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PubMed1998

Simultaneous determination of cyanide and thiocyanate in blood by ion chromatography with fluorescence and ultraviolet detection.

An ion chromatographic method for the simultaneous determination of cyanide and thiocyanate in blood has been developed. After extraction by adding water and methanol to blood, cyanide was derivatized with 2,3-naphthalenedialdehyde and taurine to give a fluorescent product of 1-cyanobenz[f]isoindole. This compound was detected with high sensitivity by fluorometry and the underivatized thiocyanate was detected by ultraviolet absorption. The detection limits were 3.8 pmol ml(-1) for cyanide and 86 pmol ml(-1) for thiocyanate, and the recoveries from blood were ca. 83% and ca. 100%, respectively. The proposed method was successfully applied to the analysis of both anions in blood from smokers, non-smokers and fire victims.

Chromatography, Ion Exchange↗
PubMed1990

[Potassium cyanide poisoning treated with hydroxocobalamin].

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.

Acidosis↗
PubMed1988

Anomalously slow cyanide binding to Glycera dibranchiata monomer methemoglobin component II: implication for the equilibrium constant.

In comparison to sperm whale metmyoglobin, metleghemoglobin a, methemoglobins, and heme peroxidases, the purified Glycera dibranchiata monomer methemoglobin component II exhibits anomalously slow cyanide ligation kinetics. For the component II monomer methemoglobin this reaction has been studied under pseudo-first-order conditions at pH 6.0, 7.0, 8.0, and 9.0, employing 100-250-fold mole excesses of potassium cyanide at each pH. At 20 degrees C, with micromolar protein concentrations, kobsd varies between 9.11 x 10(-5) s-1 at pH 6.0, 100-fold KCN mole excess, and 1.12 x 10(-2) s-1 at pH 9.0, 250-fold KCN mole excess. Our analysis shows that the concentration-independent bimolecular rate constant (k1app) is small in comparison to those of the other heme proteins. For example, at pH 7.0 it is 0.491 M-1 s-1, compared to 1.1 x 10(5) M-1 s-1 for cytochrome c peroxidase; 111 M-1 s-1 for guinea pig methemoglobin; approximately 400 M-1 s-1 for sperm whale metmyoglobin; and 692 M-1 s-1 for soybean metleghemoglobin a, at the same pH and similar temperatures. Furthermore, our results show that the dissociation rate is extremely slow, with k-1app no larger than 10(-6) s-1. Separation of the bimolecular rate constant into contributions from kCN- (the rate constant for CN- binding) and from kHCN (the rate constant for HCN binding) shows that the former is approximately 90 times greater. These results indicate that cyanide ligation reactions are not instantaneous for this protein, which is important for those attempting to study the ligand-binding equilibria.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Cyanide poisoning: treatment with hyperoxygenation and sodium thiosulphate].

A 23-year-old man survived a suicide attempt in which he had swallowed 1500 mg potassium cyanide. Initially there were cerebral seizure and marked lactacidosis. Six hours after hospital admission the cyanide blood level was 6 mg/l. The poisoning having at first not been recognized he at that time merely received supportive treatment to counteract the acidosis, as well as assisted ventilation with hyperventilation and hyperoxigenation. Afterwards, sodium thiosulphate was given additionally for 24 h at a dosage of 1 g per hour. The clinical course underlines the great importance of supportive measures in the treatment of cyanide poisoning. In the individual case the balance between risk and value of an intrinsically toxic antidote administration must be critically assessed.

Adult↗
PubMedDate not supplied

Intoxication by cyanide in fires: a study in monkeys using polyacrylonitrile.

It is suspected that hydrogen cyanide (HCN) may be an important factor in incapacitating fire victims, but the effects of sublethal exposures are not well characterized. Also, the incapacitating effects of fire atmospheres result from exposure to a mixture of toxic products so that the contribution from each component is difficult to determine. The mechanisms of incapacitation in monkeys exposed to the pyrolysis products of polyacrylonitrile (PAN) were compared to those resulting from low level HCN gas exposures. The physiological effects of the PAN atmospheres were almost identical to those of HCN gas alone. They consisted of hyperventilation, followed by loss of consciousness after 1-5 min, bradycardia with arrhythmias and T-wave abnormalities, and were followed by a rapid recovery after exposure. Hydrogen cyanide is considered to be the major toxic product formed by the pyrolysis of PAN. It is suggested that HCN may produce rapid incapacitation at low blood levels of cyanide in fires, while death may occur later due to carbon monoxide poisoning or other factors.

Acrylic Resins↗
PubMed1979

Metabolism of sodium nitroprusside and cyanide in the dog.

Blood cyanide (HCN) and thiocyanate (SCN) concentrations were measured at intervals in anaesthetized dogs given bolus doses of sodium nitroprusside (SNP) 1 mg kg-1 or potassium cyanide 1.07 mg kg-1 and in animals infused with SNP 1.5 mg kg-1 for 1 h. Cyanide appeared rapidly in the red cells to give peak concentrations which accounted for more than 90% of the total blood HCN. A delay between the peak plasma and red cell HCN concentrations confirmed that some of the SNP was degraded in the plasma. Comparison of HCN and SCN concentrations with those measured previously in patients receiving an infusion of SNP suggests that the degradation of SNP and detoxication of HCN may be more rapid in the dog. The various pathways of HCN detoxication are discussed in relation to the reduced formation of SCN in dogs receiving SNP compared with those receiving KCN.

Animals↗
PubMed1987

The induction of cyanide-resistant respiration in Hansenula anomala.

Cyanide-resistant respiration was induced in the yeast, Hansenula anomala in the presence of cyanide or antimycin A, which blocks the electron transport after ubiquinone. The de novo protein synthesis in cytosol and oxygen were deduced to be involved in this induction process. The period required for the induction varied during the growth stage, suggesting that involvement of additional physiological factor(s) in this induction process. The organism could multiply in the presence of antimycin A by developing cyanide-resistant respiration despite a decreased growth rate.

Cyanides↗
PubMed1965

ISOLATION AND CHARACTERIZATION OF THE CYANIDE-RESISTANT AND AZIDE-RESISTANT CATALASE OF LACTOBACILLUS PLANTARUM.

Johnston, M. A. (Cornell University, Ithaca, N.Y.), and E. A. Delwiche. Isolation and characterization of the cyanide-resistant and azide-resistant catalase of Lactobacillus plantarum. J. Bacteriol. 90:352-356. 1965.-Lactobacillus plantarum T-1403-5 has been shown to possess a very active cyanide- and azide-resistant catalase. By means of fractional ammonium sulfate precipitation, removal of nucleic acids with protamine sulfate, adsorption on calcium phosphate gel, and pH gradient chromatography on diethylaminoethyl cellulose, the catalase "activity" was purified approximately 14-fold. The purified enzyme preparation was insensitive to the heme poisons cyanide and azide, the metal chelating agents ethylenediaminetetraacetate and o-phenanthroline, and the sulfhydryl binding agent p-chloromercuribenzoate. The purified enzyme moved at a uniform rate in the electrophoretic field (isoelectric point, pH 4.7). The ultraviolet-light absorption spectrum was negative for heme-iron components, and fluorescence measurements yielded negative results with regard to flavin components. Acriflavin and Atabrine had no effect on enzyme activity. The nonheme catalase displayed a much broader pH range of activity than the heme-iron catalase of a control culture of Escherichia coli and the azide-sensitive catalase developed by L. plantarum NZ48 when grown in the presence of preformed hematin. The nonheme catalase was more resistant to heat inactivation. No retention of the enzyme on a chromatographic column could be obtained with Sephadex 200, nor could the enzyme be separated from crystalline beef-liver catalase by the gel filtration technique. Sedimentation was obtained in a centrifugal field of 144,000 x g for 12 hr.

Animals↗
PubMed1983

High-dose ascorbic acid decreases detoxification of cyanide derived from amygdalin (laetrile): studies in guinea pigs.

Cysteine, a sulphur-containing amino acid, is required to metabolize ascorbic acid (as ascorbate sulphate) and detoxify cyanide (to thiocyanate). In guinea pigs, conjoint use of laetrile (a cyanogenic glycoside) and ascorbic acid (in large doses) decreases the detoxification of cyanide derived from laetrile through diminishing the availability of cysteine, but not impairing hepatic rhodanese activity, which is involved in the detoxification of cyanide to thiocyanate. These results agree with the symptoms of a sublethal dose of KCN toxicity manifested by the animals. The studies, therefore, indicate that individuals taking megadoses of ascorbic acid concurrently with laetrile may be subject to self-poisoning.

Amygdalin↗
PubMed1987

Cardiorespiratory response to cyanide of arterial chemoreceptors in fetal lambs.

Cardiorespiratory response to the stimulation of the carotid and aortic receptors by sodium cyanide was examined in fetal lambs in utero at 0.8 (120 days) gestation. Injections of 50-400 micrograms cyanide into the inferior vena cava or the carotid artery of intact fetuses elicited bradycardia and respiratory responses that varied from a single gasp to rhythmic respiratory movements but no significant change in arterial blood pressure. Carotid sinus denervation eliminated the cardiorespiratory response to intracarotid injection of cyanide and sinoaortic denervation abolished the response to inferior vena caval injection. It is concluded that in fetal lamb in utero the aortic and carotid bodies are active, and hypoxic stimulation of these chemoreceptors results in cardiorespiratory response characterized by slowing of fetal heart rate, respiratory effort, and no consistent change in arterial blood pressure.

Animals↗
PubMed1989

Cyanide-induced parkinsonism: clinical, MRI, and 6-fluorodopa PET studies.

A 46-year-old man ingested 1,500 mg of potassium cyanide in a suicide attempt. He survived, but later developed a severe parkinsonian syndrome. MRI revealed multiple areas of low-signal intensity in the globus pallidus and posterior putamen. A 6-fluorodopa PET study revealed bilateral decreased uptake in the basal ganglia. This evidence of functional impairment of dopaminergic nigrostriatal neurons is related either to direct toxicity of cyanide or to the effects of cerebral hypoxia secondary to cyanide intoxication.

Cyanides↗
PubMed2006

Determination of cyanide in blood by isotope-dilution gas chromatography-mass spectrometry.

BACKGROUND: Cyanide (CN) is a lethal toxin. Quantification in blood is necessary to indicate exposure from many sources, including food, combustion byproducts, and terrorist activity. We describe an automated procedure based on isotope-dilution gas chromatography-mass spectrometry (ID GC/MS) for the accurate and rapid determination of CN in whole blood. METHODS: A known amount of isotopically labeled potassium cyanide (K13C15N) was added to 0.5 g of whole blood in a headspace vial. Hydrogen cyanide was generated through the addition of phosphoric acid, and after a 5-min incubation, 0.5 mL of the headspace was injected into the GC/MS at an oven temperature of -15 degrees C. The peak areas from the sample, 1H12C14N+, at m/z 27, and the internal standard, 1H13C15N+, at m/z 29, were measured, and the CN concentration was quantified by ID. The analysis time was 15 min for a single injection. RESULTS: We demonstrated method accuracy by measuring the CN content of unfrozen whole blood samples fortified with a known amount of CN. Intermediate precision was demonstrated by periodic analyses over a 14-month span. Relative expanded uncertainties based on a 95% level of confidence with a coverage factor of 2 at CN concentrations of 0.06, 0.6, and 1.5 microg/g were 8.3%, 5.4%, and 5.3%, respectively. The mean deviation from the known value for all concentrations was <4%. CONCLUSION: The automated ID GC/MS method can accurately and rapidly quantify nanogram per gram to microgram per gram concentrations of CN in blood.

Ascorbic Acid↗
PubMed1981

Cyanide and its relationship to nervous suffering. Physiopathological aspects of intoxication.

On the basis of personal results in man and laboratory animal, we examined some aspects of acute and chronic cyanide intoxication: physiopathological aspects, hydroxocobalamin's therapeutic action in treating acute intoxications and neurotoxic sufferings due to cyanide, and hydroxocobalamin's biological action in decreasing the level of free cyanide appearing in blood and urine, a few days after sciatic nerve clamping in rabbits.

Animals↗
PubMed1984

The cyanide content of laetrile preparations, apricot, peach and apple seeds.

Laetrile preparations obtained from a cyanide intoxicated patient were analyzed for their cyanide content by a microdiffusion colorimetric procedure. Cyanide was also determined in apricot, peach and apple seeds. The results were compared to those reported in the literature for cyanogenic glycoside containing seeds.

Amygdalin↗
PubMed1995

Antidotal efficacy of alpha-ketoglutaric acid and sodium thiosulfate in cyanide poisoning.

Alpha-ketoglutaric acid and sodium thiosulfate antagonize the toxic effects of cyanide. The present study was performed to test whether a synergistic effect may occur. The alpha-ketoglutaric acid/sodium thiosulfate solutions were injected intraperitoneally into mice prior to exposure to hydrogen cyanide (HCN) in a dynamic inhalation chamber or preceding an intraperitoneal injection of sodium cyanide (NaCN). All lethal concentration (LCT) and lethal dose (LD) values were determined after a period of 24 h. Alpha-ketoglutaric acid alone provided no protection at 250 mg/kg when challenged with HCN. Sodium thiosulfate 500 mg/kg provided a 5% protection. However, when these doses of alpha-ketoglutaric acid and sodium thiosulfate were combined, protection was increased by 18%. Alpha-ketoglutaric acid (250 mg/kg) and sodium thiosulfate (1000 mg/kg) provided an additional 48% protection against a LCT88 of HCN. A single dose of alpha-ketoglutaric acid (500 mg/kg) and sodium thiosulfate (1000 mg/kg) solutions afforded a 70% increase in survivability of the exposed animals. When mice were injected ip with 100 mg/kg of alpha-ketoglutaric acid 15 min prior to the injection of 5.5 mg/kg (LD50) of NaCN, the lethality was reduced to an LD30. Two hundred mg/kg alpha-ketoglutaric acid, challenged with the same dose of NaCN, reduced the lethality to 23%. When mice were challenged with 6.0 mg/kg of NaCN (LD70) pretreated with 100 mg/kg of alpha-ketoglutaric acid or 200 mg/kg of sodium thiosulfate, the LD was not altered in the former but reduced to an LD15 in the latter. At higher doses of sodium thiosulfate (500 mg/kg), an LD60 occurred at 13.6 mg/kg NaCN (2.5 x LD50).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1986

[High-yield synthesis of 14C labeled alicyclic amino acids with high specific radioactivity using potassium (14C) cyanide].

In order to study the tumor specificity of synthetic nonmetabolizing amino acids, 10 different 14C labeled alicyclic amino acids (3a-3j) were synthesized in high yield and with high specific radioactivity. Carbon-14 labeled alicyclic hydantoins (2a-2j) were synthesized from a small amount of radioactive potassium [14C] cyanide and corresponding ketones (1a-1j). Th 14C hydantoins (2a-2j) thus obtained were hydrolyzed without isolation to give 14C labeled alicyclic amino acids (3a-3j). The overall radiochemical yields of the amino acids (3a-3j) from potassium [14C] cyanide were 55.6-93.2% with radiochemical purity more than 99%. Specific activities of these 14C labeled compounds (3a-3j) were 209- 250 MBq/mmol (5.66-6.75 mCi/mmol). When non-radioactive potassium cyanide was not added as a carrier, 1-aminocyclopentane[14C]-carboxylic acid (3b) and 1-aminocyclooctane[14C]carboxylic acid (3e) were synthesized in the yield of 64.9 and 19.0% respectively with the specific activity exceed more than 1.85 GBq/mmol (50mCi/mmol).

Amino Acids↗
PubMed1989

Pattern of enzyme changes in rabbits administered linamarin or potassium cyanide.

Diseases like tropical ataxic neuropathy and endemic goitre have been reported to have definite correlation with a chronic ingestion of cassava (Manihot esculenta Crantz). The toxicity of cassava has been attributed to its two cyanogenic glycosides, linamarin and lotaustralin. In this study, an attempt has been made to understand the pattern of changes in certain clinically significant enzymes brought about by the chronic administration of sublethal doses of linamarin to rabbits. The profound elevation in rhodanese activity observed in the linamarin and cyanide treated rabbits indicated the attempt of the tissues to detoxify cyanide. That intact linamarin could be hydrolysed in vivo was a significant finding from the study. The mode of toxicity of linamarin was similar to that of cyanide by producing a gradual shift from aerobic to anaerobic metabolism.

Animals↗
PubMedDate not supplied

In vitro and in vivo comparison of sulfur donors as antidotes to acute cyanide intoxication.

Antidotes for cyanide (CN) intoxication include the use of sulfane sulfur donors (SSDs), such as thiosulfate, which increase the conversion of CN to thiocyanate by the enzyme rhodanese. To develop pretreatments that might be useful against CN, SSDs with greater lipophilicity than thiosulfate were synthesized and assessed. The ability of SSDs to protect mice against 2LD50 of sodium cyanide (NaCN) administered either 15 or 60 min following administration of an SSD was assessed. To study the mechanism of action of the SSD, the candidate compounds were examined in vitro for their effect on rhodanese and 3-mercaptopyruvate sulfurtransferase (MST) activity under increasing SSD concentrations. Tests were conducted on nine candidate SSDs: ICD1021 (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide dihydrochloride), ICD1022, (3-hydroxypyridin-2-yl N-[(N-methyl-3-aminopropyl)]-2-aminoethyl disulfide trihydrochloride), ICD1584 (diethyl tetrasulfide), ICD1585 (diallyl tetrasulfide), ICD1587 (diisopropyl tetrasulfide); ICD1738 (N-(3-aminopropyl)-2-aminoethyl 2-oxopropyl disulfide dihydrochloride), ICD1816 (3,3'-tetrathiobis-N-acctyl-L-alanine), ICD2214 (2-aminoethyl 4-methoxyphenyl disulfide hydrochloride) and ICD2467 (bis(4-methoxyphenyl) disulfide). These tests demonstrated that altering the chemical substituent of the longer chain sulfide modified the ability of the candidate SSD to protect against CN toxicity. At least two of the SSDs at selected doses provided 100% protection against 2LD50 of NaCN, normally an LD99. All compounds were evaluated using locomotor activity as a measure of potential adverse behavioral effects. Positive hypoactivity relationships were found with several disulfides but none was found with ICD1584, a tetrasulfide. Separate studies suggest that the chemical reaction of potassium cyanide (KCN) and cystine forms the toxic metabolite 2-iminothiazolidine-4-carboxylic acid. An alternative detoxification pathway, one not primarily involving the sulfur transferases. may be important in pretreatment for CN intoxication. Although studies to elucidate the precise mechanisms are needed. it is clear that these newly synthesized compounds provide a new rationale for anti-CN drugs, with fewer side-effects than the methemoglobin formers.

Animals↗