SEARCH · PubMed Health

Results for “Sodium Azide”

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 757 records · Page 42Linked to original sources

PubMed1982

Osmotically induced changes in the ornithine decarboxylase activity of Dictyostelium discoideum.

Myxamoebae of Dictyostelium discoideum from exponentially growing cultures showed altered ornithine decarboxylase activity upon external osmotic perturbation. On transfer to hypotonic NaCl solutions (20 mosmol/kg), cells showed high enzyme activity which was relatively independent of the concentration of the coenzyme pyridoxal phosphate (assay concentrations, 5 and 200 microM). In hypertonic solution (400 mosmol/kg) cells had a reduced level of ornithine decarboxylase activity which was dependent on the coenzyme concentration. The changes in activity were freely reversible in further external osmotic manipulation. The response to osmotic change occurred rapidly, within a few minutes. The changes still occurred at 7 degrees C but 2 mM sodium azide prevented the formation of the high activity form, although this effect was reversed when azide was removed. Cycloheximide had no effect on the osmotically induced changes. Addition of putrescine caused ornithine decarboxylase eventually to the converted to the low-activity form regardless of the osmolality of the solution. The characteristic cofactor concentration dependence of the high- and low-activity form were retained on storage of the cell extracts. No evidence was found for diffusible effectors which stabilized one or the other form of the activity. The enzymes responsible for the two forms were of the same molecular size as judged by gel filtration, and the activities had similar thermostabilities. The results are interpreted in terms of an osmotically induced interconversion of two forms of a single ornithine decarboxylase.

Azides↗

PubMed1994

Metabolic characteristics of alpha-toxin-permeabilized smooth muscle.

Rabbit portal veins were permeabilized using Staphylococcus aureus alpha-toxin, and adenosinetriphosphatase (ATPase) was measured as the formation of [3H]ADP, [3H]AMP, and [3H]adenosine from [3H]ATP in the solution bathing the muscle. The resting ATPase (1.96 +/- 0.15 mM/min, n = 13) is approximately 5-10 times higher than that measured in Triton X-100-permeabilized muscles (0.28 +/- 0.01 mM/min, n = 4), with nucleotide accumulating as ADP, AMP, and adenosine. The ATPase activity is also seen when the intact muscle is incubated in a Krebs solution containing 1 mM MgATP (2.76 +/- 0.10 mM/min, n = 73). This suggests that it is due primarily to an ecto-ATPase. The ectoenzyme is capable of hydrolyzing both ATP and ADP, and in both cases there is a higher rate at 3 than at 1 mM nucleotide. The high resting ATPase compromises the control of nucleotide concentrations within the permeabilized tissue even in the presence of an ATP-regenerating system consisting of phosphocreatine (PCr, 35mM) and creatine kinase (1 mg/ml). Treatment of the intact muscle with the ectonucleotidase inhibitor 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS) followed by alpha-toxin permeabilization and inclusion of sodium azide in subsequent solutions reduces the ecto-ATPase by approximately 70%. Addition of PCr and creatine kinase then results in the maintenance of high [ATP] and low [ADP] in the muscle, and importantly, there are no significant changes in [ATP], [ADP], [adenosine/AMP], or the ADP-to-ATP ratio upon activation of the muscle in pCa 4.5. In general, the force output in high Ca2+ increased as the metabolic profile of the muscle improved. When ATPase was measured as the appearance of [32P]Pi from [32P]PCr and [gamma-32P]ATP, the alpha-toxin-permeabilized muscle subjected to the above treatment showed only approximately 30% higher total ATPase under activated conditions compared with the freeze-glycerinated Triton-treated portal vein. The suprabasal ATPase is similar in both preparations. We conclude that the reduction of the basal ATPase by the DIDS-azide treatment permits both rigorous control of nucleotide contents and accurate measurement of ATPase activity in alpha-toxin-permeabilized smooth muscle.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1983

Mechanism of skin surface lipid peroxidation.

The correlation between the amount of lipid peroxide and squalene in skin surface lipid was observed by statistical analysis. To investigate the mechanism of skin surface lipid peroxidation, especially the role of active oxygen, squalene was irradiated by long wavelength ultraviolet light (UVA) with or without the photosensitizer, 8-methoxypsoralen (8MOP). Sodium azide (NaN3), a singlet oxygen quencher, or deuterium oxide, which elongates the life time of singlet oxygen, were also added in these experiments. The lipid peroxidation was detectable by observing malondialdehyde (MDA) formation. The MDA value in squalene solution was increased by UVA irradiation, and this effect was enhanced under the presence of 8MOP. These effects were repressed by the addition of NaN3 in the experimental system. These results may show that squalene peroxidation was mediated by singlet oxygen. Epidermal keratin could inhibit the increase of MDA values in human skin surface lipid in vitro. The inhibitory effect of epidermal protein on the deposition or the formation of lipid peroxide in skin surface was suggested.

Adult↗

PubMed1992

Oxiradical-dependent photoemission induced by a phacoemulsification probe.

Oxygen free radical formation by conventional phacoemulsification devices has been postulated as a possible mechanism of corneal endothelial damage during surgery. To test this hypothesis, phacoemulsification probe-induced free radical production was visualized using a single photon-counting camera and an O(2-)-sensitive luciferin derivative, 2-methyl-6-[p-methoxyphenyl-3,7-dihydroimidazo [1,2-a]pyrazin-3-one (MCLA), which allows the visualization of spatial and temporal alterations in free radical production. Within 1 min after starting ultrasound emission, MCLA-dependent chemiluminescence was increased significantly, the intensity of which was maximal at the tip of the probe and tapered along a gradient toward distal portions. The chemiluminescence was suppressed significantly by adding either superoxide dismutase (300 U/ml) or sodium azide (20 mmol/l). By adding deuterium to the medium, MCLA-dependent chemiluminescence significantly increased, suggesting the involvement of singlet oxygen in the reaction.

Azides↗

PubMedDate not supplied

Increased native chemiluminescence in granulocytes isolated from synovial fluid and peripheral blood of patients with rheumatoid arthritis.

Polymorphonuclear leukocytes (PMNs) isolated from peripheral blood and synovial fluid of patients with rheumatoid arthritis and from peripheral blood of volunteers were stimulated with 12-phorbol-13-myristate acetate (PMA). No significant differences in luminol-amplified chemiluminescence were found between different patients and control groups. However, two distinct patterns of native chemiluminescence were observed. Type I showed no, or only a small, increase in native chemiluminescence with integral counts over 30 min less than 3 x 10(5) cpm, and the majority of samples from volunteers were of this type. Type II was characterized by a burst of native chemiluminescence starting 8 to 15 min after cell stimulation. It was found in most PMN samples from patients with rheumatoid arthritis. Integral counts over 30 min were always higher than 10(6) cpm and as high as 10(8) cpm in some cases. A strong inhibition of the Type II native chemiluminescence was caused by desferal, catalase, thiourea, and glutathione. However, the luminol-amplified chemiluminescence remained unchanged or was only slightly decreased under the same experimental conditions. Sodium azide strongly inhibited both kinds of luminescence. Hydroxyl radicals, formed in a Fenton reaction, may be important intermediates in the Type II native chemiluminescence.

Arthritis, Rheumatoid↗

PubMed1994

Evidence for histamine uptake by murine hematopoietic progenitors.

Based on previous evidence for a role of exogenous and endogenous histamine, we have examined whether this amine can effectively interact with hematopoietic progenitors. We show that tritiated histamine is retained preferentially by bone marrow cells as compared with peritoneal, thymic or spleen cells. Cells interacting with histamine copurify with progenitors in the low density bone marrow fraction. Among this cell population, 5% are labeled as assessed by autoradiography. The characteristics of histamine retention by these cells are consistent with active uptake rather than binding to a known receptor since (a) it is almost completely abrogated at 4 degrees C, by sodium azide or chloroquine, (b) histamine is internalized, and (c) relatively high concentrations of classical receptor antagonists are required to inhibit histamine retention by bone marrow cells.

Animals↗

PubMed1990

A lectin-like receptor on murine macrophage is involved in the recognition and phagocytosis of human red cells oxidized by phenylhydrazine.

Phenylhydrazine (Phz) is a powerful hemolytic agent which has several effects on both normal and G6PD deficient red blood cells (RBCs). We have studied the mechanism of removal of Phz-damaged human RBCs by murine macrophages. Phagocytosis of Phz-treated RBCs was found to be 50 RBCs/100 mac as compared to 2 RBCs/100 mac of the controls. EGTA and sodium azide inhibited the phagocytosis, indicating a requirement for both calcium ions and energy. Incubation of macrophages with sugars such as D-galactose or D-mannose reduced phagocytosis of Phz-treated RBCs by up to 60%, indicating the involvement of a macrophage lectin-like receptor in the recognition of Phz-treated RBCs. The presence of serum in the phagocytosis assay did not affect either phagocytosis of Phz-treated RBCs or inhibition by sugars. beta-Galactosidase, but not neuraminidase, treatment of RBCs caused a significant inhibition in phagocytosis of Phz-treated RBCs. These results suggest that galactosyl residues are exposed on RBC membrane during oxidation, probably not as a result of desialization. We conclude that Phz-treated RBCs are detected as damaged cells mainly due to sugar changes on their membrane, which are directly recognized by lectin-like receptors on the macrophages.

Animals↗

PubMed1987

High mutagenic activity of 3-azido-1,2-propanediol (azidoglycerol, AG) in strain D7 of Saccharomyces cerevisiae.

3-Azido-1,2-propanediol (azidoglycerol, AG) showed a high mutagenicity in strain D7 of Saccharomyces cerevisiae. At 5 mM it increased the spontaneous frequency of isoleucine revertants 3500 times and the frequency of gene convertants 3000 times during 24 h of growth, reducing the growth rate to 30%. In non-growth conditions, treatment with 150 mM of AG for 3 h reduced cell survival to 60% and enhanced the frequency of isoleucine revertants 490 times and tryptophan-independent convertants 50 times. At equal survival levels, AG was found to be 3000-fold more mutagenic and 200-fold more convertogenic than sodium azide.

Azides↗

PubMed1983

Luminol-dependent chemiluminescence analysis of the variables of the phagocytic response by canine granulocytes.

Variables which influence the oxygen-dependent chemiluminescence (CL) response of canine polymorphonuclear leukocytes (PMN) to zymosan were examined in a luminol-dependent CL assay system. Maximal CL responses were obtained when 5 x 10(6) canine PMN, isolated from heparinized blood, were assayed at 37 degrees C in a Luminometer. The response was enhanced by the addition of 0.05 mM Luminol and inhibited by the addition of 0.06 mM sodium azide and 60 micrograms superoxide dismutase. Repeatability on a given day was very good; however, day to day variations in CL activity prevented direct comparison of phagocytic activity between days. Opsonization of zymosan in equine serum significantly reduced the CL response by canine PMN as compared to opsonization of zymosan in autologous or homologous canine serum and bovine serum. The present results show that luminol-dependent CL analysis can be used to measure phagocytosis by canine granulocytes in a luminometer and has potential use in clinical situations.

Animals↗

PubMed1994

Effects of acidic pH on the formation of vinblastine-induced paracrystals in Chinese hamster ovary cells.

The pH-related change in morphology of vinblastine (VLB)-induced paracrystals formed in Chinese hamster ovary (CHO) cells was examined immunohistochemically in order to determine both the mechanism of tubulin crystallization and the influence of acidic pHs on cytoskeletal microtubules. Lowering the extracellular pH (pHe) rapidly reduced the intracellular pH (pHi) in CHO cells. Lowering the pHi to near the neutral range significantly accelerated the growth of VLB-induced paracrystals, compared to that of paracrystals formed at a physiological pHe. However, further cytoplasmic acidification caused by the addition of sodium azide into the culture medium induced the disappearance of typical paracrystals and the appearance of a highly organized meshwork of tubulin appearing as short, thick filaments at the light microscopic level. Treatments using different concentrations of VLB at different pHe's showed that low pHi's (6.7 and 6.3) suppressed paracrystal-formation at lower concentrations of VLB (5 x 10(-6) M and 10(-5) M). At higher concentrations of VLB (5 x 10(-5) M and 10(-4) M), only short filaments were formed at pHi 6.3. Electron microscopy revealed that the filaments had a ladder-like structure probably consisting of a stacked series of fused rings. This indicates that paracrystals may be modified by extremely low pH. These results show that paracrystals are unstable in living cells and that their formation is regulated by environmental pH.

Acids↗

PubMed1994

Characterization of a method for the detection of drugs with free radical scavenging activity using porcine leukocytes.

The effects of a range of free-radical scavenging drugs on luminol-enhanced chemiluminescence (CL) generated by porcine leukocytes, following activation by two nonreceptor-mediated stimulants, phorbol myristate acetate (PMA; a protein kinase activator) and ionomycin (a cation ionophore), and by xanthine plus xanthine oxidase (X-XO), have been examined. Superoxide dismutase (0.1 units/mL) and catalase (50 units/mL) inhibited X-XO, but they were ineffective in leukocyte suspensions except at concentrations 500 times and 20 times higher. Sodium azide (10(-5) to 10(-3) M) caused a marked inhibition in CL production in activated leukocytes, but not of X-XO CL. The antioxidants, glutathione (10(-3) M) and L-ascorbic acid (10(-3) M) were ineffective in activated leukocytes, but caused total inhibition of X-XO-induced CL. Mannitol (100 mM) had no effect on chemiluminescence in either system. Captopril (10(-3) M) produced an inhibition of CL in both systems and this inhibition was significantly modified by pH. Thus, the present study has established a standard screening procedure for the assessment of free-radical scavenging activity using activated porcine leukocytes and xanthine-xanthine oxidase.

Animals↗

PubMed1988

Luminol-dependent photoemission from single neutrophil stimulated by phorbol ester and calcium ionophore--role of degranulation and myeloperoxidase.

Luminol-dependent photonic burst from phorbol ester-treated single neutrophil was visually investigated by using an ultrasensitive photonic image intensifier microscope. Neutrophils stimulated by phorbol myristate acetate (0.1 microgram/ml) alone produced a negligible level of photonic activities in the presence of luminol (10 micrograms/ml). The additional application of 0.1 microM Ca2+ ionophore A23187 induced explosive changes of photonic burst corresponding to the distribution of neutrophils, and these photonic activities were gradually spread to extracellular space. Sodium azide, which prevents myeloperoxidase activity, inhibited Ca2+ ionophore-induced photonic burst from phorbol ester-treated neutrophil. These findings suggest a prerequisite role of degranulation and myeloperoxidase release in luminol-dependent photoemission from stimulated neutrophils.

Azides↗

PubMed1997

Neutrophil-mediated activation of mitoxantrone to metabolites which form adducts with DNA.

In this study we have shown that phorbol ester-stimulated human neutrophils are able to oxidatively activate mitoxantrone and result in covalent incorporation of the drug into cellular DNA. The use of the myeloperoxidase inhibitor sodium azide confirmed that the activation and covalent binding of mitoxantrone to cellular DNA was due to its metabolism by the haem enzyme myeloperoxidase. Phorbol ester-stimulated neutrophils were also able to oxidatively metabolise mitoxantrone and facilitate extracellular covalent binding of the drug to calf thymus DNA. These results suggest that myeloperoxidase may contribute to the mode of action of mitoxantrone.

Animals↗

PubMed1981

Effects of free fatty acids on the organization of cytoskeletal elements in lymphocytes.

Treatment of mouse lymphocytes with cis-unsaturated free fatty acids produced alterations in the immunofluorescence patterns of the cytoskeleton and contractile proteins. Saturated free fatty acids and trans-unsaturated free fatty acids had no effect. In untreated cells, the microtubular pattern exhibited radiation from an organizing center, resembling the spokes of an umbrella. The addition of linoleic acid produced a polarized submembranous aggregate. Under control conditions, staining for actin revealed a diffuse pattern over the entire cell, but the addition of linoleic acid caused the formation of a single large patch, or polarized submembranous aggregate. The pattern for alpha-actinin normally revealed intense perinuclear staining on a diffuse background. Linoleic acid caused the loss of this pattern and the formation of a polarized submembranous aggregate. Linoleic acid treatment also caused the pattern for myosin to change from diffuse to uniform submembranous patching around the periphery of the cell. For all of these proteins, calcium (8 mM), but not magnesium, partially reversed the effects of linoleic acid. Sodium azide had little effect on the normal distribution of actin, tubulin, and alpha-actinin; however, myosin staining revealed prominent patch formation. Colchicine treatment caused diffuse staining, some polarized submembranous aggregate formation of tubulin, and some patching of myosin, but not as extensively as did treatment with linoleic acid. Actin and alpha-actinin were unaffected. These results, in view of the previously shown facts that pretreatment of cells with linoleic acid followed by anti-immunoglobulin inhibits capping of surface immunoglobulin (Klausner, et al., Proc. Natl. Acad. Sci. U.S.A. 77:437-441, 1980) and that free fatty acids partition into the surface membrane (Klausner et al., J. Biol. Chem. 255:1286-1295, 1980), suggest that the perturbation of the plasma membrane with unsaturated free fatty acids alters the interaction of surface receptors with the cytoskeleton, which in turn affects cytoplasmic distribution of the proteins.

Actins↗

PubMed1984

An improved fixation technique for ultrastructural preservation of embryonic lenses.

Substandard ultrastructural preservation of mitochondria in rat lenses, resulting from glutaraldehyde fixation, prompted us to apply the technique of Minassian and Huang which involved the addition of 0.1% sodium azide (NaN3), an inhibitor of mitochondrial respiration, to the fixative. As had been found in other tissue types by these investigators, we determined that the presence of NaN3 greatly improved the ultrastructure of mitochondria in embryonic lenses. That the effect of NaN3 was not strictly osmotic was established by comparison of lenses fixed in azide solution with those fixed in non-azide solutions of comparable and higher osmolalities.

Animals↗

PubMed1983

Receptor-mediated endocytosis of transferrin in K562 cells.

Human diferric transferrin binds to the surface of K562 cells, a human leukemic cell line. There are about 1.6 X 10(5) binding sites per cell surface, exhibiting a KD of about 10(-9) M. Upon warming cells to 37 degrees C there is a rapid increase in uptake to a steady state level of twice that obtained at 0 degree C. This is accounted for by internalization of the ligand as shown by the development of resistance to either acid wash or protease treatment of the ligand-cell association. After a minimum residency time of 4-5 min, undegraded transferrin is released from the cell. Internalization is rapid but is dependent upon cell surface occupancy; at occupancies of 20% or greater the rate coefficient is maximal at about 0.1-0.2 min-1. In the absence of externally added ligand only 50% of the internalized transferrin completes the cycle and is released to the medium with a rate coefficient of 0.05 min-1. The remaining transferrin can be released from the cell only by the addition of ligand, suggesting a tight coupling between cell surface binding, internalization, and release of internalized ligand. There is a loss of cell surface-binding capacity that accompanies transferrin internalization. At low (less than 50%) occupancy this loss is monotonic with the extent of internalization. Even at saturating levels of transferrin, the loss of surface receptors upon internalization never exceeds 60-70% of the initial binding capacity. This suggests that receptors enter the cell with ligand but are replaced so as to maintain a constant, albeit reduced, receptor number on the cell surface. In the absence of ligand, the cell surface receptor number returns at 37 degrees C. Neither sodium azide nor NH4Cl blocks internalization of ligand. However, they both prevent the release of transferrin from the cell thus halting the transferrin cycle. Excess ligand can overcome the block due to NH4Cl but not azide although the cycle is markedly slower. Iron is delivered to these cells by transferrin at 37 degrees C with a rate coefficient of 0.15 to 0.2 min-1. The iron is released from the transferrin and the majority is found in intracellular ferritin. There is a large internal receptor pool comprising 70 to 80% of the total cell receptors and this may be involved in maintaining the steady state iron uptake.

Ammonium Chloride↗

PubMed1982

E rosette dissociation: evidence for a role of the cytoskeleton.

When put into 37 degrees C incubation, the E rosettes dissociate spontaneously and the sheep erythrocytes (SRBC) form caps at one pole of the lymphocytes. This process is associated with changes in cell morphology such as uropod formation or membrane budding. The disintegration of E rosettes and the capping of SRBC can be retarded by addition of cytochalasin B plus colchicine, chlorpromazine or sodium azide. These findings suggest a pivotal role of the cytoskeleton in the dissociation process of E rosettes. However, other mechanisms of disintegration are to be considered since none of the drugs can prevent the dissociation of E rosette entirely.

Adolescent↗

PubMed1989

Genotoxicity of azidoalanine in mammalian cells.

Sodium azide mutagenesis is mediated through a metabolic intermediate in bacteria and plant species. However, very little is known about the interaction of this intermediate with nucleic acids, its genotoxic potential, or its mechanism of action, especially in mammalian cells. Chinese hamster cells and normal human skin fibroblasts were treated with extracts from Salmonella typhimurium or Hordeum vulgare (barley) containing a crude mutagenic metabolite, as well as with synthetically produced azidoalanine. The cells were evaluated for the induction of sister chromatid exchanges and the ability to perform unscheduled DNA synthesis. With the purified azidoalanine and the azide-treated extracts from Hordeum vulgare, there was a statistically significant increase in the frequency of sister chromatid exchanges observed in both Chinese hamster cells and human fibroblasts. This increase was about twofold, as compared with the control. On the other hand, there was no detectable genotoxic response when cells were exposed to azide-treated extract from Salmonella typhimurium. The results imply that azidoalanine and the crude mutagenic metabolite from Hordeum vulgare are weakly genotoxic in mammalian cells.

Alanine↗