Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The extent of blast transformation for human and BALB/c mouse lymphocytes has been examined over a wide range of glutamine concentrations with several agents which initiate blastogenesis. Maximum [3H] thymidine incorporation was seen at 0.5 mM glutamine for lymphoid tissues stimulated in the following manner: human and BALB/c splenic and peripheral blood lymphocytes with phytohemagglutinin, BALB/c splenic lymphocytes with lipopolysaccharide, and BALB/c vs C3H/HeJ two-way mixed lymphocyte cultures. The inhibition of blastogenesis exerted by glutamine concentrations greater than 0.5 mM could not be reversed by washing and reculturing the cells at 0.5 mM glutamine. To elucidate the reason for inhibition by higher glutamine concentrations, the products of spontaneous glutamine decomposition, L-2-pyrrolidone-5-carboxylic acid and ammonia were tested for their in vitro influence on BALB/c splenocyte blastogenesis. Pyrrolidone-carboxylic acid, in concentrations up to 5 mM, was without effect. In contrast, ammonia concentrations exceeding 1 mM became increasingly more inhibitory. The genesis of inhibitory levels of ammonia in culture medium was confirmed and has been considered as primarily responsible for inhibiton by high glutamine. Addition of Escherichia coli glutaminase (pH optimum 4.9) to cultures of BALB/c splenocytes or human peripheral blood lymphocytes had no effect on either the extent of blastogenesis of these tissues or the glutamine levels in their culture medium.
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PMID:The influence of glutamine, its decomposition products, and glutaminase on the transformation of human and mouse lymphocytes. 108 49

The effect of endotoxin on renal glutamine metabolism and ammoniagenesis was investigated in vivo in the rat to gain further insight into the altered glutamine flow that characterizes critical illness. Studies were done 15 hours following a single dose of Escherichia coli lipopolysaccharide (10 mg/kg). Renal blood flow and arterial glutamine concentration were similar in control and study rats, but the kidney switched from an organ of slight glutamine uptake in controls (129 +/- 52 nmol/100 g of body weight per minute) to net release in the endotoxin-treated animals (-273 +/- 170 nmol/100 g of body weight per minute). Simultaneously, the specific activity of renal glutamine synthetase increased by almost 50% (374 +/- 40 nmol/mg of protein per hour in rats given endotoxin vs 253 +/- 12 nmol/mg of protein per hour in controls), while glutaminase was unchanged. Urinary ammonia excretion was reduced by 35% in the endotoxin-treated animals (47 +/- 6 mumol/12 h in endotoxin-treated animals vs 70 +/- 8 mumol/12 h in controls) despite a 10% fall in the arterial bicarbonate value. Endotoxin alters the net flux of glutamine across the kidney which appears to be partially regulated enzymatically. This may impair the kidneys' ability to maintain acid/base homeostasis.
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PMID:Endotoxin and renal glutamine metabolism. 167 Jul 57

THI is a component of ammonia caramel, a widely used food colouring. The effect of THI on the immune system has been determined in the male F344 rat. THI was given in the drinking water at doses of 1, 10 and 50 mg/l (equivalent to 0.1, 1 and 5 mg/kg per day) to animals on a vitamin B6-deficient diet. After 1 week, the immune competence of the animals was assessed under continued THI treatment. No marked changes in thymus or spleen weight were observed after THI treatment, although there was an increased number of pyknotic cells in the thymic cortex, mainly engulfed by macrophages and there appeared to be a slight thinning of the cortex area. THI produced a significant loss in T and B lymphocytes in peripheral blood but not in the spleen. No change in natural killer (NK) cell activity against YAC-1 target cells was observed in the spleen. The observed increase in NK cell activity in peripheral blood was due to an increase in circulating large granular lymphocytes (LGL). Although the serum antibody titre against keyhole limpet haemocyanin (KLH) was not affected by THI treatment, B cells showed less proliferation when cultured with lipopolysaccharide. T cell function was impeded as measured in mitogen-induced proliferation assay, delayed-type hypersensitivity assay and host versus graft (popliteal lymph node) assay. The results indicate that THI is an immunosuppressor in the rat, in whom it can produce profound lymphopenia and suppression of cell-mediated immunity.
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PMID:Immunosuppressive effects of 2-acetyl-4-tetrahydroxybutyl imidazole (THI) in the rat. 186 15

Germ-free (GF) rats were maintained on a diet marginally adequate in protein, with and without a supplement of NH4Cl. Their urinary excretion of total nitrogen, nitrate, urea and creatinine was measured before and for 4 days after injection of Escherichia coli endotoxin (lipopolysaccharide; LPS). Although more nitrogen was excreted by rats on the diet supplemented with NH4Cl, nitrate excretion was increased to a similar extent in rats on both diets. This suggests that oxidation of ammonia released by deamination of amino acids is an unlikely pathway of nitrate synthesis. In a second experiment, nitrate excretion before and after injection of LPS was measured in GF and conventional (CV) rats given high- or low-protein diets. Urinary 3-methylhistidine (3MH) was measured as an index of breakdown of tissue protein. In both environments, nitrate excretion was significantly greater, before and after LPS administration, by rats on the high-protein diet than by their counterparts on the low-protein diet, and was generally greater by GF than by CV rats. Since only small, non-significant rises in urinary 3MH were observed after LPS treatment, it was concluded that the bulk of the nitrogen required for nitrate synthesis in response to endotoxin is derived from dietary protein rather than from nitrogenous products of tissue breakdown.
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PMID:Influence of dietary protein and gut microflora on endogenous synthesis of nitrate induced by bacterial endotoxin in the rat. 187 66

Ammonia-induced cell envelope injury was examined in pure cultures of Escherichia coli and Enterobacter aerogenes. Cell injury, as determined by the ratio of colony-forming units on m-T7 agar to colony-forming units on m-Endo agar, increased with exposure to increasing concentrations of ammonia. Cell envelopes appeared to be the site of injury as indicated by increasing susceptibility to lysozyme with increasing ammonia concentration. Cells exposed to ammonia also exhibited more cellular leakage than control cells. Leakage from cells exposed to ammonia included proteins, and all leaked substances increased in concentration as ammonia concentrations increased. The concentration of 2-keto-3-deoxyoctonate (KDO) in the outer membrane of E. coli increased with ammonia exposure, while KDO concentration in the outer membrane of E. aerogenes decreased. The results suggest that exposure of E. coli cells to high concentrations of ammonia disrupts the outer membrane and lipopolysaccharide-associated proteins, while E. aerogenes cells are affected through the disruption of bonds between KDO and the outer membrane.
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PMID:Ammonia-induced cell envelope injury in Escherichia coli and Enterobacter aerogenes. 224 77

Lipopolysaccharide from Escherichia coli C interacts with polyvalent cations at low ionic strength at more than one site. The first site has high affinity with a KD value of 10(-8) M for Ca2+ and even stronger binding for [(NH3)5CoNH2Co(NH3)5]5+ and La3+. The high-affinity site for the latter cations is beyond the sensitivity of the assay method. The second, low-affinity, site for bivalent cations has a Km of 10(-3) M, whereas, for tervalent and quinquevalent metal cations and spermine and hexacyclen (1,4,7,10,13,16-hexa-azacyclo-octadecane), this constant has a value of 10(-5) M. Binding of cations to the high-affinity site does not alter the aggregation state of the lipopolysaccharide, but combination with the low-affinity site gives particles twice the size of those of the sodium salt. Very high Ca2+ concentrations (30 mM) give particles eight times the size of those of the sodium salt.
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PMID:The interaction of cations with lipopolysaccharide from Escherichia coli C as shown by measurement of binding constants and aggregation reactions. 268 35

The macrophage cell line RAW 264.7 when activated with Escherichia coli lipopolysaccharide and interferon-gamma synthesized nitrite (NO3-) and nitrate (NO3-). Medium change after the activation showed that L-arginine was the only amino acid essential for this synthesis. D-Arginine would not substitute for L-arginine. Other analogues that could replace L-arginine were L-homoarginine, L-arginine methyl ester, L-arginamide, and the peptide L-arginyl-L-aspartate. L-Argininic acid, L-agmatine, L-ornithine, urea, L-citrulline, and ammonia were among the nonprecursors, while L-canavanine inhibited this L-arginine-derived NO2-/NO3- synthesis. When morpholine was added to the culture medium of the activated RAW 264.7 macrophages, N-nitrosation took place, generating N-nitrosomorpholine. GC/MS experiments using L-[guanido-15N2]arginine established that the NO2-/NO3- and the nitrosyl group of N-nitrosomorpholine were derived exclusively from one or both of the terminal guanido nitrogens of arginine. Chromatographic analysis showed that the other product of the L-arginine synthesis of NO2-/NO3- was L-citrulline. The role of the respiratory burst in NO2-/NO3- synthesis was examined using the macrophage cell lines J774.16 and J774 C3C. Both cell lines synthesized similar amounts of NO2-/NO3-. However, J774 C3C cells do not produce superoxide and hence do not exhibit the respiratory burst. Additional experiments also ruled out the involvement of the respiratory burst in NO2-/NO3- synthesis.
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PMID:Macrophage synthesis of nitrite, nitrate, and N-nitrosamines: precursors and role of the respiratory burst. 281 72

The metabolic fate of an oral dose of 3.5 mmol 15N-labelled nitrate was investigated in young adults. An average of 60% of the 15N-nitrate dose appeared in the urine within 48 h; less than 0.1% appeared in the faeces. Some of the 15N label of nitrate was found in the urine (3%) and faeces (0.2%) in the form of ammonia and urea; the remainder of the dose was attributed to nitrate loss via metabolism to other reduced nitrogen compounds. Studies with germ-free rats indicated that half of the nitrate metabolism is due to mammalian processes. These and previous studies show that not all of the nitrate excreted in the urine is of dietary origin but evolves from endogenous synthesis. An oral dose of 15N-ammonium acetate was incorporated into urinary 15N-nitrate in rats, suggesting that ammonia is a precursor of nitrate. Furthermore, Escherichia coli lipopolysaccharide was found to be a potent stimulus of nitrate excretion (nine-fold increase), due to an increased rate of synthesis. Two other types of experimentally induced inflammatory states - injection of carrageenan and of turpentine - enhanced nitrate synthesis. It is proposed that the pathway of nitrate biosynthesis may be the result of oxidation of reduced nitrogen compounds by oxygen radicals generated by an activated reticuloendothelial system.
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PMID:Mammalian nitrate biochemistry: metabolism and endogenous synthesis. 653 15

Helicobacter pylori is now accepted as the major cause of chronic gastritis. The initial response to infection is acute neutrophilic gastritis, which progresses to active chronic gastritis in most people. To confirm the pathogenic role of H. pylori, both the individual histological features of chronic gastritis and its topographical patterns must be shown to be caused by the infection. Surface epithelial degeneration is a probable result of direct tissue injury by bacterial products. Candidates are ammonia or ammonium products, cytotoxins, phospholipases and pro-inflammatory products such as lipopolysaccharide and platelet-activating factor. Neutrophil polymorph and chronic inflammatory cell infiltration are consequences of the mucosal immune response to bacterial antigens. Complement products and interleukin (IL)-8 are polymorph chemotaxins, and monocyte processing of antigens, followed by T helper cell and B lymphocyte responses, explain the presence of these cells in the mucosa. Atrophy may be a consequence of autodestructive products of neutrophil and monocyte activation, such as reactive oxygen metabolites and proteases. Intestinal metaplasia is most probably an adaptive response, possibly to H. pylori infection, exacerbated by other injurious agents such as bile reflux and dietary irritants. Pangastritis is the usual outcome after H. pylori infection. This is followed by multifocal atrophy and intestinal metaplasia. The latter changes weaken mucosal defences further and peptic ulceration may ensue. Patients with an increased parietal cell mass who become infected with H. pylori will exhibit antral restriction of the gastritis because the high acid output protects the corpus mucosa from bacterial adhesion and the inflammatory consequences. Such patients also have acid-induced gastric metaplasia in the proximal duodenum.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology of Helicobacter pylori infection. 804 28

In this paper we discuss the following: 1. Synthesis of [Co(H3CsarNHCH2pyRu(NH3)5)] (PF6)5, (CoRu). 2. Interaction of CoRu with calf thymus DNA and with lipopolysaccharide from Escherichia coli C (LPS) has been estimated using the absorption of the complex at 242 and 420 nm. 3. DNA and LPS increase the rate of fall of absorption at 420 nm due to autooxidation of the complex. 4. The fall in absorption of CoRu(II) at 420 nm can be used to give an approximate measure of binding to DNA and to LPS. 5. Both macromolecules are aggregated by CoRu at high concentrations and the cation and macromolecule complex can be removed by low speed centrifugation. 6. The DNA-CoRu complex can also be removed by high speed centrifugation when the cation concentration is too low to cause aggregation (20 microM CoRu/155 microM DNA-P). Absorption of redissolved complex at 420 nm is restored by reduction with ascorbic acid. 7. At saturation the ratio of mole CoRu bound/mole DNA-P is 0.16.
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PMID:The binding of a complex cobalt ruthenium polyamine by deoxyribonucleic acid and a lipopolysaccharide: a model for a novel class of drugs. 847 25


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