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PubMed1982

Contact dermatitis from cyanide plating solutions.

Two cases of contact dermatitis from electroplating solutions were attributed to irritation from cyanide salts. Both demonstrated similar clinical features. In neither could concomitant contact allergy to other constituents of the plating solutions be demonstrated. In one case, irritation could not be attributed to the alkalinity of the plating solution. Contact dermatitis from cyanide plating solutions may be associated with systemic symptoms, since cyanide is rapidly absorbed through the skin. Poor handling and hygiene techniques in the workplace should be corrected immediately.

Adolescent↗
PubMedDate not supplied

[Respiratory resistance of methylotrophic bacteria to formate and cyanide].

Whole cells and cell-free preparations of the methylotrophic bacteria, Pseudomonas sp. AM 1 and Achromobacter parvulus, can oxidize formate at tis concentration in the reaction medium up to 1 M. The respiration of whole cells is registered at a concentration of formate greater than 10(-2) M, while that of cell-free extracts at a formate concentration greater than 5 X 10(-5) M. This seems to be due to the presence of a permeability barrier in cells for formate. The oxidation of reduced TMPD and exogenous cytochrome c by the membrane preparations of the two bacteria is inhibited by formate and cyanide; Ki50% = 2.5 X 10(-2) and 10(-6) M, respectively. The oxidation of NADH by the membrane preparations of the bacteria is not inhibited by 1 M formate and 5 X 10(-4) M cyanide but is inhibited by formaldehyde with Ki50% = 3 X 10(-2) M. Formaldehyde has no effect on the oxidation of reduced TMPD and cytochrome c at concentrations greater than 2 X 10(-1) M. These data indicate that respiration of the studied methylotrophic bacteria in the presence of high formate concentrations should be attributed in the presence of a branched electron transport chain in them; one branch of the chain is resistant to formate and cyanide, but is sensitive to formaldehyde.

Alcaligenes↗
PubMed1981

Binding of saframycin A, a heterocyclic quinone anti-tumor antibiotic to DNA as revealed by the use of the antibiotic labeled with [14C]tyrosine or [14C]cyanide.

Saframycin A is antitumor antibiotic structurally characterized by twin heterocyclic quinone skeletons and alpha-cyanoamine moiety. The binding of saframycin A to DNA was investigated using the antibiotic labeled at different positions. Heterocyclic quinone skeletons were biosynthetically labeled with [14C]tyrosine. The cyano residue of saframycin A was specifically labeled as a result of the reaction of [14C]cyanide with a derivative of saframycins, decyanosaframycin A, in the culture filtrate. When calf thymus DNA was incubated with [14C]tyrosine-labeled saframycin A in the presence of dithiothreitol, radioactivities were progressively recovered from DNA fraction. In contrast, saframycin A in the absence of dithiothreitol was completely devoid of reactivity toward DNA. When [14C]cyanide-labeled saframycin A was reacted with DNA, however, none of the radioactivity was associated with DNA. The release of cyano residue from the antibiotic was triggered by the reduction. Thus, conversion of quinone to hydroquinone skeletons as well as conversion of alpha-cyanoamine to immonium or alpha-carbinolamine is the consequence of the reduction. The fact that dithiothreitol-inducible binding of saframycin A to DNA was blocked by the addition of excess cyanide indicates that immonium or alpha-carbinolamine is the actual species involved in the interaction with DNA. The striking similarities between saframycin A and anthramycin in regard to the mode of binding to DNA are discussed.

Animals↗
PubMed1978

Analytical precautions in measurement of blood cyanide.

Solutions of KCN in 0.1 mol/liter NaOH, stored for six months at 4 degrees C, were unchanged as determined by silver titration and color development with pyridine-pyrazalone reagent. At room temperature the cyanide concentration of such solutions decreased by 0.079% per day (half life = 880 days) and the extent of color development changed in direct proportion to the change in silver titer. Rubber stoppers adsorb (or dissolve) HCN when in contact with this gas. The cyanide tends to come out of the stopper long after the source of the gas is removed. Rubber stoppers and expired air contaminated by HCN must be carefully avoided during cyanide analysis. Expired air contains HCN, generally in larger amounts for persons who smoke.

Colorimetry↗
PubMed1980

Cyanide concentrations in blood after amygdalin (laetrile) administration in rats.

Toxic amounts of cyanide are released into the blood of rats following the oral administration of amygdalin (laetrile); cyanide blood concentrations and toxicity are markedly less when amygdalin is given intravenously. Analysis of the time course of cyanogenesis suggests that cyanide could accumulate in blood after repeated oral doses of amygdalin.

Administration, Oral↗
PubMed1981

[Therapeutic attitude in cyanide poisoning (author's transl)].

According to experimental and clinical data, the present treatment of acute cyanide poisoning depends basically on: 1) Dicobaltetracemate in cases of occupational pathology to be given at the working area, to patients with giddiness or mental confusion, 2) Oxygen by assisted ventilation, associated to hydroxocobalamine and sodium thiosulfate, to be administered after admission (patients in coma or circulatory failure). Initial cardio-respiratory arrest requires immediate cardiac massage and assisted ventilation. The rapid cyanide metabolism makes useless the dialysis methods. Frequent complications as metabolic acidosis and acute pulmonary oedema respond to symptomatic treatment. If these therapeutic measures are rapidly applied in confirmed cyanide poisoning, the notion of lethal blood level should be reconsidered. Survivals have been observed with initial plasma levels of 6 mg/l.

Antidotes↗
PubMed1980

Cyanide, protein and iodine interactions in the performance, metabolism and pathology of pigs.

Performance and metabolic and pathological changes were evaluated in 48 growing pigs fed different levels of dietary protein, cyanide and iodine. Protein deficiency reduced urinary iodine excretion and the concentrations in serum of protein, protein bound iodine and thiocyanate. It also reduced liver rhodanese activity and caused a decrease in urinary thiocyanate excretion which was not significant. Dietary cyanide increased urinary thiocyanate and iodine excretion and serum thiocyanate concentration while the basal diet reduced urinary iodine excretion and serum PBI. Pathological studies showed that cyanide treatment had no marked effect on the microanatomy of the tissues examined. Dietary protein deficiency caused histological changes in the thyroid gland and bone which suggested a decline in metabolic activity. Iodine deficiency caused hyperplastic goitre in the experimental animals.

Animals↗
PubMed1981

Behavioural, electroencephalographic and histological study of the protective effect of etomidate against histotoxic dysoxia produced by cyanide.

The acute toxicity of cyanide is largely due to the inhibition of cytochrome oxidase, and the subsequent breakdown of cellular metabolism. Breakdown in cellular metabolism, leading to a disruption of cellular integrity lies at the heart of the permanent neurological damage resulting from ischemic/hypoxic brain insult. In 200 g male Wistar rats treated with 5 mg/kg KCN i.v. and ventilated until spontaneous breathing restarted, the cornea reflex, tail-pinch reaction and righting reflex disappeared for about 20 min. In curarized and artificially ventilated rats the EEG remained flat for a similar period before slowly returning. Saline treated animals which survive the KCN injection die significantly earlier than non-KCN treated animals when injected with 120 mg/kg metrazol s.c. one week later. Histological examination of KCN treated animals revealed swollen mitochondria at 20 min, and microvacuolization and ischemic cell changes at 1 week. In rats pretreated with etomidate 10 mg/kg s.c. 30 min before cyanide the cornea, tail-pinch and righting reflex were absent for the same time as in controls. The EEG was similar to that seen in saline/KCN animals, however, the time to EEG was similar to that seen in saline/KCN animals, however, the time to EEG silence was doubled. One week after the cyanide injection their reaction to the metrazol injection was similar to animals treated one week earlier with saline. Although there was evidence of swollen mitochondria 20 min after KCN, one week after KCN there was no evidence of ischemic hypoxic brain damage. These results demonstrate that under similar conditions of dysoxia, etomidate treated animals appear to be protected from the behavioural and histological sequelae of those conditions.

Animals↗
PubMed1980

[Autoradiographic distribution of 14C after administering tracer-marked nitroprusside, cyanide and thiocyanate to pregnant mice and rats (author's transl)].

Doses of ca. 2--3 mg/kg of nitroprusside, cyanide and thiocyanate, tracer-marked with 14C, were applied i.v. to pregnant mice and rats. Autoradiograms of the whole animal were taken 1 min, 10 min and 60 min after administration. After administering nitroprusside two phases of the tracer pattern could be distinguished: the phase of removal of the cyanide poisoning with tracer-markings predominant in the liver and the lungs, followed by the phase of thiocyanate excretion, with tracer-markings predominantly in the stomach and urinary system. Tracer-markings in the foetuses were observed during the thiocyanate phase, but not during the cyanide phase. The therapeutic consequences are discussed.

Animals↗
PubMed1980

Effect of hyperbaric oxygen on cyanide intoxication: in situ changes in intracellular oxidation reduction.

To evaluate the efficacy of hyperbaric oxygen on cyanide intoxication, changes in the intracellular oxidation-reduction state of the renal cortex were observed in situ in 16 New Zealand white rabbits by detecting the reduced pyridine nucleotide fluorescence that represents the degree of cyanide blockade of the respiratory chain. The data indicated that 100% oxygen at 2 ATA exerted both prophylactic and therapeutic antagonistic effects on the cyanide poisoning. Administration of hyperbaric oxygen could constitute a significant treatment if proper chemical treatment is carried out concomitantly.

Animals↗
PubMed1995

Seizures and selective CA-1 hippocampal lesions induced by an excitotoxic cyanide metabolite, 2-iminothiazolidine-4-carboxylic acid.

Excitatory amino acid (EAA)-like and excitotoxic properties of the secondary metabolite of cyanide, 2-iminothiazolidine-4-carboxylic acid, (2-ICA) were evaluated because of its possible role in cyanide-induced neurotoxicity. Intracerebroventricular (i.c.v.) injections of 2-ICA in mice produced wild-running seizures that were qualitatively and quantitatively similar to seizures observed with glutamate. 2-ICA, kainate and proline seizures were prevented by both the NMDA and non-NMDA antagonists, MK-801 and CNQX, respectively. In contrast, NMDA-induced seizures were prevented by MK-801, but not CNQX. When infused i.c.v. in rats over a seven day period, 2-ICA produced extensive and selective loss of CA-1 pyramidal neurons of the hippocampus. In hippocampal slices preloaded with D-[3H]aspartate, 2-ICA superfusion did not evoke release nor significantly augment potassium stimulated release of the radiolabeled transmitter. These findings indicate 2-ICA has excitotoxic properties and its role in cyanide neurotoxicity deserves further study.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1994

Simultaneous measurement of alcohols and hydrogen cyanide in biological specimens using headspace gas chromatography.

We attempted to analyze biological specimens simultaneously for alcohols and hydrogen cyanide. A headspace gas chromatographic method with thick film wide bore column (PEG 20M) for the simultaneous determinations of methanol, ethanol, n-propanol and hydrogen cyanide in blood has been developed. This method was applied for the determinations of methanol, ethanol and hydrogen cyanide in a forensic autopsy case and animal experiments.

1-Propanol↗
PubMed1994

Protein kinase C modulation of rhodanese-catalyzed conversion of cyanide to thiocyanate.

Detoxification of cyanide is catalyzed by a sulfurtransferase, rhodanese, a phosphoprotein regulated by unknown protein kinases. In this study, we determined if a Ca2+/phospholipid-modulated phosphotransferase, protein kinase C (PKC) could modify rhodanese activity. Thiocyanate (SCN-) production as an estimate of rhodanese activity in vitro was measured in the presence or absence of exogenously added purified PKC, or 12-O-tetradecanoylphorbol acetate (TPA), a pharmacologic activator of the endogenous PKC. HI-6 (1-(2-(hydroximino)methyl))pyridinium-2-(4-(aminocarbonyl) pyridinium dimethylether) is an oxime that may dephosphorylate phosphoproteins due to the proposed phosphatase-like activity of the oximes. We examined HI-6's effect on rhodanese-catalyzed SCN- production. Bovine kidney rhodanese (0.40 mg/ml protein) was reacted with 4 mM KCN and SCN- production determined spectrophotometrically following the method of Westley (1981). Preincubating rhodanese with 20 or 100 ng of purified PKC (alpha, beta, gamma isozymes) for 5 min before initiating the reaction with 4 mM KCN as the substrate increased SCN- production by 17 or 40%, respectively, over the control (P < 0.05). Rhodanese formation of SCN- decreased when the preincubation was conducted with 1 nM or 100 nM of TPA. With HI-6 at 1 or 10 microM used in place of PKC, or TPA, rhodanese activity was increased by 6 or 14% (P < 0.05), respectively, compared to control. Under the conditions examined, exogenous PKC acting as a possible phosphate acceptor, and HI-6, a potential dephosphorylating compound, increased rhodanese activity. These data are consistent with the observation that rhodanese can exist as a phosphorylated enzyme which is not active and a dephosphorylated form which is active. It is suggested that addition of purified, exogenous PKC may accept phosphate from phosphorylated rhodanese or HI-6 may dephosphorylate rhodanese, both of which stimulate the conversion of cyanide anion to the less toxic SCN-. These observations support the possibility that rhodanese may be regulated by protein phosphorylation and treatments that alter the phosphorylation state of rhodanese may affect cyanide detoxification via SCN- formation.

Animals↗
PubMed1993

N-methyl-D-aspartate receptors mediate cyanide-induced cytotoxicity in hippocampal cultures.

We reported previously that glutamate excitotoxicity may contribute to cyanide-induced neuronal injury. Cyanide stimulates glutamate release which can activate glutamate receptors to initiate excitotoxic processes. This study examines the role of EAA receptor subtypes in mediating cyanide-induced cytotoxicity. Cytotoxicity was assessed in primary rat hippocampal cultures by measuring lactate dehydrogenase (LDH) in the culture media. NaCN (0.1-10 mM) or glutamate (0.01-1 mM) produced concentration-dependent cytotoxicity following 18 hrs of incubation. Glutamate-induced cytotoxicity was partially blocked by the non-NMDA antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX) and the NMDA antagonist, 2-amino-5-phosphonovalerate (APV). Simultaneous exposure of cultures to both CNQX and APV provided complete protection against glutamate cytotoxicity. NaCN-induced cytotoxicity was not blocked by CNQX, but completely blocked by APV and simultaneous exposure to CNQX and APV did not offer added protection. These results indicate that in hippocampal cultures, both non-NMDA and NMDA receptors mediate glutamate excitotoxicity, whereas NaCN-induced cytotoxicity is mediated primarily by activation of the NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1994

Structural factors governing azide and cyanide binding to mammalian metmyoglobins.

The structural factors governing azide and cyanide binding have been examined by measuring the effects of 46 mutations at key topological positions in the distal pocket in sperm whale, pig, and human myoglobin. Replacement of His64 (E7) with smaller amino acids results in dramatic increases in the association rate constant for azide binding primarily due to relief of steric hindrance imposed by the imidazole side chain. Gln64 and His64 (native) metmyoglobins have abnormally low rate constants for azide dissociation (0.1-0.3 s-1) due to direct hydrogen bonding between the N epsilon atoms of these residues and the bound ligand. Mutations at positions 67(E10) and 68(E11) produce large but complex changes in the azide binding parameters as a result of both steric and electrostatic effects, which alter water coordination, influence the rate of anion movement into the distal pocket, and affect the stability of the Fe-N3 bond. Replacement of Phe46 with Leu or Val and substitution of Arg(Lys)45 with Glu and Ser cause disorder in the position of the distal histidine side chain and result in 4-700-fold increases in both k'N3 and kN3 but produce little change in overall azide affinity. All of these results suggest strongly that azide enters the distal pocket of native myoglobin through a polar channel that is regulated by a His64 "gate." In contrast to azide binding, the rate constant for cyanide association decreases 4-300-fold when the distal histidine is replaced with apolar residues. His64, Gln64, and distal pocket water molecules appear to facilitate deprotonation of HCN, which is the major kinetic barrier to cyanide binding at neutral pH.

Animals↗
PubMed1993

Rapid multicomponent analysis of hemoglobin derivatives for controlled antidotal use of methemoglobin-forming agents in cyanide poisoning.

When cyanide poisoning is treated with a methemoglobin-forming agent, oxidative metabolism is protected at the expense of the oxygen capacity of the blood. The affinity of methemoglobin for CN- is high enough to compete with cytochrome oxidase, which protects the latter from becoming blocked, but all hemoglobin used for this purpose is lost for the transport of oxygen. Therefore, the fractions of the various hemoglobin derivatives present in the blood should be carefully monitored during this kind of treatment. After we had developed a multiwavelength spectrophotometric method for this purpose, we studied the feasibility of using a modified commercial six-wavelength hemoglobin photometer (Radiometer OSM3) for easy and rapid analysis of methemoglobin and methemoglobin cyanide in small samples of blood. All conditions appeared to be fulfilled for the construction of a practical multiwavelength photometer for reliably monitoring methemoglobin therapy in patients with cyanide poisoning, even in the presence of carboxyhemoglobin, as often occurs in fire victims.

Adult↗
PubMed1977

Cyanide intoxication in sheep: therapeutic value of oxygen or cobalt.

The combination of cobalt salts and oxygen with the traditional sodium nitrite-sodium thiosulfate antidote may have value as cyanide antidotes. Results reported previously in mice were extended to sheep in the present experiments. Cobaltous chloride (15 mg/kg of body weight) or oxygen with or without sodium nitrite and sodium thiosulfate were compared with respect to the median lethal dose of oral sodium cyanide. Although cobaltous chloride or oxygen used alone did result in a significant increase in the median lethal dose of sodium cyanide in sheep, the protection was minor compared with the overall protection provided by the classic antidotal combination of sodium nitrite and sodium thiosulfate. Cobaltous chloride combined with sodium nitrite and sodium thiosulfate did not provide any increase in protection more than that observed with sodium nitrite and sodium thiosulfate alone. Oxygen used in combination with sodium nitrite and sodium thiosulfate did significantly increase the protection. However, the increase in protection was not of sufficient magnitude to recommend it as a practicable addition to the present therapeutic regimen.

Animals↗
PubMed1996

Interference in glucose and other clinical chemistry assays by thiocyanate and cyanide in a patient treated with nitroprusside.

A 3-year-old patient treated with nitroprusside for congestive heart failure had 6.5 mmol/L thiocyanate (toxic, >1.5 mmol/L) and 110 micromol/L cyanide (toxic, >5 micromol/L) present in her blood. At this time a whole-blood glucose concentration assayed on the Nova Stat Profile 5 Plus (Stat Profile) was 25.1 mmol/L. Plasma from that specimen analyzed on a Kodak Ektachem 700 analyzer (E700) indicated 5.2 mmol/L glucose. We investigated the potential interference of dissolved thiocyanate or cyanide on glucose and other routine assays. Toxic concentrations of thiocyanate increased Stat Profile glucose values and E700 total calcium, chloride, and creatinine values. Stat Profile ionized calcium values were decreased by toxic concentrations of thiocyanate. Cyanide (100 micromol/L) decreased alanine aminotransferase activity measured on the E700. Interference with the Stat Profile glucose assay may have been caused by thiocyanate oxidation at the glucose electrode.

Blood Chemical Analysis↗