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PubMed2004

[The problem and improvement of colorimetric method for determination of sulfite in foods containing sulfur compounds].

The modified Rankine colorimetric method for measuring sulfite added to food as a food additive has a low determination limit and is little influenced by interfering substances from foods. However, it can give erroneous results for foods containing Liliaceae Allium. So, four different methods, alkaline titration, a colorimetric method, ion chromatography and qualitative analysis with potassium iodate-starch paper, were examined. It was found that the sodium azide used in the colorimetric method forms sulfur dioxide during bubbling and heating. The proposed colorimetric method can be applied to food containing sulfur compounds, if sodium azide is omitted and 1% triethanolamine solution is used as an absorbent instead of 0.1 mol/L sodium hydroxide solution.

Colorimetry↗

PubMed2005

Kinetic modelling of the intestinal transport of sarafloxacin. Studies in situ in rat and in vitro in Caco-2 cells.

The absorption kinetics of sarafloxacin, as a model of fluoroquinolone structure, were studied in the rat small intestine and in Caco-2 cells. The objective of the study was to investigate the mechanistic basis of the drug's intestinal transport in comparison with other members of the fluoroquinolone family and to apply a mathematical modelling approach to the transport process. In the rat small intestine, sarafloxacin showed dual mechanisms of intestinal absorption with a passive diffusional component and an absorptive carrier-mediated component. The characteristics of the animal study design made it suitable for population analysis, thus allowing the accurate estimation of transport parameters and their inter and intra-individual variances. The transport system in the rat model was ATP-dependent, as sodium azide was able to decrease the absorption rate constant in a concentration-dependent fashion. The inhibition mechanism of sodium azide was modelled based on its ATP depletion capacity. The rationale of this approach was to consider the inhibitor-carrier interaction as a concentration- dependent response. This interaction was accurately described by a non-competitive mechanism. In Caco-2 cells, sarafloxacin showed a concentration dependent permeability in both directions apical to basal, and basal to apical. The permeability values and ratios of permeability values at different concentrations suggested the presence of two carriers (absorption and efflux carriers). The passive diffusion component in both systems was compared to that predicted by the absorption-partition correlation, previously established for two series of fluoroquinolones. The discrepancy between the experimental and predicted value suggested the presence of an efflux mechanism similar to that already described for other fluoroquinolones. The differences and similarities of the in situ and the in vitro results are discussed as well as the usefulness of the modelling approach.

Adenosine Triphosphate↗

PubMed1999

Energy metabolism inhibition impairs amyloid precursor protein secretion from Alzheimer's fibroblasts.

The present study investigates the influence of aglycemia and sodium azide (a Cytochrome c Oxidase inhibitor) on sAPP secretion from skin fibroblasts derived from sporadic AD patients and control subjects. Aglycemia reduced sAPP release in the medium of both AD and control fibroblasts to a similar extent after 2 h incubation. Treatment for 2 h with increasing azide concentrations (1 microM-100 mM) under glucose deprivation did not significantly affect sAPP secretion from control fibroblasts, but was able to significantly inhibit sAPP secretion from AD fibroblasts (maximal inhibition 51%). The failure of antioxidants like glutathione (GSH) or N-acetylcysteine (NAC) to antagonize the azide effect on AD fibroblasts and lipoperoxidation data seemed to rule out the possibility that oxidative stress could mediate the sodium azide effect on sAPP release from AD fibroblasts.

Acetylcysteine↗

PubMed1984

Pseudomonas aeruginosa exoproteases inhibit human neutrophil chemiluminescence.

The present study was designed to examine the effect of Pseudomonas aeruginosa alkaline protease and elastase on human polymorphonuclear leukocyte chemiluminescence. Both a luminol-enhanced and a nonenhanced chemiluminescence system using opsonized zymosan were utilized. It was found that alkaline protease and elastase at concentrations of 25 micrograms/ml strongly inhibited luminol-enhanced myeloperoxidase-mediated chemiluminescence, whereas inhibition of the nonenhanced chemiluminescence response was about 50%. In an attempt to determine the mechanism of inhibition of neutrophil chemiluminescence by these proteases, we examined the effect of various inhibitors of neutrophil oxidative metabolism on chemiluminescence, namely, superoxide dismutase, sodium azide, and catalase. It was shown that the pattern of inhibition of chemiluminescence by alkaline protease and elastase was similar to that of sodium azide, inhibitor of myeloperoxidase. The present study demonstrates that alkaline protease and elastase, extracellular products of P. aeruginosa, are capable of inhibiting myeloperoxidase-mediated chemiluminescence, one of the major antimicrobial systems of polymorphonuclear leukocytes. These findings provide further evidence for the role of P. aeruginosa exoproteases as virulence factors in the pathogenesis of infections caused by this microorganism.

Azides↗

PubMed1989

Antimutagenicity of some citrus fruits in Salmonella typhimurium.

The antimutagenic effect of 10 citrus fruit juices was observed against the mutagenicity of N-nitro-o-phenylenediamine (NPD) in TA97a and sodium azide in TA100 tester strains of Salmonella typhimurium using the Ames test. It was noticed that the juices of all these fruits reduced significantly the NPD and sodium azide induced revertant colonies. The inhibitory activity was enhanced if the mutagen and juice were co-incubated for about 30 min at 37 degrees C prior to performing the mutagenicity assay. Dilution with distilled water led to the reduction in the inhibitory activity. The antimutagenic activity of synthetic ascorbic acid or citric acid or combined ascorbic acid and citric acid was also seen. But the results with fruit juices tempted us to believe that in addition to ascorbic acid and citric acid, the presence of other factor(s) possessing antimutagenic properties cannot be ruled out.

Azides↗

PubMed2006

Mechanism of L-ascorbic acid uptake by rabbit corneal epithelial cells: evidence for the involvement of sodium-dependent vitamin C transporter 2.

PURPOSE: To investigate the mechanism of L-ascorbic acid uptake by rabbit corneal epithelial cells and to functionally characterize the specific transporter involved in this translocation process. METHODS: Uptake studies were carried out with SIRC (Statens Seruminstitut Rabbit Cornea) and rPCEC (rabbit Primary corneal epithelial cell culture) in 12-well plates using [14C] Ascorbic acid (AA). Uptake was done in the presence of L-ascorbic acid and D-isoascorbic acid to delineate stereospecificity. Inhibition studies were performed in the presence of D-glucose a substrate for GLUT and also para amino hippuric acid (PAHA) a substrate for organic anion transporter. Effects of pH and sodium on the uptake of AA were characterized. Concentration dependency studies were performed. Energy dependence of AA uptake was investigated with ouabain and sodium azide in rPCEC. Reverse Transcription-polymerase chain reaction (RT-PCR) was also performed. RESULTS: Uptake of AA was inhibited by about 90% and 50% respectively in the presence of L-ascorbic acid and D-isoascorbic acid in both SIRC and rPCEC. Uptake was unaltered by D-glucose and PAHA. The process was sodium dependent and saturable at higher concentrations. Ouabain and sodium azide significantly diminished the uptake process. It also decreased with a reduction in pH. The RT-PCR results showed the presence of SVCT2 but not SVCT1. CONCLUSIONS: Uptake of AA across rabbit corneal epithelial cells appears to be a carrier mediated active process. A saturable, sodium dependent, and pH sensitive transporter with high specificity for L-ascorbic acid was functionally characterized and was identified as SVCT2.

Animals↗

PubMed1999

Photogenotoxicity of fluoroquinolones in Chinese hamster V79 cells: dependency on active topoisomerase II.

The Chinese hamster V79 lung cell in vitro micronucleus assay was adapted to detect and quantify phototoxicity and photogenotoxicity of fluoroquinolones. Using this assay, the quinolones were ranked in terms of decreasing phototoxicity: clinafloxacin >> lomefloxacin, sparfloxacin >> trovafloxacin, nalidixic acid, ofloxacin, ciprofloxacin > enoxacin, norfloxacin. This rank order agrees well with published studies utilizing various other phototoxicity models and establishes this approach as a fast and sensitive way to characterize the phototoxic potential of quinolones. Nearly complete inhibition of phototoxicity was observed if the cells were pretreated for as little as 1 min with 10-20 mM sodium azide prior to the addition of quinolone. An identical azide effect was seen in unirradiated quinolone- and etoposide-treated cells. These findings are consistent with a model in which sodium azide renders DNA topoisomerase II catalytically inactive. In this state, topoisomerase II cannot initiate DNA strand cleavage and the DNA/topoisomerase complex becomes insensitive to quinolones and other topoisomerase II inhibitors. The fact that azide reduces both UV-dependent and UV-independent toxicity and clastogenicity strongly suggests a common mechanism of toxicity dependent on the formation of topoisomerase-induced DNA double-strand breaks.

Animals↗

PubMed1997

The reaction of peroxynitrite with tert-butyl hydroperoxide produces singlet molecular oxygen.

Peroxynitrite, a biological oxidant, can induce lipid peroxidation in biological membranes which leads to the formation of various hydroperoxides. Here, we report the formation of singlet oxygen (1O2) in the reaction of peroxynitrite with tert-butyl hydroperoxide (t-BOOH) used as a model compound for organic hydroperoxides. The formation of singlet oxygen was observed by (i) dimol emission in the red spectral region, (ii) monomol emission in the infrared region at 1270 nm and by (iii) chemical trapping of singlet oxygen with anthracene-9,10-diyldiethyl disulfate (EAS). The emission signal was increased when H2O was replaced by deuterium oxide and was quenched by sodium azide. When singlet oxygen was generated in the reaction of peroxynitrite with t-BOOH, the 1O2 quenching rate constant for sodium azide was estimated from a Stern-Volmer plot as 1.3 x 10(8) M(-1) S(-1) which is in line with known values. The 1O2 generation in the peroxynitrite/t-BOOH reaction was also detected by the formation of the endoperoxide of EAS. These data establish the generation of 1O2 in the reaction of peroxynitrite with t-BOOH and suggest a potential involvement of 1O2 in peroxynitrite-mediated reactions in biological systems.

Deuterium Oxide↗

PubMed1986

Comparative evaluation of the effect of pharmacological agents on endocytosis and coendocytosis of IgE by rat basophilic leukaemia cells.

The aggregation of IgE bound to rat basophilic leukaemia (RBL) cells leads to the exocytosis of mediators, the endocytosis of the antigen-aggregated mouse IgE anti-DNP, as well as the coendocytosis of some unaggregated monomeric rat IgE (IR162) and/or unbound receptors. We describe here the relative effect on endocytosis and coendocytosis of various pharmacological agents that block or enhance exocytosis. We have previously shown that, unlike exocytosis, endocytosis by RBL and normal rat mast cells was independent of extracellular calcium. We show here that the presence of calcium chelators or antagonists also had no effect on endocytosis of cross-linked IgE. However, coendocytosis of non-cross-linked IgE was partially inhibited by the elimination of extracellular calcium and the addition of calcium chelators such as EDTA or EGTA-Mg2+. Moreover, the addition of calcium antagonists such as Ni2+ and Co2+ (5 mM) to an incubation mixture containing Ca2+ (1 mM) resulted in the complete inhibition of coendocytosis without affecting endocytosis. Other inhibitors of exocytosis such as sodium azide (10-2M), quercetin (10-4M) and dibutyryl cyclic AMP (10-2 M) blocked coendocytosis completely but had no effect on endocytosis. Sodium azide (10 mM) in combination with 2-deoxyglucose (10 mM) effectively inhibited (90%) endocytosis. Cytochalasin B (10-4 M), which was shown to enhance serotonin release, had no effect on the extent of endocytosis or coendocytosis observed 20 min after the initiation of aggregation. Thus, in RBL cells, endocytosis, coendocytosis and exocytosis exhibit distinguishable sensitivities to some pharmacological drugs.

Animals↗

PubMed2000

Simultaneous production of nitric oxide and peroxynitrite by plant nitrate reductase: in vitro evidence for the NR-dependent formation of active nitrogen species.

We examined the ability of plant nitrate reductase (NR) to produce nitric oxide (NO) using in vitro assays. Electrochemical and fluorometric measurements both showed that NO is produced by corn NR in the presence of nitrite and NADH at pH 7. The NO production was inhibited by sodium azide, a known inhibitor for NR. During the reaction, absorbance of 2',7'-dichlorodihydrofluorescein increased markedly. This change was completely suppressed by sodium azide, glutathione or depletion of oxygen. We conclude that plant NR produces both NO and its toxic derivative, peroxynitrite, under aerobic conditions when nitrite is provided as the substrate for NR.

Aerobiosis↗

PubMed1997

Singlet oxygen involvement in ultraviolet (254 nm) radiation-induced formation of 8-hydroxy-deoxyguanosine in DNA.

In the present article, we report that ultraviolet (UV 254 nm) radiation substantially induced the formation of 8-hydroxy-2'-deoxyguanosine (8-OHdG) in purified DNA. The formation of 8-OHdG, a hallmarker of oxidative DNA damage, increased linearly up to 25 kJ/m2 and was dependent on the presence of oxygen in the solution. Deoxygenation by nitrogen significantly reduced the yield of 8-OHdG by UV radiation, whereas oxygenation with 100% oxygen substantially enhanced the yield. The hydroxyl radical (HO.) scavenger dimethysulfoxide (DMSO) dramatically quenched the formation of 8-OHdG by the ionizing radiation and Fenton reaction, but enhanced the formation of UV-induced 8-OHdG. Further studies showed that DMSO and mannitol, two predominant HO. scavengers, enhanced the levels of UV-induced 8-OHdG in a dose-dependent fashion, suggesting that UV-induced 8-OHdG is independent of the generation of HO.. The use of deuterium oxide (D2O), which prolongs the half life of singlet oxygen (1O2), substantially enhanced the yield of 8-OHdG by UV radiation, but not that by Fenton reaction. In contrast, sodium azide, a more and less specific 1O2 quencher, substantially reduced the levels of 8-OHdG by both UV radiation and Fenton reaction, indicating that sodium azide lacks the quenching specificity of 1O2 and HO.. It is proposed that UV induced 8-OHdG proceeds through a singlet oxygen involvement mechanism, rather than the generation of hydroxyl radicals.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed1975

Polar appearance and nonligand induced spreading of measles virus hemagglutinin at the surface of chronically infected cells.

Fixation with glutaraldehyde (GA) and paraformaldehyde (PFA) preserved measles virus hemagglutinin at the surface of chronically infected cells. Cells fixed with PFA but not with GA exhibited hemadsorption with green monkey cells. PFA fixation, in contrast to GA fixation, also preserved the immunogenicity of measles virus hemolysin. These fixatives and the removal of the measles virus hemagglutinin from the cell surface by trypsin enabled studies of the appearance of the hemagglutinin at the surface membrane. Results obtained by immunofluorescence technique and by hemadsorption indicated that measles virus hemagglutinin appeared polarly at the cell membrane and then spread around the surface. This was substantiated by measurements of the immunofluorescence intensity at the single cell level per membrane unit and per cell, and by measuring the binding of iodinated immunoglobulins per 10(6) cells. The appearance was inhibited by sodium azide and cytochalasin B. The spreading was not inhibited by sodium azide, but was influenced by cytochalasin B. The spreading did not proceed at 4 degrees C. On the basis of these findings, a hypothetical model for appearance and spreading of measles virus hemagglutinin was proposed.

Antibodies, Viral↗

PubMed1982

Energy-dependent lysosomal wrapping mechanism (LWM) during autophagolysosome formation.

The relation of lysosomes to autophagy, in particular the lysosomal wrapping mechanism (LWM) is investigated ultracytochemically from the viewpoint of demonstrations of energy dependency of the LWM. An induction of the LWM was made in mouse subcutaneous histiocytes by subcutaneous administration of ovalbumin. Prior administration of the inhibitor of glycolysis (2-deoxyglucose) alone and of the oxidative phosphorylation (sodium azide or 2,4-dinitrophenol) alone did not prevent the occurrence of the LWM following ovalbumin administration, but a prior administration of a mixture of 2-deoxyglucose and 2,4-dinitrophenol or 2-deoxyglucose and sodium azide prevented the occurrence of the LWM. These results suggest that in order for the LWM to take place ATP is required as an energy source.

2,4-Dinitrophenol↗

PubMed1979

Interference of azide with cysteine biosynthesis in Salmonella typhimurium.

The growth inhibition of Salmonella typhimurium aziA mutants by sodium azide is reversed by cystine and related compounds. NADPH-sulphite reductase (hydrogen-sulphide:NADP+ oxidoreductase; EC 1.8.1.2), an enzyme of cysteine biosynthesis, is inhibited in cell extracts by sodium azide. AziB mutants which are able to grow in the presence of the inhibitor without cystine were isolated. About half of them were mapped in the cysK gene and have only residual activity of its product, O-acetylserine sulphydrylase A [O-acetyl-L-serine acetate-lyase (adding hydrogen-sulphide); EC 4.2.99.8]. Sensitivity of wild type and aziA mutants to azide was also reversed by a constitutive mutation in cysB, the regulatory gene of cysteine biosynthesis. CysK and cysB mutants showed cross-resistance to azide and 1,2,4-triazole. It is suggested that the resistance of these mutants to azide is due to an increased activity of NADPH-sulphite reductase.

Azides↗

PubMed1987

Use of a sensitive receptor binding assay to discriminate between full-length and truncated human recombinant tumor necrosis factor proteins.

A radioreceptor assay (RRA) capable of detecting picomolar concentrations of human recombinant tumor necrosis factor (TNF) was used to compare the relative binding affinities of genetically engineered full-length and truncated TNF proteins. The specific cell-surface receptors for TNF present on the human cervical carcinoma cell line ME-180 were characterized as having a Kd of 0.2 nM and a density of 2700 sites/cell. Conditions were then defined for an RRA that maximized the specific binding of 125I-TNF to this adherent cell line. Incubation of ME-180 cells with 125I-TNF at 37 degrees C in the presence of 0.02% sodium azide resulted in a 4-fold increase in assay sensitivity and a doubling of specific counts bound, as compared to binding done at 4 degrees C with or without sodium azide. Inhibition of receptor-ligand internalization under these conditions was a likely reason for the increases. This system was utilized to compare low concentrations of the full-length TNF protein and a genetically altered TNF protein (mutein) which lacks the 10 N-terminal amino acids and contains an N-terminal methionine. Previous studies showing the truncated TNF to be 2- to 3-fold lower in cytotoxic activity on a variety of tumor cell lines were corroborated by our findings that the mutein was also three and one-half times lower in relative affinity for the TNF receptor on ME-180 cells. These results suggest a possible role for these residues in receptor binding and illustrate the use of a highly sensitive RRA for the evaluation of TNF molecules altered by recombinant DNA technology.

Amino Acid Sequence↗

PubMedDate not supplied

Adenosine diphosphate ribose dilates bovine coronary small arteries through apyrase- and 5'-nucleotidase-mediated metabolism.

Cyclic adenosine diphosphate ribose and adenosine diphosphate ribose (ADPR) play an important role in the regulation of intracellular Ca(2+) release and K(+) channel activity in the coronary arterial smooth muscle. The role of these signaling nucleotides in the control of vascular tone has yet to be determined. The present study was designed to determine whether ADPR produces vasodilation in coronary arteries and to explore the mechanism of action of ADPR. ADPR (10-60 micromol/l) was found to produce endothelium-independent relaxation in a concentration-dependent manner in isolated and pressurized small bovine coronary arteries. The ADPR-induced vasodilation was substantially attenuated by adenosine deaminase (0.2 U/ml), and the P(1) purinoceptor antagonist 8-(p-sulfophenyl)theophylline (50 micromol/l), with maximal inhibitions of 60 and 80%, respectively. When the coronary arterial homogenates were incubated with ADPR, the production of adenosine and 5'-AMP was detected. The adenosine production was blocked by the 5'-nucleotidase inhibitor, alpha,beta-methylene adenosine 5'-diphosphate (MADP, 1 mmol/l), which was accompanied by a corresponding accumulation of 5'-AMP. This 5'-AMP accumulation was substantially inhibited by the apyrase inhibitor sodium azide (10 mmol/l). Moreover, ADPR was hydrolyzed into 5'-AMP by purified apyrase. In agreement with their inhibitory effect on the adenosine production, MADP and sodium azide significantly attenuated the vasodilator response to ADPR. The metabolism of ADPR to adenosine was only detected in cultured coronary arterial smooth muscle cells but not in endothelial cells. We concluded that ADPR produces vasodilation in small coronary arteries and that the action of ADPR is associated with the adenosine production via an apyrase- and 5'-nucleotidase-mediated metabolism.

5'-Nucleotidase↗

PubMed1981

Uptake of free and liposome-entrapped 125I-labelled PVP by rat intestinal sacs in vitro: evidence for endocytosis.

The uptake of free and liposome-entrapped 125I-labelled PVP was measured in and intestinal-sac preparation from adult rats. Uptake of the free macromolecule was directly proportional to the substrate concentration and was reduced by colchicine and sodium azide. Uptake of the liposome-entrapped macromolecule was greater than that of the free macromolecule, was not directly proportional to substrate concentration, showed signs of saturation at high liposome concentrations, and was also reduced by sodium azide and colchicine. These results suggest that gut epithelial cells take up the free macromolecule by fluid-phase endocytosis and the liposome-entrapped macromolecule by adsorptive endocytosis.

Animals↗

PubMed1996

Mutation induction and mutation spectra of S. typhimurium TA100 after exposure to isohistidines.

L-Isohistidine and D,L-isohistidine, but not D-isohistidine, caused an increase of the number of mutant colonies in S. typhimurium strain TA100. Spontaneous and also sodium azide or 2-aminoanthracene induced mutant numbers were enhanced by L-isohistidine and by an isomeric mixture of D,L- and L-isohistidine. These effects could not be attributed to a growth-enhancing property. The colony probe hybridization procedure was used to investigate the effects of the histidines on the spontaneous and azide-induced spectra of the hisG46 allele in strain TA100. D,L-Isohistidine, but not the D-isomer, caused and increase of transitions (CCC-->CTC) and transversions (CCC-->CAC) in the spontaneous spectrum. Sodium azide alone induced a strong increase of CCC-->CTC transitions; combination with the D,L-isohistidine led to a further enhancement of this type of base substitutions, whereas with the L-isomer, no such effect was observed. This supports the hypothesis that the activity of D,L-isohistidine is probably not due to DNA-damaging properties, but rather to indirect mechanisms, such as enhancement of the infidelity of DNA replication and/or interference with DNA-repair or proofreading functions.

Alleles↗