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PubMed1992

Cytogenetic effects of sodium azide encapsulated in liposomes on heteroploid cell cultures.

Lipid vesicles (liposomes) have been shown to be a useful vehicle for the delivery of a variety of compounds to cultured cells. Using multilamellar vesicles (MLV) and small unilamellar vesicles (SUV) we were able to deliver the classical mutagen, sodium azide, into human heteroploid HEp-2 cells. With this method sodium azide is not diluted in culture medium, but it is 'focused' into cells, producing chromosomal aberrations and other major genetic damages. Our results indicate that liposomes are suitable vectors for introducing clastogenic substances into cultured human cells.

Azides↗
PubMed1990

Embryotoxic effects of sodium azide infusions in the Syrian hamster.

Pairs of osmotic minipumps containing 400 mg/ml (6.15 M) sodium azide in distilled water were subcutaneously implanted in timed pregnancy Syrian golden hamsters. The total delivered dose was calculated as 6 X 10(-2) mmol kg-1 hr-1 at the maximal pumping rate. Most dams exhibited obvious signs of toxicity during the period of pump implantation which was Days 7 through 9 of gestation. After removal of the pumps the dams were euthanized on Day 13 of gestation, and the uteri were removed for counting of the number of living, malformed, and resorbed fetuses. This dose rate resulted in a significantly increased incidence of resorptions of embryos over that in a control group implanted with pumps delivering only distilled water. The incidence of gross malformations exclusively in the form of encephaloceles was not different between control and azide-infused groups. The extent of nitrosylation of circulating hemoglobin was followed with time and found to involve only about 0.1% of the total blood pigment. Thus, this commercially important and widely distributed chemical with high acute toxicity is not considered to be teratogenic in hamsters, and it produces embryotoxicity only at dose rates that result in toxic signs in the dams.

Abnormalities, Drug-Induced↗
PubMed1989

Sodium-azide-evoked noradrenaline and catecholamine release from peripheral sympathetic nerves and chromaffin cells.

1. The spontaneous release of [3H]noradrenaline [( 3H]NA) has been measured from rabbit pulmonary arteries and bovine chromaffin cells in the presence of neuronal uptake blocker cocaine (3 x 10(-5) M). 2. The Na+-pump inhibitor sodium-azide (NaN3, 2mM) produced a moderate increase of [3H]NA release from both preparations and relaxed the arteries. The [3H]releasing action of NaN3 was accompanied by a 30% inhibition of 86Rb-uptake into chromaffin cells. 3. In both preparations, ouabain (10(-4) M) markedly increased the release of [3H], contracted the arteries and inhibited the 86Rb-uptake of chromaffin cells by about 75%. A combined application of NaN3 and ouabain produced a similar inhibition of 86Rb-uptake of chromaffin cells and failed to increase further the release of [3H] in comparison to that found in response to ouabain alone. 4. Removal of K+ from the external medium increased both the release of [3H]NA and the tone of pulmonary arteries. NaN3 further increased the transmitter release in "K+-free" solution but relaxed the muscle. In the absence of external K+ and in the presence of azide, ouabain further enhanced the transmitter release but failed to produce significant contraction. 5. Reactivation of the Na+-pump by readmission of K+ (5.9 mM) to the external medium abolished the transmitter releasing action of NaN3 in arteries. 6. It is concluded that in peripheral sympathetic nerves and chromaffin cells, NaN3 inhibits the Na+-pump producing NA and CA release respectively and in nerves even if NA release had already been increased by K+-removal.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

Effects of sodium azide on motor activity, motor coordination, and learning.

Because of the proposed importance of cytochrome oxidase in some neurological disorders, an inhibitor of this enzyme was evaluated in a battery of tests measuring exploration, motor coordination, and learning. Mice injected with sodium azide (6 or 12 mg/kg) were slower to initiate a response in a T maze and had less rears in a small chamber than mice injected with placebo. Drugged mice did not alternate spontaneously even at a minimal retention interval (0 min), but were not impaired in water maze spatial and visual discrimination learning tasks. No group differences emerged in terms of horizontal motor activity and its habituation, number of grooming episodes, and motor coordination. These results indicate that azide-induced slowing of motor activity is situation-specific and is accompanied by abnormalities in choice behavior in a T maze.

Animals↗
PubMed1983

Quaternary structure and spin-state transition in azide methemoglobin A.

The temperature-dependent ultraviolet and visible absorption changes of human azide methemoglobin with and without inositol hexaphosphate (IHP) were examined in a 4'-35 degrees C range. The 537-nm absorption change of IHP-free hemoglobin was about 1.2-fold larger than that of IHP-bound hemoglobin. The data were analyzed by considering the thermal spin equilibrium within the R and T conformers and the quaternary equilibrium between the two conformers. The spin equilibrium analysis suggested that the T conformer has a larger high-spin content than the R conformer. The quaternary equilibrium analysis, on the other hand, showed that the T conformer is more populated at lower temperature. The thermodynamic values for the quaternary equilibrium were determined to be delta H = -13.3 kcal/mol and delta S = -47.6 eu. The large negative delta H and delta S values were compensated for each other to give a small energy difference between the two quaternary states, e.g., delta G4 = 670 cal/mol of tetramer at 20 degrees C. The coincidence of the temperature-dependent IHP-induced changes in the visible and ultraviolet absorptions of heme and aromatic chromophores at the subunit boundaries suggested that the quaternary transition energy is not localized at heme moiety. The reverse temperature dependence of the T conformer fraction as compared with the high-spin fraction of heme iron was interpreted as indicating that the appearance of the T state is not directly coupled with an increase in the strain of Fe-N(F8 His) linkage in azide methemoglobin A.

Azides↗
PubMed1989

Substrate oxidation by the heme edge of fungal peroxidases. Reaction of Coprinus macrorhizus peroxidase with hydrazines and sodium azide.

The peroxidase from Coprinus macrorhizus is inactivated by phenylhydrazine or sodium azide in the presence of H2O2. Inactivation by phenylhydrazine results in formation of the delta-meso-phenyl and 8-hydroxymethyl derivatives of the prosthetic heme group and covalent binding of the phenyl moiety to the protein but not in the detectable formation of Fe-phenyl- or N-phenylheme adducts. Alkylhydrazines are catalytically oxidized but do not inactivate the enzyme. Catalytic oxidation of sodium azide produces the azidyl radical and results in its addition to the delta-meso position of the prosthetic heme group. Comparison of the heme adducts obtained with C. macrorhizus peroxidase with those generated by horseradish peroxidase shows that the regiochemistry of the addition reactions is the same in both cases. The results suggest that substrates interact primarily or exclusively with the heme edge rather than the ferryl oxygen of C. macrorhizus peroxidase and indicate that the interaction occurs with the same sector of the heme edge as in horseradish peroxidase. The active-site topologies of this pair of plant and fungal peroxidases thus appear to be similar, although the observation that alkylhydrazines add to the heme edge of horseradish but not C. macrorhizus peroxidase clearly shows that there are significant differences in the two active sites.

Agaricales↗
PubMed1990

Epidemic hypotension in a dialysis center caused by sodium azide.

The water used for dialysate (dialysis fluid) in hemodialysis centers is produced by water treatment systems (WTS), which require careful and frequent monitoring. On November 3, 1988, nine patients receiving hemodialysis treatments at a single dialysis center suddenly developed hypotension within 30 minutes of onset of dialysis. Eight patients exhibited symptoms and two experienced syncopal episodes; there were no deaths. The incidence of dialysis-associated hypotension occurring within 30 minutes after dialysis onset for these patients was significantly higher during outbreak treatments than during preoutbreak (September 1 through November 2, 1988) treatments, (9 of 9 vs. 0 of 238, P less than 0.00001, Fisher's t-test). Sodium azide, a potent hypotensive agent, was identified as the probable contaminant within the WTS of the dialysis center at the time of the outbreak because: 1) it was mixed with glycerine as the preservative solution of each of the four ultrafilters that were put on-line in the WTS without rinsing, 12 hours before the outbreak; and 2) high levels of total organic carbons were detected from dialysis water collected at point-of-use sites at the time of the outbreak, suggesting contamination of the WTS with the sodium azide-glycerine preservative solution. To prevent similar occurrences, we recommend that ultrafilters (and other components of the WTS) be rinsed free of potentially toxic chemicals prior to use. Dialysis center personnel need to be aware of the potential affects that each modification of disinfection of the WTS may have upon the product water used to prepare dialysate for patient treatments.

Aged↗
PubMed1993

Sodium azide mutagenesis: preferential generation of A.T-->G.C transitions in the barley Ant18 gene.

The molecular basis for the absence of anthocyanins and proanthocyanidins in four independent sodium azide-induced ant18 mutants of barley was examined by sequencing the gene encoding dihydroflavonol 4-reductase in these mutants. Sodium azide generated 21 base substitutions, which corresponds to 0.17% of the 12,704 nucleotides sequenced. Of the substitutions, 86% were nucleotide transitions, and 14% were transversions. A.T-->G.C base pair transitions were about 3 times more frequent than G.C-->A.T transitions. No deletions or mutation hot spots were found. The absence of dihydroflavonol 4-reductase activity in ant18-159, ant18-162, and ant18-164 plants is caused by missense mutations in the respective genes. By using microprojectile bombardment, a plasmid harboring the wild-type Ant18 gene was introduced into ant18-161 mutant cells and resulted in the development of anthocyanin pigmentation, which demonstrates that the mutation is corrected by expression of the introduced gene. On the other hand, a plasmid derivative with the two ant18-161-specific base transitions at the 5' splice site of intron 3 prevented complementation. It is concluded that the absence of detectable mRNA for dihydroflavonol 4-reductase in ant18-161 cells is due to the mutations in the pre-mRNA splice donor site.

Alcohol Oxidoreductases↗
PubMedDate not supplied

[The use of sodium azide as a fecal preservative for studying the eggs of Schistosoma mansoni and of other helminths by the Kato-Katz method: a study in an endemic area].

In two aliquots of 208 samples of stool, tests have been made by the Kato-Katz method, one being made after the use of 0.2mg of sodic azide for 200mg, and the other without the aforesaid conservant. The resulted percentages with or without the conservant were, respectively, for Ancylostomideos: 12.5 and 25.9; for Ascaris lumbricoides: 71.6 and 72.5; for Schistosoma mansoni: 7.6 and 17.7, and for Trichuris trichiura: 86 and 85. The count of the eggs with and without the conservant was, respectively, 264 and 539 for Ancylostomideos, 13186 and 33751 for A. lumbricoides, 55.5 and 63.5 for S. mansoni, and 1345 and 2068 for T. trichiura. The authors did not confirm the advantage of using sodic azide for study in endemic areas. They suggest that the exsiccation of the stool and the low intensity of infections can explain the unfavourable results of the present clinical trial.

Animals↗
PubMed1986

A case of fatal sodium azide ingestion.

A fatal case of sodium azide poisoning in which exchange blood transfusions, charcoal hemoperfusion, hemodialysis and potent vasopressor agents failed to prevent the development of circulatory collapse associated with a wide complex cardiac rhythm is presented. The cellular toxin sodium azide resulted in the development of an altered mental status, profound metabolic acidosis, cardiac arrhythmia (atrial fibrillation and terminal wide complex arrhythmias), a relative decrease in cardiac output, hypotension and non-cardiogenic pulmonary edema. Further animal studies are needed to gain new approaches for the treatment of this rare cause of human poisoning.

Acidosis↗
PubMed1992

[Detection of an inhibition of benzo(a)pyrene and sodium azide induced mutagenesis by extracts from human feces].

Low levels of mutagenic activities were detected in only 5-25% of the feces of people on a normal mixed-western diet, when feces were extracted by solvents and extracts were analyzed for mutagenicity with Ames' standard Salmonella/microsome assay. Since mutagens are know to be present in this type of diet and may be synthesized endogenously by bacteria in the large bowel, the question is if antimutagenic compounds mask the presence of genotoxic substances. We therefore tested the inhibition of known mutagens--benzo(a)-pyrene and sodium azide--by acetone/ethyl-acetate extracts of lyophilized feces in model experiments. These extracts completely suppressed the mutagenicity of benzo(a)pyrene and reduced the mutagenicity of sodium azide by about 60%, but were non-cytotoxic. Using gel filtration over Sephadex LH-20 and subsequent silica gel column chromatography we found that the inhibitors were polar organic compounds with molecular weights about 500 or more. The inhibitory effect could not be changed by esterification or saponification methods but was completely abolished by alkaline potassium permanganate oxidation. We therefore conclude that the antimutagenic activities might be identical with bile pigments.

Antimutagenic Agents↗
PubMed1991

The catalytic site of manganese peroxidase. Regiospecific addition of sodium azide and alkylhydrazines to the heme group.

Manganese peroxidase (MnP), which normally oxidizes Mn2+ to Mn3+, is rapidly and completely inactivated in an H2O2-dependent reaction by 2 equivalents of sodium azide. The inactivation is paralleled by formation of the azidyl radical and high yield conversion of the prosthetic heme into a meso-azido adduct. The meso-azido enzyme is oxidized by H2O2 to a Compound II-like species with the Soret band red-shifted 2 nm relative to that of native Compound II. The time-dependent decrease in this Compound II-like spectrum (t1/2 = 2.3 h) indicates that the delta-meso azido heme is more rapidly degraded by H2O2 than the prosthetic heme of control enzyme (t1/2 = 4.8 h). MnP is also inactivated by phenyl-, methyl-, and ethylhydrazine. The phenylhydrazine reaction is too rapid for kinetic analysis, but KI = 402 microM and kinact = 0.22/min for the slower inactivation by methylhydrazine. Reaction with phenylhydrazine at pH 4.5 does not yield iron-phenyl, N-phenyl, or meso-phenyl heme adducts. Ethylhydrazine inactivates the enzyme both at pH 4.5 and 7.0, but only detectably produces delta-meso-ethyl-heme at pH 7.0. Reconstitution of apo-MnP with hemin or delta-meso-ethylheme yields enzyme with, respectively, 50 and 5% of the native activity. The delta-meso-alkyl group thus suppresses most of the catalytic activity of the enzyme even though a Compound II-like species is still formed with H2O2. Finally, Co2+ inhibits the enzyme competitively with respect to Mn2+ but does not inhibit its inactivation by azide or the alkylhydrazines. The results argue that substrates interact with the heme edge in the vicinity of the delta-meso-carbon. They also suggest that Mn2+ and Co2+ bind to a common site close to the delta-meso-carbon without blocking the approach of small molecules to the heme edge. An active site model is proposed that accommodates these results.

Azides↗
PubMed1983

Lack of correlation between cyclic GMP elevation and relaxation of nonvascular smooth muscle by nitroglycerin, nitroprusside, hydroxylamine and sodium azide.

Recent reports have suggested that the smooth muscle relaxant effects of drugs such as nitroprusside and nitroglycerin are mediated by increases in tissue levels of cyclic GMP. This hypothesis was examined by comparing the effects of nitroprusside, nitroglycerin, hydroxylamine and sodium azide on tension and cyclic GMP levels in rat vas deferens, rat myometrium and guinea-pig taenia coli. All four of the agents were capable of increasing cyclic GMP levels in these tissues but there did not appear to be a good correlation between cyclic GMP elevation and muscle relaxation in any of the tissues studied. For example, nitroprusside markedly elevated cyclic GMP levels in rat vas deferens and myometrium but had no relaxant effect on either tissue. Nitroglycerin was less effective than nitroprusside in elevating cyclic GMP levels, but was an effective relaxant in both tissues. Significant increases in myometrial cyclic GMP were seen with 0.1, 1 and 5 mM concentrations of hydroxylamine but only the highest concentration had a definite relaxant effect on the muscles. A similar concentration of nitroprusside produced a greater elevation of cyclic GMP than did hydroxylamine, but had no relaxant effect in this preparation. In guinea-pig taenia coli, significant increases in cyclic GMP levels were obtained with concentrations of sodium azide and hydroxylamine which had no effect on the contractile activity of the preparations. These results, together with previous results from this laboratory, suggest that the relaxant effects of this group of drugs in rat vas deferens, rat myometrium and guinea-pig taenia coli are not mediated by increases in tissue levels of cyclic GMP. Further experiments are necessary to determine whether a causal relationship exists between cyclic GMP elevation and relaxation in other types of smooth muscle.

Animals↗
PubMed1984

[Pharmacological sensitivity of the photopic c-wave in the electroretinogram of the chicken. I. Effects of sodium azide, adrenaline, and a barbiturate].

The c-wave recorded in the chicken electroretinogram proved to be cone-triggered. The effect of various drugs active on pigment epithelium and on c-waves in scotopic retinas were tested in order to determine whether a similar mechanism may underlie both rod- and cone-triggered c-waves. Our results indeed point to such a similar reactivity of both types of c-waves. Pentothal, a short-acting barbiturate induced--as it does in the sheep--a transient disappearance of the c-wave. Sodium azide and adrenaline produced very similar effects: when injected i.v., these drugs produced a transient increase in the resting potential of the eye (the "azide potential"). When injected im or i.p., both drugs provoked--as they do in rabbit or in rat retinas--an increase in the voltage of the c-wave, but this increase was preceded in the chicken by a partial or total suppression of this component.

Animals↗
PubMedDate not supplied

[Sodium azide--an activator of serum lipoproteins peroxidation].

Addition of even small amounts of sodium azide to preparations of blood serum lipoproteins of various classes, isolated by ultracentrifugation, intensified peroxidation of their lipids. At the same time, physical structure of blood serum lipoproteins was impaired as shown by activation of chemoluminescence using fluorescent probes pyrene and I-aniline naphthalene-8-sulphonate simultaneously with an increase in content of malonic dialdehyde. The data obtained suggest that the results of studies of protein-lipid structures in media containing azides have to be interpreted very carefully to avoid unwarranted conclusions.

Animals↗
PubMed1998

Determining sodium azide concentration in blood by ion chromatography.

We describe a simple method for measuring sodium azide concentrations in aliquots of blood and other tissues. Aliquots are acidified, converting azide to volatile hydrazoic acid (HN3) which is then trapped in sodium hydroxide. We analyze the resulting aliquots by ion chromatography, using a sodium tetraborate eluent and suppressed conductivity detection. The method is sensitive to at least 100 ng/mL.

Azides↗
PubMed1994

Enhanced mutagenic effect of a 60 Hz time-varying magnetic field on numbers of azide-induced TA100 revertant colonies.

Forty-eight hours exposure to a two Gauss (0.2 mT) rms 60 Hz time varying sinusoidal electromagnetic field increased the number of azide induced TA100 revertant colonies of Salmonella typhimurium 14% as compared with controls in the ambient < 2 milli-Gauss 60 Hz field. In the absence of the electromagnetic field, the numbers of mutant colonies grown within and outside the non-energized coil were nearly identical. Without azide, the number of "spontaneous" mutant colonies forming in the experimental field was not statistically significant from numbers of colonies not exposed to field effects. Experimental temperature variation of 2 degrees C had little effect on colony formation, and the enhanced production of revertant colonies in the presence of the magnetic field was maintained during continued culture for 5 additional days.

Azides↗