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PubMed1975

Fatal self-administration of sodium azide.

A 19-year old woman ingested an unknown amount of sodium azide (NaN3). The earliest symptoms were nausea and loss of vision. Within a few hours her clinical features were dominated by central nervous system signs, acute pulmonary edema, lactic acidosis, and hypothermia. The patient died within 12 hours, hypotension and shock occurring as preterminal events. This was the first recorded case in which antidotal methemoglobin production was attempted. Sodium nitrite administration resulted in methemoglobinemia but did not appreciably alter the clinical course and may not be of major benefit. Gross examination post-mortem showed marked pulmonary edema, visceral hemorrhage and congestion, and slight cerebral edema. Microscopically, the lungs showed alveolar and interstitial edema and a polymorphonuclear infiltrate. There were petechial hemorrhages and severe nonspecific changes in the brain.

Adult↗
PubMed1989

Effect of Emblica officinalis Gaertn. (Indian gooseberry) fruit extract on sodium azide and 4-nitro-o-phenylenediamine induced mutagenesis in Salmonella typhimurium.

Water, acetone and chloroform extracts of E. officinalis fruit reduced sodium azide and NPD induced his+ revertants significantly in TA100 and TA97 a strains respectively of S. typhimurium. The chloroform extract was less active as compared to water and acetone extracts. Autoclaving of water extract for 15 min did not reduce its activity. The enhanced inhibitory activity of the extracts on pre-incubation suggests the possibility of desmutagens in the extracts. Besides ascorbic acid, a constituent of the extract, the role of other antimutagenic factors in the extract cannot be ruled out.

Azides↗
PubMed2001

Mild and selective sodium azide mediated cleavage of p-nitrobenzoic esters.

[reaction: see text] A mild and selective cleavage of p-nitrobenzoic esters by sodium azide in methanol is reported. This new methodology is mild enough for use with acid- or base-sensitive compounds. No elimination byproducts are formed. Fmoc- and trifluoroacetyl-amino protecting groups, benzyl esters, and ethyl esters remain unaffected. Less reactive compounds are discussed in terms of steric factors, and yields are increased by altering the azide solvation.

Amino Acids↗
PubMed1993

[Antimutagenic action of superoxide dismutase on sodium azide- and nitrosoguanidine-induced mutagenesis in Salmonella typhimurium TA 1535].

It was shown that superoxide dismutase (SOD) decreased the mutagenic action of sodium azide (NaN3) and N-methyl-N'-nitro-N-nitrosoguanidine in Salmonella typhimurium TA1535. Catalase and quenchers of hydroxyl radicals showed, unlike SOD no effect on the mutagenicity of NaN3. Cell extract from propionic acid bacteria also possessed the antimutagenic activity, only partially depending on the SOD activity.

Antimutagenic Agents↗
PubMed2000

Rapid inhibition by sodium azide of the phosphoinositide-mediated calcium response to serotonin stimulation in human platelets: preservation in Alzheimer's disease.

The effect of sodium azide (NaN(3)) upon platelet Ca(2+) signalling has been investigated. A 60 s preincubation with 1 mM NaN(3) reduced the Ca(2+) response to 1 microM serotonin without a corresponding reduction in the responses to 52 mU/ml thrombin or 70 microM beta-amyloid(25-35) (A beta(25-35)). The effect of NaN(3) upon the response to serotonin, which was not blocked by either glutathione ethyl ester (GTEE) or dithiothreitol (DTT), was similar in platelets obtained from patients with Alzheimer's disease and from age- and gender-matched controls. After a preincubation time of 5 min was used, the Ca(2+) response to thrombin was greatly reduced by 1 mM NaN(3), but not by 50 microM 4-hydroxynonenal (HNE, 50 microM). Platelet levels of HNE and malondialdehyde were not significantly affected by up to 30 min of incubation with NaN(3) at room temperature. It is concluded that the rapid effect of NaN(3) upon the Ca(2+) response to serotonin in human platelets is not mediated by an inhibition of cytochrome c oxidase, and is due to an action proximal to phosphoinositide-specific phospholipase C.

Adult↗
PubMed1997

Allium cepa anaphase-telophase root tip chromosome aberration assay on N-methyl-N-nitrosourea, maleic hydrazide, sodium azide, and ethyl methanesulfonate.

The Allium anaphase-telophase assay was used to show genotoxicity of N-methyl-N-nitrosourea (MNU), maleic hydrazide (MH), sodium azide (NaN3) and ethyl methanesulfonate (EMS). All agents induced chromosome aberrations at statistically significant levels. The rank of the lowest doses with positive effect was as follows: NaN3 0.3 mg/l < MH 1 mg/l < MNU 41 mg/l < EMS 100 mg/l. The results were compared with results from other plant assays (Arabidopsis, Vicia, Tradescantia) and for MH and MNU the values were found to be within the same range, whereas the results in the Allium test for NaN3 and EMS were in a lower range than that found for the other plant assays. EMS and MMS (methyl methanesulfonate), two chemicals used as positive controls in mutagenicity testing, were compared in the Allium test, and MMS was found to be about ten times more potent in inducing chromosome aberrations than EMS. Recording of micronuclei in interphase cells showed that this endpoint does not give more information of clastogenicity than recording of chromosome aberrations in anaphase-telophase cells.

Allium↗
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↗
PubMed2002

[Changes of thioredoxin mRNA level in neurons insulted by sodium azide].

Oxidative stress has been considered to be associated with many neurodegenerative diseases, while mitochondrial damage is one of the important reasons that aggravate oxidative stress. Sodium azide (NaN3) is a specific inhibitor of mitochondrial cytochrome c oxidase (COX), which can be used to mimic neuronal damage induced by mitochondrial deficiency. In this experiment, the neurotoxic effects of NaN3 on cultured primary neurons were detected by means of cell viability measurement (MTT assay) and morphological observation, and an in vitro model of neuronal injury induced by NaN3 were established. Further the changes of thioredoxin mRNA level in cultured neurons insulted by NaN3 were analyzed by semiquantitative RT-PCR in order to explore the role of Trx, an important redox regulatory protein, in the process of neuronal injury. It was found that cultured neurons could be damaged by NaN3 in a dose- and time-dependent manner and the expression of Trx decreased during certain dose (0-32mmol/L) and time (0-4hr) of NaN3 treatment. The above data suggest that decreased the expression of Trx may be associated with oxidative stress induced by neuronal respiratory chain injury, which could impair neuronal protective mechanism.

Animals↗
PubMed1980

SAMA/PMA position: safe disposal of laboratory wastes containing sodium azide.

While it is well established that the disposal of laboratory wastes containing sodium azide might be hazardous, evidence proving such a risk when the wastes are disposed of properly remains inconclusive. The Scientific Apparatus Makers Association and the Pharmaceutical Manufacturers Association oppose any general policy requiring the elimination of the preservative from laboratory reagents. Rather, they endorse the concept of alerting users to its presence and advising them of proper handling procedures. The following position paper, prepared by the SAMA/PMA Task Force, explains these suggestions.

Azides↗
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↗
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↗
PubMed1983

Sodium azide enhancement of interleukin-2 production.

The production of large quantities of Interleukin-2 (IL-2) from normal human lymphocytes has been limited by the short production and release period, as well as its absorption by the responsive cell population. We report the utilization of sodium azide (NaN3, 0.01% final concentration) to allow continued production of IL-2 as long as 72-96 hr and thereby increase the yield significantly. Cell cycle analysis performed by flow cytometry indicates that NaN3 blocks cells at the G0-G1 transition and the G1-S transition, depending on the time of addition of NaN3 to the cultures.

Animals↗
PubMedDate not supplied

Mutation spectrum of a binary mixture of mutagens (methapyrilene and sodium azide) in strain TA1535 of Salmonella.

Methapyrilene (MP) is a rat-liver carcinogen and cocarcinogen that exhibits a narrow spectrum of mutagenic activity in Salmonella typhimurium, inducing only a 2-fold increase in revertants only in the base-substitution strain TA1535; it also enhances the mutagenic activity of sodium azide (NaN3) in the same strain. To examine the effects of MP at the molecular level, we used the colony probe hybridization procedure developed by Cebula and Koch (Mutation Res., 229 (1990) 79-87) to identify the base substitutions in approximately 800 background, MP-, NaN3-, and MP + NaN3-induced revertants of the hisG46 allele of strain TA1535. The predominant mutation in all 4 mutation spectra was a CCC-->CTC transition. The results suggest a mechanism by which MP enhances the infidelity of the DNA replication complex or inhibits a DNA repair or proofreading function, resulting in the production of more of the same error that occurs normally and that is also induced by NaN3. Such a mechanism might be the basis for the carcinogenic and cocarcinogenic activities of MP. To our knowledge, this is the first report of the molecular analysis of mutants produced by exposure of cells to a binary mixture of mutagens.

Azides↗
PubMed1984

Chromium (VI) potentiates mutagenesis by sodium azide but not ethyl methanesulfonate.

A fluctuation test using Salmonella typhimurium strain 1535 has been used in an experimental protocol to assess biological effects of interactions between chromium (VI), such as K2CrO4, and two DNA-damaging agents, ethyl methanesulfonate (EMS), and sodium azide. Mutagenicity, expressed as the average number of mutations induced over a parallel control, was determined for the compounds alone and in combination. The significance of the differences between the "expected" response, calculated by simple addition of the responses from the individual tests, and the observed response when the combination was tested, were estimated by chi square. For the combination of K2CrO4 and NaN3, the response was significantly greater than expected suggesting a possible potentiation of mutagenesis. The opposite (a less-than-additive response) was found for the K2CrO4/EMS combination. Both effects were found to be dose related to the concentration of potassium chromate used. Toxicity of the compounds or their combinations to the bacteria could not explain the results.

Azides↗