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At least 19 recordsLinked to original sources
PubMed1995

Oxidation of cysteine and methionine residues during acid hydrolysis of proteins in the presence of sodium azide.

Sodium azide is widely used as bacteriostatic agent during downstream processing of proteins. Amino acid composition analysis of protein samples, subjected to hydrolysis with hydrochloric acid in a buffer containing sodium azide, revealed the presence of cysteic acid, methionine sulfoxide, and methionine sulfone in addition to the expected reaction products. Hydrolysis with methanesulfonic acid in the presence of sodium azide resulted in detection of only methionine sulfoxide in addition to the expected products. When the proteins were hydrolyzed in a buffer containing no sodium azide or after its removal by dialysis, no oxidation products were detected (except for minor amounts of methionine sulfoxide). The generation of the particular oxidation products was affected by the concentration of sodium azide in the protein solution. Therefore, presence of sodium azide in protein samples intended for amino acid composition analysis may lead to wrong conclusions concerning oxidation of cysteine and methionine residues.

Amino Acids↗
PubMed1975

Activation of guanylate cyclase from rat liver and other tissues by sodium azide.

Sodium azide, hydroxylamine, and phenylhydrazine at concentrations of 1 mM increased the activity of soluble guanylate cyclase from rat liver 2- to 20-fold. The increased accumulation of guanosine 3':5'-monophosphate in reaction mixtures with sodium azide was not due to altered levels of substrate, GTP, or altered hydrolysis of guanosine 3':5'-monophosphate by cyclic nucleotide phosphodiesterase. The activation of guanylate cyclase was dependent upon NaN3 concentration and temperature; preincubation prevented the time lag of activation observed during incubation. The concentration of NaN3 that resulted in half-maximal activation was 0.04 mM. Sodium azide increased the apparent Km for GTP from 35 to 113 muM. With NaN3 activation the enzyme was less dependent upon the concentration of free Mn2+. Activation of enzyme by NaN3 was irreversible with dilution or dialysis of reaction mixtures. The slopes of Arrhenius plots were altered with sodium azide-activated enzyme, while gel filtration of the enzyme on Sepharose 4B was unaltered by NaN3 treatment. Triton X-100 increased the activity of the enzyme, and in the presence of Triton X-100 the activation by NaN3 was not observed. Trypsin treatment decreased both basal guanylate cyclase activity and the responsiveness to NaN3. Phospholipase A, phospholipase C, and neuraminidase increased basal activity but had little effect on the responsiveness to NaN3. Both soluble and particulate guanylate cyclase from liver and kidney were stimulated with NaN3. The particulate enzyme from cerebral cortex and cerebellum was also activated with NaN3, whereas the soluble enzyme from these tissues was not. Little or no effect of NaN3 was observed with preparations from lung, heart, and several other tissues. The lack of an effect with NaN3 on soluble GUANYLATE Cyclase from heart was probably due to the presence of an inhibitor of NaN3 activation in heart preparations. The effect of NaN3 was decreased or absent when soluble guanylate cyclase from liver was purified or stored at -20degrees. The activation of guanylate cyclase by NaN3 is complex and may be the result of the nucleophilic agent acting on the enzyme directly or what may be more likely on some other factor in liver preparations.

Animals↗
PubMedDate not supplied

Comparison of the bronchodilator and vasodilator activity of sodium azide and sodium nitroprusside in the guinea-pig.

1. Sodium azide and sodium nitroprusside are potent dilators of the intact guinea-pig tracheal preparation in vitro. 2. Both substances are bronchodilators in the anaesthetized guinea-pig in vivo when administered intravenously or by aerosol inhalation. 3. Sodium azide and sodium nitroprusside are also potent vasodilators in the guinea pig. 4. At all doses and by route of administration, including aerosol inhalation, the hypotensive effect predominates over bronchodilatation.

Airway Resistance↗
PubMed1985

Photopic c-wave in the chicken ERG: sensitivity to sodium azide, epinephrine, sodium iodate, barbiturates, and other general anesthetics.

The c-wave recorded in the chicken electroretinogram proved to be a cone-triggered component. The questions arose whether its reactivity to various specific drugs (sodium iodate, sodium azide, epinephrine, or barbiturates) were similar to those described for classic rod-triggered c-waves. We also tested the sensitivity of the chicken c-wave to various general anesthetics. Urethane was found to be the drug that best preserves the c-wave in electrophysiological recordings.

Anesthetics↗
PubMed1987

Suicidal sodium azide ingestion.

Sodium azide (NaN3) is a highly reactive, toxic, widely used chemical. Although industrial exposure is common, fatal ingestion is rare. We describe the case of a 30-year-old man who ingested 15 to 20 g of sodium azide. He became comatose within two hours and eventually expired from a combination of acidosis, respiratory depression, and ventricular fibrillation. In sufficient doses, sodium azide is rapidly fatal and there is no effective treatment.

Administration, Oral↗
PubMed1996

Exposures and health effects: an evaluation of workers at a sodium azide production plant.

Sodium azide is the principal gas-generating agent used to inflate automobile supplemental restraint systems, more commonly called airbags. Although sodium azide is known to affect the cardiovascular system by causing peripheral vasodilation, there is no published literature describing occupational exposures to sodium azide in the rapidly growing automobile airbag industry. In 1994-1995, the National Institute for Occupational Safety and Health (NIOSH) conducted a cross-sectional study of health complaints reported by sodium azide production workers at the only continuous sodium azide production facility in the United States. The NIOSH evaluation consisted of a plant industrial hygiene survey, a symptom questionnaire, ambulatory blood pressure monitoring, and blood azide analysis. Personal breathing zone air monitoring revealed exposures to sodium azide and hydrazoic acid (a reactant product) at levels greater than the NIOSH Recommended Exposure Limits (RELs). In some cases, exposures exceeded the REL despite the use of air-supplied respirators. The questionnaire revealed that most workers reported headache (10 of 11 [91%]), episodes of low blood pressure (9 of 11 [82%]), and palpitations (8 of 11 [73%]) occurring in the production areas within the 6 months preceding the study. Mild headache (4 of 11 [36%]) was the only symptom reported during our 24-hr medical survey. Ambulatory blood pressure monitoring revealed one asymptomatic employee with a drop in blood pressure (defined as a drop in systolic [at least 20 mm Hg] and diastolic [at least 10 mm Hg] blood pressure) during a period of exposure to sodium azide at a level five times the NIOSH REL. Improvements in plant engineering controls, increased attention to employee hygiene practices, and a more comprehensive respiratory protection program were recommendations made by NIOSH to reduce exposures at the plant. All facilities handling sodium azide should be aware of the potential toxicity of sodium azide and hydrazoic acid.

Adult↗
PubMed1977

Stimulation of guanylate cyclase by sodium nitroprusside, nitroglycerin and nitric oxide in various tissue preparations and comparison to the effects of sodium azide and hydroxylamine.

Sodium nitroprusside, nitroglycerin, sodium azide and hydroxylamine increased guanylate cyclase activity in particulate and/or soluble preparations from various tissues. While sodium nitroprusside increased guanylate cyclase activity in most of the preparations examined, the effects of sodium azide, hydroxylamine and nitroglycerin were tissue specific. Nitroglycerin and hydroxylamine were also less potent. Neither the protein activator factor nor catalase which is required for sodium azide effects altered the stimulatory effect of sodium nitroprusside. In the presence of sodium azide, sodium nitroprusside or hydroxylamine, magnesium ion was as effective as manganese ion as a sole cation cofactor for guanylate cyclase. With soluble guanylate cyclase from rat liver and bovine tracheal smooth muscle the concentrations of sodium nitroprusside that gave half-maximal stimulation with Mn2+ were 0.1 mM and 0.01 mM, respectively. Effective concentrations were slightly less with Mg2+ as a sole cation cofactor. The ability of these agents to increase cyclic GMP levels in intact tissues is probably due to their effects on guanylate cyclase activity. While the precise mechanism of guanylate cyclase activation by these agents is not known, activation may be due to the formation of nitric oxide or another reactive material since nitric oxide also increased guanylate cyclase activity.

Animals↗
PubMed1995

Interference of sodium azide with the quantitation of bilirubin: modification of Fog's method to eliminate azide interference.

Interference of sodium azide with bilirubin estimation was studied at different concentrations of sodium azide. At an azide concentration (0.08% or 12.3 mM), 99% inhibition of the color reaction was observed. Similar results were obtained when the effect of sodium azide was studied by fixing bilirubin concentration and increasing the azide concentration. The decrease in color reaction can be explained on the basis of competition of the two compounds, i.e., bilirubin and sodium azide for diazosulfanilic acid. The method was modified to measure the concentration of bilirubin in various serum samples containing different amounts of sodium azide.

Azides↗
PubMed1977

Membrane-bound adenosine triphosphatase of Escherichia coli. III. Effects of sodium azide on the enzyme functions.

1) Sodium azide and diphenyl phosphorazidate (DPPA) inhibited purified membrane-bound ATPase [coupling factor of oxidative phosphorylation; EC 3.6.1.3] of Escherichia coli non-competitively with Ki values of 39 and 51 micrometer, respectively. 2) Sodium azide and DPPA inhibited the activity of ATPase bound to the membrane as effectively as that of the purified enzyme. 3) The effects of sodium azide on succinate-dependent ATP synthesis, Pi-ATP exchange, and ATP hydrolysis reactions by the membrane vesicles were compared under the same conditions. At concentrations below 1.0 mM, sodium azide inhibited ATP hydrolysis, but Pi-ATP exchange and ATP synthesis were almost unaffected. At 10 mM sodium azide, both Pi-ATP exchange and ATP synthesis reactions were completely inhibited, probably because at this concentration, sodium azide acted as a proton-conducting uncoupler.

Adenosine Triphosphatases↗
PubMed1975

Requirement for a macromolecular factor for sodium azide activation of guanulate cyclase.

Sodium azide, a highly nucleophilic agent and a potent metabolic inhibitor, markedly increased guanylate cyclase activity from supernatant fractions of rat liver homogenates. The effect of sodium azide was not observed with partially purified guanulate cyclase from liver or crude soluble guanylate cyclase from cerebral cortex. However, the effect of sodium azide could be restored by the readdition of a fraction isolated from rat liver homogenates. The macromolecular factor required for the sodium azide effect was separated from soluble guanylate cyclase of rat liver with DEAE-cellulose column chromatography, and some of its properties were examined. The factor was nondialyzable and heat labile.

Animals↗
PubMed1991

Sodium azide: ineffective as a faecal preservative for parasitological diagnosis.

Sodium azide was compared with 10% formalin to evaluate sodium azide's effectiveness as a faecal preservative for intestinal helminths and protozoa. Faecal specimens collected from Haiti were preserved in sodium azide and in 10% formalin and analysed after 1.5, 6.5 and 11.5 weeks by examining direct wet-mount preparations. Sodium azide did not preserve the morphology of either helminths or protozoa as well as 10% formalin did. However, sodium azide prevented embryogenesis of helminth eggs, while some helminth eggs in 10% formalin contained living larvae. Biosafety guidelines regarding the toxicity, reactivity, and disposal of sodium azide were strictly followed. Use of 10% formalin is a significantly better choice than sodium azide for preserving parasites when accurate identification of parasites and biosafety are the main concerns.

Adolescent↗
PubMed1980

Effects of pH on the mutagenicity of sodium azide in Neurospora crassa and Salmonella typhimurium.

Sodium azide at various pH values did not cause a significant increase in the frequency of forward mutation above the control frequency at the adenine-3 (ad-3) region in resting conidia and in conidia from growing cultures of heterokaryons 12 and 59 of Neurospora crassa. Conidia from ad-3 mutants were plated with sodium azide at various pH values, and no obvious increase in reverse mutation above the controls was observed. Data are presented showing that sodium azide at pH 3 is inactivating conidia by interacting with the cytoplasma rather than the nucleus, and this may be the primary reasons that no mutation at the ad-3 region was detected. The dependence of sodium azide mutagenicity on pH was investigated in histidine-requiring mutants of Salmonella typhimurium using a suspension test. There were no significant differences in the reversion frequencies among the pH values (3-8) tested. Thus, no pH dependence is associated with sodium azide mutagenicity, nor are growth and/or DNA replication required for mutagenicity by sodium azide, in S. typhimurium.

Adenine↗
PubMed1996

Occupational health data as a basis for process engineering changes: development of a safe work environment in the sodium azide industry.

The development of an occupational health system for a plant manufacturing sodium azide has had to confront biological and hygienic difficulties related to the nature of sodium azide. Sodium azide in pellet form is used as the nitrogen generant for automobile air bags; however, it is manufactured as a very fine powder making exposure control more difficult. Sodium azide is a rapidly active, vasodilatory hypotensive agent that causes headaches and drops in blood pressure. Occupational health assessment of the plant and its employees demonstrated the need for exposure control, based on inspection, interviews, health data, process and site review. Targeted studies demonstrated the nature and magnitude of health effect problems at this plant and the relationship to azide exposure. Engineering and hygiene changes were developed in response to the evidence of worker exposure demonstrated by the targeted studies. The occupational health surveillance system provided a monitor for temporal changes. Results appear to demonstrate over the period of the development of the program, the following changes: (1) reductions in evidence of subjective symptoms from azide exposure (health incident reports of headaches and other symptoms), (2) reductions in objective signs of effects from azide exposure (drops in cross-shift mean arterial blood pressures), and (3) reductions in measured levels of azide exposure. Future studies need to validate the evidence of exposure changes and to further identify additional sources of exposure. Interventions designed to reduce exposures need to be demonstrated to be effective and need to be monitored to demonstrate continuing effectiveness.

Azides↗
PubMed1997

Sodium azide induces mitotic recombination in Drosophila melanogaster larvae.

Sodium azide (NaN3), a potent mutagen for bacteria and barley, was tested for somatic mutation and mitotic recombination induction in wing imaginal disc cells of Drosophila melanogaster. Comparisons were made among inversion-free flr3/mwh, inversion-heterozygous TM3, Ser/mwh, and inversion-free, high bioactivation OR(R), flr3/mwh flies. Third instar larvae were exposed chronically for 48 h to sodium azide at 0.5, 0.63, 0.75, 0.88 and 1.0 mM. The frequencies of spots per wing obtained in the three kinds of progeny scored were compared. In inversion-free flies, sodium azide induced large single and total spots at all concentrations tested, and small single and twin spots at 0.75 mM and higher concentrations. In contrast, it failed to increase the frequency of small and large single spots in inversion-heterozygous flies. In high bioactivation flies (which are inversion-free), sodium azide increased the frequency of large single spots at 0.63, 0.88 and 1.0 mM and the frequency of total spots at 0.63 mM. From the absence of genotoxic activity observed in inversion-heterozygous flies it is concluded that sodium azide induces exclusively mitotic recombination in wing somatic cells of Drosophila melanogaster larvae after chronic exposure. This recombinogenic activity is reduced in the presence of high bioactivation capacity.

Animals↗
PubMed1980

The effects of sodium azide on mammalian cells cultivated in vitro.

Sodium azide acted cytostatically to cytotoxically on 2 lines of mammalian cells. After application of the substance in an acid environment the highest cytostatic effect was noted. The results of the DNA-synthesis inhibition test suggest that sodium azide does not damage the DNA of the observed fibroblasts with any of the tested modes of application. In Chinese hamster cells neither 20-h treatment in medium nor 60-min treatment in an acid environment gave rise to significantly increased occurrence of 6-TG-resistant mutations. The results of the DNA-synthesis inhibition test, as well as the mutagenicity testing, do not suggest the possibility that treatment with sodium azide might induce DNA damage in the observed human and Chinese hamster cells. The cytostatic effect of sodium azide on the fibroblasts studied is probably not accompanied by a genotoxic effect.

Animals↗
PubMed1989

[Acute poisoning caused by sodium azide].

Until now, only few cases of intoxication with sodium azide have been published. The case of suicidal sodium azide ingestion reported here and a survey of the relevant literature serve to demonstrate the pharmacological mode of action and the symptoms of acute poisoning, as well as the diagnostic proof of the toxic agent. Only symptomatic treatment can be implemented at present. Due to the restricted accessibility of the azide there is a close connection in the known cases of intoxication to the patient's profession or his (her) place of work: 17 out of 20 cases involved persons working in laboratories, whilst in 2 cases sodium azide was administered to patients by mistake. Knowledge of this connection may be of great help in making the diagnosis of acute sodium azide poisoning.

Adult↗