did not modify toxin activity. The ability of several modifiers of membrane function to alter expression of toxicity for HEp-2 cells was also examined. One compound known to enhance endocytic activity, Tuftsin, had no effect, whereas poly-L-ornithine provided partial protection. Of the two compounds known to alter membrane fluidity, cytochalasin B provided partial protection for HEp-2 cell cultures, whereas colchicine had no effect. Agents that bind to sulfhydryl groups on the cell surface had no apparent effect on toxicity, suggesting that the initial toxin-cell interaction does not involve sulfhydryl groups. Those compounds that provide virtually full protection against the action of diphtheria toxic on cell monolayers (i.e., ammonium chloride, sodium fluoride, and sodium arsenite) had no inhibitory effect on the in vitro enzyme activity associated with fragment A of the toxin.

Ammonium Chloride↗
PubMed1977

Nonenzymic spectrophotometric determination of potential poison ivy cross-reactors.

I describe an inexpensive, nonenzymic analytical system for prescreening substances that might cross-react as Rhus toxing (e.g., poison ivy, poison oak, and sumac allergens) on human skin. By spectrophotometric assay after incubation with an oxidizing mixture of Cu(II)ammine complex and ammonium persulfate, I could accurately and reproducibly determine o-quinoidal products of several potential synthetic cross-reactors and native poison ivy allergen, and could distinguish these from catecholamines, resorcinol, p-hydroquinone, and a closely related phenol. A good correlation was obtained between this nonenzymic technique and an enzymic assay. This Cu(II)ammine/persulfate oxidative assay, however, is inexpensive and obviates any spectral interference from enzymic proteins.

Allergens↗
PubMedDate not supplied

Enzyme inhibition by tobacco smoke: a comparison of the effects of four filters.

The effects of four types of cigarette filters on the inhibition of glyceraldehyde-3-phosphate dehydrogenase by aqueous solutions of the free gas phase of tobacco smoke have been studied. Commercial cellulose acetate-charcoal filters or experimental wool filters containing a polyethyleneimine-quaternary ammonium additive were particularly effective in removing the inhibitor(s) from smoke under prescribed experimental conditions. Inhibition was dependent in all cases on both the age and the amount of free gas phase solution as well as contact time. Transient enzyme activation was observed. It is suggested that hydrogen sulfide is the main inhibitor present in the gas phase of cigarette smoke.

Acetates↗
PubMedDate not supplied

[Antiheparin activity of polymers based on the alkaloid, lupinine].

Antiheparin activity and acute toxicity of a monomer and polymer quaternary ammonium salts obtained on the basis of the alkaloid lupinine were investigated. The monomer was shown to have no antiheparin activity even when administered in high doses. Lupinine polymetakryloyl iodoethylate is a selective heparin antagonist. This activity of polymers is relative to the extent of polymerization. A compound with a molecular weight of 20 000 turned out the most effective in the tested series of ready-made polymers. Acute toxicity of polycations is considerably less than that elicited by the monomer. The effect of heparin complete neutralization is accompanied by transitory thrombocytopenia.

Alkaloids↗
PubMed1976

Innate and drug-induced resistance to acute lung damage caused in rats by alpha-naphthyl thiourea (ANTU) and related compounds.

During the 3rd and 4th weeks of life rats were highly resistant to the toxic effects of alpha-naphthyl thiourea (ANTU) and of thiourea and its derivatives but toxicity developed rapidly during the following 2 weeks. Marked resistance to lung damage by toxic thioureas could be induced in older, mature rats by pretreatment with the toxic agent itself (tachyphylaxis), with other toxic and non-toxic antithyroid drugs or with iodine or iodide--even if the rats were pretreated at an early age before susceptibility to the agent developed. ANTU-tachyphylaxis was dose-dependent. Total thyroidectomy did not affect either lung damage induced by ANTU or the resistance due to tachyphylaxis or to pretreatment with iodide or the antithyroid drugs thiourea, 1-ethyl-1-phenyl thiourea or propyl thiouracil. Neither total nor medullary adrenalectomy affected ANTU toxicity. Marked resistance to ANTU-induced lung damage was induced in rats by pretreatment with either an activator (3-4 benzypyrene) or an inhibitor (SKF 525-A) of drug-metabolizine mixed-function microsomal enzyme systems; the inhibitor, sodium phenobarbitone, had no significant effect on toxicity. The sulphydryl compound, AET, induced marked resistance to ANTU; cysteine was less effective. Neither autonomic blockade with nicotine and atropine nor actinomycin D had significant effects on toxicity to ANTU. The acute pulmonary oedema induced in rats by high pressure oxygen, chemical convulsants, pressor agents and ammonium sulphate differed in many respects from that induced by toxic thioureas; it was typically haemorrhagic in nature, did not result in significant pleural effusion, did not exhibit tachyphylaxis, and was not influenced by pretreatment with iodide or derivatives of thiourea.

Age Factors↗
PubMed1978

Effects of ammonia on monoamine oxidase and enzymes of GABA metabolism in mouse brain.

Acute and chronic ammonia toxicity was produced in the mice by intraperitoneal injection of ammonium chloride (200 mg/kg) and by exposure of mice to ammonia vapours (5% v/v) continuously for 2 days and 5 days respectively. The ammonia content was elevated in the cerebellum, cerebral cortex and brain stem and in liver. In acute ammonia intoxication there was a decrease in the monoamine oxidase (MAO) activity in all the three regions of brain. In chronic ammonia toxicity (2 days of exposure) a significant increase in the activity of MAO was observed in the cerebral cortex while in cerebellum and brain stem there was a significant decrease. In cerebral cortex and cerebellum there was a rise in the activity of MAO as a result of exposure to ammonia vapours for 5 days. A significant decrease was observed in the activity of glutamate decarboxylase (GAD) in all the three regions of the brain both in acute and chronic ammonia toxicity (2 days). There was a decrease in the activity of this enzyme only in the cerebral cortex in the animals exposed to ammonia for 5 days. The activity of GABA-aminotransferase (GABA-T) showed a significant rise in cerebellum and a fall in the brain stem in acute ammonia toxicity. In chronic ammonia toxicity GABA-T showed a rise in all the three regions of brain. Chronic ammonia toxicity produced a significant decrease in the content of glutamate in all the three regions without a significant change in the content of aspartate. GABA and glutamine. The content of alanine increased in all the three regions of brain under these experimental conditions. The ratio of glutamate + aspartate/GABA and glutamate/glutamine showed a decrease in all the three regions as a result of ammonia toxicity.

4-Aminobutyrate Transaminase↗
PubMed1979

Neisseria meningitidis infection in mice: influence of iron, variations in virulence among strains, and pathology.

The influence of iron on Neisseria meningitidis infection in C-57 mice was examined. Iron sulfate, ferric ammonium citrate, and iron sorbitol citrate all proved to be too toxic for use as infection-enhancing agents. Iron dextran displayed an extremely low toxicity, enhanced infection in a dose-dependent manner, and resulted in infection enhancement factors approaching 10(9) for virulent strains of N. meningitidis. Fatal iron dextran-enhanced infection was shown to be reversible by in vivo chelation of iron. Virulent strains of N. meningitidis produced symptoms of infection and pathological lesions in mice both with and without iron pretreatment, but an avirulent strain failed to produce symptoms of infection or pathological lesions, regardless of iron administration. Iron dextran-enhanced infection in mice proved to be a useful model for the examination of virulence of various N. meningitidis strains. All of 9 isolates from clinical disease possessed virulence, whereas only 3 of 10 isolates from carriers possessed virulence, when examined by using this model.

Animals↗
PubMed1977

Inactivation of Clostridium haemolyticum toxic fluids and their antigenicity.

One hundred fifty-one isolates of Clostridium haemolyticum were examined for consistent toxin production following repeated serial transfers in laboratory media. Most of these isolates produced only small amounts of toxic materials and serial transfers appeared to reduce toxigenic characteristics. Eleven of the isolates consistenly produced measurable amounts of toxic materials. One of these isolates was used for production of toxic fluids that were concentrated by lyophilization and reconstitution to a smaller volume or by precipitation with ammonium sulphate followed by dialysis against water and glycerol. Known amounts of these substances were inactivated with formalin, heat, beta-propiolactone, ultra-violet irradiation and glutathione. The resulting toxoids were inoculated into guinea pigs and most were judged to be nonimmunogenic because the animals were unable to resist dermal challenge. Toxic materials with added glycine were inactivated with formaldehyde as readily as those without the amino acid but the resulting toxoids were immunogenic while those prepared without the amino acid were not.

Animals↗
PubMed1978

Specific inhibition of in vitro Candida-induced lymphocyte proliferation by polysaccharidic antigens present in the serum of patients with chronic mucocutaneous candidiasis.

A specific inhibitory activity of in vitro proliferative responses of normal human lymphocytes to Candida metabolic antigen was found in the serum of 6 out of 23 children with chronic mucocutaneous candidiasis. In each of the six patients, the presence of an inhibitory activity was associated with Candida-specific cellular defects, characterized by a negative-skin test and a lack of in vitro lymphocyte proliferation. The presence of a circulating inhibitor was detected during relapses of the disease and disappeared under antifungal therapy. This inhibitory effect was not associated with any toxicity on tested lymphocytes. The factor was shown to be nondialysable, thermostable, nonprecipitable with ammonium sulfate and absorbable on anti-Candida antibodies or concanavalin A-coupled agarose columns. Altogether, these results suggest that the inhibitory factor is not an immunoglobulin, but rather a polysaccharidic antigen of Candida albicans. An inhibition of Candida-induced proliferative response of normal human lymphocytes was also obtained by addition of polysacharide antigens or purified mannans from C. albicans to cultures. Candida polysaccharidic antigens appeared, therefore, to be involved in specific depression of cellular functions observed in chronic candidiasis.

Adolescent↗
PubMed2026

Zebrafish as a Model Organism to Study Neurotoxicity: A Potential Tool for Neuroprotective Drug Discovery.

INTRODUCTION: Danio rerio, the zebrafish, serves as an excellent model in neuroprotective drug discovery due to its conserved nervous system organization, neurotransmitter pathways, antioxidant defenses, and genomic similarity to mammals. METHODS: A systematic literature search following PRISMA 2020 guidelines was conducted across Pub- Med, Scopus, Web of Science, and Google Scholar. Studies published between 2020 and 2025 were prioritized, with earlier key papers included for context. The data on larval, adult, and genetically modified zebrafish models were analyzed for neurotoxic effects, focusing on study design, toxicants, and neurobehavioral or molecular outcomes. RESULTS: Neurotoxicants such as chlorpyrifos, bisphenol, triphenyl phosphate, aluminum, ammonium acetate, arsenic, zinc, acrylamide, methylmercury, and tris (1,3-dichloro-2-propyl) phosphate were shown to cross the zebrafish blood-brain barrier. These exposures caused significant behavioral alterations, neurotransmitter imbalances, oxidative stress, and gene or protein expression changes related to brain function. Analysis of the transgenic zebrafish revealed notable alterations in neuronal development and axonal morphology upon exposure to various neurotoxic chemicals. DISCUSSION: Zebrafish display neurotoxic responses with a close resemblance to mammals, supporting their translational value in neurotoxicity and drug discovery studies. However, limitations such as a less complex brain compared to mammals, quick neuronal regeneration, limited tissue access, and difficulties in drug absorption quantification warrant refinements in zebrafish models. CONCLUSION: Zebrafish offer a versatile, cost-effective, and genetically tractable system for neurotoxicity and neuroprotection research. This systematic review highlights their crucial role in neuroprotective drug discovery while emphasizing the need for improved methodological approaches to enhance translational reliability.

Animals↗
PubMedDate not supplied

[Use of Cetremide in the surgery of hydatid cysts].

The satisfactory treatment for hydatid disease is surgical removal of the cyst. The use of different chemical scolicide such as formalin, alcohol and hypertonic solution of NaCl intra-cavity are common. The purpose of this paper is to present the use of a new scolicide agent CETRIMIDE (cetyl trimethyl ammonium bromide), first experimentally then in 7 patients with hydatid disease in different location. The special techniques described, no sign of toxicity or recurrence noticed. I have found this is a reliable method of preventing recurrences. No recurrence was found in our series after 2 years of follow-up.

Adult↗
PubMed1977

[Isolation and purification of a preparation possessing leukocytosis-stimulating properties from pertussis bacteria].

A homogeneous protein LSF-2 preparation was extracted from the cultural fluid of Bordetella pertussis strains of the 1.0.3 serological type by means of precipitation with ammonium sulphate and electrofocussing; this preparation proved to produce a marked leukocytosis-stimulating and a weak toxic action of delayed type in experiments on animals. Intraperitoneal administration of 5 mug of the LSF-2 preparation caused a rise of leukocytosis in mice to 100,000 cells per 1 mm3, a delay in the gain in weight beginning from the 3rd day of the administration and a late death of the animals in 5% of cases. The LSF-2 preparation protected the mice in infection with a virulent pertussis strain No. 18323 in the amount of from 12 to 91%, depending on the immunizing dose; its ImD50 was equal to 2.0 -2.4 mug of protein. The results of investigations carried out permitted to assess the role of this substance in the formation of specific immunity in pertussis infection.

Animals↗
PubMed1977

Response of skin to ammonium persulphate.

In order to investigate the histamine liberating actions of ammonium persulphate, skin slices from three species (guinea pig, rat and monkey) were incubated in vitro with concentrations of ammonium persulphate ranging from 1 to 1000 microgram/ml. None of these concentrations released significant amounts of histamine in guinea pig or monkey skin. In the rat the highest concentration (1000 microgram/ml) released 20-24% of the histamine content of the skin, but the intensitivity of this response to cooling indicates a non-specific "toxic" action on mast cells. By contrast a known chemical histamine liberator, compound 48/80, released significant amounts of histamine from skin at much lower concentrations in all three species. Ammonium persulphate is clearly not a potent histamine liberator. Ammonium persulphate dermatitis is presumably a result of increased sensitivity of skin mast cells, due to immunological or other factors, in susceptible individuals.

Ammonium Sulfate↗