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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↗
PubMedDate not supplied

Human health effects of sodium azide exposure: a literature review and analysis.

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.

Air Bags↗
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↗
PubMed1991

NTP Toxicology and Carcinogeneis Studies of Sodium Azide (CAS: 26628-22-8) in F344 Rats (Gavage Studies).

Sodium azide is a white crystalline solid used in the manufacture of the explosive lead azide. It is the principal chemical used to generate nitrogen gas in automobile safety airbags and airplane escape chutes and is a broad-spectrum biocide used in both research and agriculture. Toxicology and carcinogenicity studies were conducted by administering sodium azide (greater than 99% pure) in distilled water by gavage to groups of male and female F344/N rats once daily, 5 days per week for 14 days, 13 weeks, or 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary cells. 14-Day Studies: Rats received 0, 5, 10, 20, 40, or 80 mg/kg sodium azide. All male and female rats receiving 40 or 80 mg/kg and two of five female rats receiving 20 mg/kg died during the first week of the studies. Clinical findings of toxicity included lethargy and inactivity. No grossly observable lesions were present in any of the dose groups. 13-Week Studies: Rats received 0, 1.25, 2.5, 5, 10, or 20 mg/kg sodium azide. Seven of 9 males and all 10 females receiving 20 mg/kg died before the end of the studies. Final mean body weights of treated rats were within 10% of those of the controls. Compound-related clinical findings of toxicity in the 20 mg/kg dose groups included lethargy and labored breathing. Histopathologic lesions induced by sodium azide were limited to the brain (necrosis of the cerebrum and thalamus) and lung (congestion, hemorrhage, and edema), and were observed in rats receiving 20 mg/kg that died during the studies. Body Weights, Feed Consumption, and Survival in the 2-Year Studies: Because compound-related deaths were observed in the groups receiving 20 mg/kg in the 13-week studies, lower dose levels were used in the 2-year studies. Two-year studies were conducted by administering 0, 5, or 10 mg/kg sodium azide to groups of 60 male and 60 female rats. Dose-related depression in mean body weight was observed throughout the study period. Mean feed consumption values in low- and high-dose groups were lower than control values. Survival of high-dose rats of each sex was significantly (P<0.05) lower than controls (males-control, 24/60; low-dose, 27/60; high-dose, 9/60; females-37/60; 43/60; 21/59). The reduced survival was attributed to brain necrosis and cardiovascular collapse induced by sodium azide. Neoplastic and Nonneoplastic Effects in the 2-Year Studies: There were no compound-related increases in incidences of neoplasms in rats. Significantly decreased incidences were observed for certain neoplasms, including mononuclear cell leukemia in male rats (control, 33/60; low-dose, 28/60; high-dose, 14/60), adrenal gland pheochromocytoma in male rats (26/55; 16/56; 6/54), mammary gland fibroadenoma in female rats (20/60; 11/60; 8/59), and pituitary gland neoplasms in female rats (37/60; 28/60; 17/59). These decreases reflected to some extent, but could not be attributed solely to, the reduced survival of the high-dose groups. Compound-related nonneoplastic brain lesions (necrosis of the cerebrum and thalamus) were observed at significantly (P<0.001) increased incidences in high-dose male and female rats. The increased incidence of lung congestion observed in this dose group was considered due to cardiovascular collapse secondary to brain necrosis. Genetic Toxicology: Sodium azide was mutagenic in Salmonella typhimurium strains TA100 and TA1535, with or without exogenous metabolic activation (S9); it was not mutagenic in strain TA1537 or TA98. In cytogenetic tests with Chinese hamster ovary cells, sodium azide induced sister chromatid exchanges, but not chromosomal aberrations, in the presence and the absence of S9. Conclusions: Under the conditions of these 2-year gavage studies, there was no evidence of carcinogenic activity of sodium azide in male or female F344/N rats administered 5 or 10 mg/kg. Sodium azide induced necrosis in the cerebrum and the thalamus of the brain in both male and female rats. Synonyms: Azide, Azium, Smite

Journal Article↗
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↗
PubMed2001

[A case of fatal acute sodium azide poisoning].

A case of fatal sodium azide poisoning induced by suicidal ingestion was reported. When the patient arrived, her vital signs such as consciousness and blood pressure, were normal. But 25 hours after ingestion, she died from metabolic acidosis, ARDS (acute respiratory distress syndrome) and acute cardiac failure. We detected the azide ion in patient's serum using GCMS method and measured the blood concentration of sodium azide using the GC/NPD method. The half-life period of sodium azide in blood was calculated as about 2.5 hours.

Acidosis↗
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↗
PubMed2006

Effect of sodium azide on the metabolic activity of cultured fetal cells.

Sodium azide is a highly toxic substance. However, the mechanism of its toxicity has not been fully established. In the present study, we attempted to investigate the toxicity of sodium azide in various cultured fetal cells, using changes in cellular respiration as an indicator of metabolic inhibition to elucidate tissue-specificity. The human fetal cell lines used in this study included myocardial cells, nerve cells, fibroblasts, hepatocytes and renal tubular epithelial cells. The cells were seeded in wells at a density of 2 x 10(6)cells/2mL, sodium azide was added at a concentration of 0.01 ng/mL to 10 microg/mL, and the respiration of each type of cell was measured 1 h later using a dissolved oxygen meter. The concentration at which sodium azide inhibited metabolic activity was lower in the nerve and myocardial cells than in the fibroblasts, hepatocytes and renal tubular epithelial cells. These findings may serve to clarify the dynamic mechanisms of sodium azide toxicity in vivo.

Cell Respiration↗
PubMed1991

Acute neurotoxicity of sodium azide and nitric oxide.

Sodium azide is a chemical of rapidly growing commercial importance with a high acute toxicity and an unknown mechanism of action. Although it has some chemical properties and biological effects in common with cyanide, its lethality does not appear to be due to inhibition of cytochrome oxidase. Unlike cyanide it is a potent vasodilator and inhibitor of platelet aggregation presumably by virtue of its conversion to nitric oxide in vivo and in isolated preparations of blood vessels and thrombocytes. It is not clear whether the high toxicity of azide is due to nitric oxide or to the parent anion. Of a number of possible azide antagonists tested in intact mice only phenobarbital in both anesthetic and subanesthetic doses afforded statistically significant protection against death. Diazepam, phenytoin, and an anesthetic dose of a ketamine/xylazine combination had no effect. Major motor seizures are sometimes seen in human azide poisoning, and these are a regular feature of azide poisoning in laboratory rodents. Solutions of nitric oxide given systemically to mice produced no signs of toxicity, but doses 1,000-fold lower placed in the cerebroventricular system of rats produced brief but violent tonic convulsive episodes. A dose of 0.61 mmol/kg azide as given systemically regularly produced convulsions whereas a dose of 6 mumol/kg given icv produced seizures in rats. The icv convulsive dose of azide was 50-fold larger than the icv dose of nitric oxide. These results suggest that azide lethality is due to enhanced excitatory transmission in the central nervous system perhaps after its conversion to nitric oxide.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2001

Catalase catalyzes nitrotyrosine formation from sodium azide and hydrogen peroxide.

Sodium azide (NaN3) is known as an inhibitor of catalase, and a nitric oxide (NO) donor in the presence of catalase and H2O2. We showed here that catalase-catalyzed oxidation of NaN3 can generate reactive nitrogen species which contribute to tyrosine nitration in the presence of H2O2. The formation of free-tyrosine nitration and protein-bound tyrosine nitration by the NaN3/catalase/H2O2 system showed a maximum level at pH 6.0. Free-tyrosine nitration induced by peroxynitrite was inhibited by ethanol and dimethylsulfoxide (DMSO), and augmented by superoxide dismutase (SOD). However, free-tyrosine nitration induced by the NaN3/catalase/H2O2 system was not affected by ethanol, DMSO and SOD. NO2- and NO donating agents did not affect free-tyrosine nitration by the NaN3/catalase/H2O2 system. The reaction of NaN3 with hydroxyl radical generating system showed free-tyrosine nitration, but no formation of nitrite and nitrate. The generation of nitrite (NO2-) and nitrate (NO3-) by the NaN3/catalase/H2O2 system was maximal at pH 5.0. These results suggested that the oxidation of NaN3 by the catalase/H2O2 system generates unknown peroxynitrite-like reactive nitrogen intermediates, which contribute to tyrosine nitration.

Animals↗
PubMed1999

[Sodium azide: a review of biological effects and case reports].

This report reviews the biological effects and case reports of suicidal or accidental ingestion of, and occupational exposure to sodium azide. Ingested doses of sodium azide were estimated for the 6 survival and 4 fatal cases studied. The lowest dose among survival cases was 5-10 mg. The patient reported headache, sweating, and faintness within approximately 5 minutes of ingestion. Four victims ingested 20 to 40 mg and recovered within 2 hours. However, a man who took 80 mg reported chest pain for 6 months after ingestion. The smallest doses among fatal cases were 0.7-0.8 g for women and 1.2-2 g for men. All victims suffered from hypotension, tachycardia, hyperventilation, diaphoresis, vomiting, nausea, and diarrhea. There is no antidote for sodium azide. Detoxicants for cyanide such as sodium nitrite or thiosulfate were tried, but were unfortunately, ineffective. Sodium nitrite may worsen the hypotension caused by sodium azide, and is not recommended. Occupational exposure to sodium azide is thought to be common, however, fatal exposure is rare. NIOSH "Recommended Exposure Limits" for sodium azide is 0.3 mg/m3.

Adolescent↗
PubMedDate not supplied

Three fatal sodium azide poisonings.

We report 3 cases and review the published literature on sodium azide ingestion. A 38-year-old man intentionally ingested 2 tablespoonsful of sodium azide in water and developed seizures, coma, hypotension and fatal ventricular arrhythmias within 2 hours. A 33-year-old male ingested an unknown quantity of sodium azide. In the emergency department he was unconscious and underwent immediate intubation and gastric lavage. Nitrite therapy was instituted without improvement. He remained acidotic despite bicarbonate therapy and developed hypotension which was unresponsive to pressor agents. He died approximately 8 hours after admission despite resuscitative efforts. A 52-year-old male ingested 1.5 to 2g of sodium azide and survived for 40 hours. Nitrite therapy was ineffective. The role of sodium nitrite in treating sodium azide toxicity by producing methaemoglobin which complexes with azide is discussed.

Adult↗
PubMed1977

Induction of DNA single-strand breaks in barley by sodium azide applied at pH 3.

Sodium azide (1 to 50 mM), adjusted to pH 3 and applied for 2 h to presoaked barley seeds, induced a dose-dependent frequency of single-strand breaks in DNA of non-germinating embryos. This was demonstrated by sedimentation analyses of isolated DNA samples in alkaline sucrose gradients and in neutral sucrose gradients with 80% formamide. The doses applied also inhibited dose dependently the root length, seed germination and partially the seedling height. Only the sub-lethal doses (10 and 12.5 mM) induced a low frequency of chromatid breaks and translocations in the root tip metaphases. The sedimentation rate (in alkaline sucrose gradients) of calf thymus DNA treated with sodium azide at pH 3, was similar to that of the control DNA treated with buffer (pH 3) alone.

Azides↗
PubMed1997

Sodium azide induces relaxation of the canine gastric body by activating a guanylate cyclase-dependent pathway.

In order to study the inhibitory mechanism by which sodium azide eliminates smooth muscle contraction in vivo and in vitro, gastrointestinal motility was monitored via chronically implanted force transducers in the stomach and duodenum of conscious dogs. Circular smooth muscle strips with myenteric plexus from the canine gastric body were used for in vitro measurement of isometric tension. In conscious dogs, sodium azide (50 micrograms kg-1, i.v.) abolished both the spontaneously occurring phase III contractions and postprandial motility. Exogenous motilin (100 ng kg-1)- and bethanechol (50 micrograms kg-1)-induced contractions were also abolished by sodium azide. In vitro, sodium azide and electrical field stimulation (EFS) caused a concentration- or frequency-dependent nonadrenergic noncholinergic relaxation in the gastric body strips. The relaxation induced by EFS, but not sodium azide, was abolished by tetrodotoxin. NG-nitro-L-arginine and oxyhaemoglobin failed to attenuate the relaxant effect of sodium azide, but strongly inhibited EFS-induced relaxation. Methylene blue inhibited both sodium azide- and EFS-induced relaxation. cGMP concentrations in muscle strips were markedly increased by sodium azide. These findings indicate that sodium azide induces relaxation in the canine gastric body through a direct action on smooth muscle, by activating a guanylate cyclase-dependent pathway; endogenous NO synthesis does not participate in this inhibitory mechanism.

Adrenergic alpha-Antagonists↗