Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Cyanides”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 487 records · Page 27Linked to original sources
PubMedDate not supplied

Role of cytochrome P-450 IIE1 and catalase in the oxidation of acetonitrile to cyanide.

Acetonitrile is a common industrial solvent and laboratory agent, which can be toxic if ingested. The toxicity of nitriles appears to be due to the production of cyanide, and detailed studies by Freeman and Hayes [(1988) Biochem. Pharmacol. 37, 1153-1159; (1987) Fundam. Appl. Toxicol. 8, 263-271] have shown that microsomes oxidize acetonitrile to cyanide. Treatment of rats with inducers of cytochrome P-450 IIE1 such as pyrazole, 4-methylpyrazole, and ethanol resulted in a 4- to 5-fold increase in cyanide production from acetonitrile by isolated microsomes. Phenobarbital treatment had a small stimulatory effect, whereas 3-methylcholanthrene treatment decreased microsomal oxidation of acetonitrile. Pyrazole treatment increased Vmax per milligram of microsomal protein and per nanomole of P-450 but did not affect the apparent km for acetonitrile, whereas the 4-methylpyrazole treatment increased Vmax and the apparent affinity for acetonitrile. Cyanide production was inhibited by carbon monoxide as well as by substrates and compounds that interact with the P-450 IIE1 isozyme such as ethanol, 2-butanol, DMSO, and 4-methylpyrazole. Oxidation of acetonitrile to cyanide by microsomes from rats treated with pyrazole or 4-methylpyrazole was nearly completely inhibited by anti-P-450 3a IgG. These results implicate a role for P-450 in the oxidation of acetonitrile to cyanide and suggest that P-450 IIE1 may be an especially effective catalyst for this oxidation. Acetonitrile oxidation was not affected by hydroxyl radical scavengers or by desferrioxamine, indicating no role for hydroxyl radicals in the overall mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetonitriles↗
PubMed1998

Biodegradation of cyanides, cyanates and thiocyanates to ammonia and carbon dioxide by immobilized cells of Pseudomonas putida.

Pseudomonas putida utilizes cyanide as the sole source of carbon and nitrogen. Agar, alginate, and carrageenan were screened as the encapsulating matrices for P. putida. Alginate-immobilized cells of P. putida degraded sodium cyanide (NaCN) more efficiently than non-immobilized cells or cells immobilized in agar or carrageenan. The end products of biodegradation of cyanide were identified as ammonia (NH3) and carbon dioxide (CO2). These products changed the medium pH. In bioreactors, the rate of cyanide degradation increased with an increase in the rate of aeration. Maximum utilization of cyanide was observed at 200 ml min-1 of aeration. Immobilized cells of P. putida degraded cyanides, cyanates and thiocyanates to NH3 and CO2. Use of Na[14C]-CN showed that 70% of carbon of Na[14C]-CN was converted into 14CO2 and only 10% was associated with the cell biomass. The substrate-dependent kinetics indicated that the Km and Vmax values of P. putida for the substrate, NaCN were 14 mM and 29 nmol of oxygen consumed mg protein-1 min-1 respectively.

Agar↗
PubMed1967

Effect of carbonyl cyanide m-chlorophenylhydrazone on respiration and respiration-dependent phosphorylation in Escherichia coli.

1. The interference mechanism of carbonyl cyanide m-chlorophenylhydrazone with the respiratory process and with phosphorylation coupled to respiration has been investigated in resting cells of Escherichia coli. 2. Preincubation of the cells with carbonyl cyanide m-chlorophenylhydrazone in the absence of substrate caused strong inhibition of succinate oxidation. The inactivation of the respiratory system proved to be time-dependent and temperature-dependent and could be arrested by adding the substrate. Inhibition of incorporation of (32)P into acid-soluble organic phosphate esters exceeded the inhibition of oxygen uptake. 3. In contrast with succinate, the rate of oxidation of glucose was increased by carbonyl cyanide m-chlorophenylhydrazone. The sensitivity of other substrates to the inhibitor was less than that of succinate. 4. Various observations are described in support of the view that respiratory inhibition induced by carbonyl cyanide m-chlorophenylhydrazone is a result of its interference with ATP synthesis. The capacity of a given substrate to increase intracellular ATP concentration appeared to be directly related to its resistance to inhibition. In cell-free extracts carbonyl cyanide m-chlorophenylhydrazone still suppressed (32)P incorporation but had no effect on respiration. 5. Carbonyl cyanide m-chlorophenylhydrazone-induced stimulation of glucose oxidation and the acceleration of succinate oxidation by ADP or AMP in cells rendered permeable to nucleotides are tentatively interpreted as an indication that a certain part of respiration in E. coli is under phosphate-acceptor-mediated control.

Adenine Nucleotides↗
PubMed1980

Energy conservation by the plant mitochondrial cyanide-insensitive oxidase. Some additional evidence.

Several measures of energy conservation, namely ADP/O ratio, P/O ratio, ATP/O ratio and phosphorylation detected by continuous assay with purified firefly luciferase and luciferin, all show phosphorylation can occur with mung-bean mitochondria at cyanide concentrations sufficient to inhibit the cytochrome oxidase system. Phosphorylation in the presence of cyanide is uncoupler- oligomycin- and salicylhydroxamate-sensitive. The participation of phosphorylation site 1 is excluded, phosphorylation being attributable to a single phosphorylation site associated with the cyanide-insensitive oxidase. The cyanide-insensitive oxidase has also been shown to support a variety of other energy-linked functions, namely, Ca2+ uptake, reversed electron transport and the maintenance of a membrane potential detected by the dye probes 8-anilinonaphthalene-1-sulphonate and safranine. High concentrations of cyanide have uncoupler-like activity, decreasing the ADP/O ratio and the t 1/2 for the decay of a pH pulse through the the mitochondrial membrane. This uncoupler-like effect is most marked with aged mitochondria. The observations of energy conservation attributable to the cyanide-insensitive oxidase are compared with other reports where it is concluded that the alternative oxidase is uncoupled.

Adenosine Triphosphate↗
PubMed1996

Cyanide-induced apoptosis and oxidative stress in differentiated PC12 cells.

Terminally differentiated PC12 cells are a useful neuron-like model for studying programmed cell death in response to nerve growth factor (NGF) deprivation. This in vitro model was used to investigate the mechanism by which cyanide-induced histotoxic hypoxia produces neuronal degeneration. Treatment of undifferentiated PC12 cells with 0.1 mM KCN for 24 h did not produce cell death. In contrast, treatment of differentiated PC12 cell cultures with 0.1 mM KCN for 24 h increased cell death by 43% when compared with control cultures, as measured by trypan blue dye exclusion and lactate dehydrogenase release assays. The Ca2+/Mg(2+)-dependent endonuclease inhibitor aurintricarboxylic acid and the transcriptional inhibitor actinomycin D partially attenuated hypoxic toxicity, suggesting roles for endonuclease activation and transcription in this model of neuronal death. Extracted DNA from cyanide-treated neurons demonstrated cleavage into oligonucleosomal fragments on gel electrophoresis. Transmission electron microscopic analysis showed morphological changes consistent with apoptotic cell death, including membrane blebbing and convolution, as well as chromatin condensation and margination to the nuclear membrane. Addition of either ascorbate or catalase to the cultures partially attenuated the loss of cell viability induced by cyanide, and decreased the incidence of apoptotic cells after treatment, based on the in situ detection of DNA strand breaks. The ability of cyanide to elevate intracellular oxidant species was determined by microfluorescence in differentiated PC12 cells loaded with the oxidant-sensitive dye 2',7'-dichlorofluorescin. Exposure of cells to 0.1 mM KCN produced a rapid generation of oxidants that was blocked approximately 50% by ascorbate or catalase. These observations indicate that cyanide induces apoptosis in terminally differentiated, and not undifferentiated, PC12 cells, and that antioxidants significantly reduce the incidence of cyanide-induced apoptosis.

Animals↗
PubMed1978

Prevention of nitroprusside-induced cyanide toxicity with hydroxocobalamin.

To investigate hydroxocobalamin's role in preventing cyanide intoxication from sodium nitroprusside, we studied two groups of patients. One group received nitroprusside alone, and the other received nitroprusside and hydroxocobalamin. Red-cell and plasma cyanide levels were 83.44 +/- 23.12 and 3.51 +/- 1.01 microgram per 100 ml after nitroprusside alone and were 33.18 +/- 17.29 and 2.18 +/- 0.65 microgram per 100 ml after nitroprusside plus hydroxocobalamin. Acidosis developed in patients with red-cell cyanide levels higher than 75 microgram per 100 ml. When hydroxocobalamin infusion was stopped before sodium nitroprusside infusion was discontinued, blood cyanide levels and base deficit increased in a manner similar to that in the untreated group. The dose of nitroprusside used in each group did not differ statistically. These data show that hydroxocobalamin prevents cyanide transfer from red cells and plasma to tissue after nitroprusside metabolism, and thereby prevents cyanide toxicity from large intravenous doses of the drug.

Adult↗
PubMed1991

Mechanism of cyanide inhibition of the blood-clotting, vitamin K-dependent carboxylase.

Cyanide is a competitive inhibitor of carbon dioxide in the vitamin K-dependent glutamate carboxylase system, which plays a central role in the function of the blood clotting cascade. The mechanism of cyanide inhibition has been obscure for some time. At pH 7.2, cyanide (pKa = 9.21) will exist in solution as hydrogen cyanide to the extent of 99%. Hydrogen cyanide is linear triatomic molecule able to serve as a surrogate for carbon dioxide at the enzyme active site. Hydrogen cyanide is an acid; it will quench the deprotonated glutamate carbanion precursor to gamma-carboxyglutamate, resulting in inhibition of the carboxylation sequence.

Amino Acid Sequence↗
PubMedDate not supplied

Ion chromatographic determination of cyanide released from flaxseed under autohydrolysis conditions.

Flaxseed is increasingly being used in some food products because of its high content of alpha-linolenic acid and dietary fibre. However, flaxseed contains cyanogenic glycosides which release toxic hydrogen cyanide in the presence of water (autohydrolysis). A method for estimation of cyanide in flaxseed under these conditions is described. The determination is carried out by homogenizing the sample with water, letting it stand, filtering it through a membrane and then injecting the filtrate into an HPLC system consisting of an anion exchange column and an electrochemical (amperometric, oxidation) detector. The homogenate is analysed at various intervals until a maximum value of cyanide is observed. The cyanide content of ten cultivars of flaxseed, when analysed by this method, was found to range from 124 to 196 micrograms/g. The release of cyanide showed a maximum at about 3 h of hydrolysis. Virtually no cyanide was detected on boiling the homogenate or the flaxseed before determination.

Anions↗
PubMed2000

Dietary cyanide from insufficiently processed cassava and growth retardation in children in the Democratic Republic of Congo (formerly Zaire).

Dietary cyanide exposure from cyanogenic glucosides in insufficiently processed cassava has been advanced as a contributing factor in child growth retardation. Whether cyanide exposure aggravates children's growth retardation was studied by comparing two populations of children from the northern and the southern zones of the Bandundu region, Democratic Republic of Congo (former Zaire), using dietary interviews, anthropometry and urine analyses. Both populations consumed cassava as their staple diet, but whereas in the north the cassava was well processed, in the south it was inadequately processed. The mean urinary thiocyanate was much higher in the south, whereas mean urinary sulphate excretion was equally low in the two areas. However, the mean urinary SCN/SO4 molar ratio was higher in the south (0.20), indicating that 10-20% of sulphur amino-acids were used for cyanide detoxication. No significant differences were found between the two populations in weight-for-height and weight-for-age indices but the height-for-age index was significantly lower in children from the south, indicating more severe growth retardation in children exposed to dietary cyanide. Because of the preferential use of sulphur amino-acids for cyanide detoxification in the human body, dietary cyanide exposure from cassava may be a factor aggravating growth retardation in Bandundu.

Anthropometry↗
PubMed1979

Effects of prolonged cyanide and thiocyanate feeding in rats.

Male weaning rats were fed a semipurified diet containing 10% casein; this diet restricted in methionine, vitamin B12, and iodine; or the complete and restricted diets supplemented with either 1500 ppm potassium cyanide or 2240 ppm potassium thiocyanate for 11.5 mo. There were no deaths or clinical signs of toxicity. Cyanide, but not thiocyanate, caused a consistent reduction in weight gain in the complete and restricted groups. Both cyanide and thiocyanate caused decreased thyroid gland activity in young rats, particularly in the restricted groups. Plasma thyroxine concentrations were maintained in the mature cyanide-treated rats, even though secretion rates were decreased. However, the mature thiocyanate-treated animals showed decreased plasma thyroxine concentrations, despite thyroid gland enlargement. Modest primary myelin degeneration in the spinal cord white matter was found in the restricted group and in rats receiving this diet supplemented with either cyanide or thiocyanate. The lesions did not resemble those of a vitamin B12 deficiency in appearance or those of acute cyanide intoxication in distribution. Because of tissue autolysis, it could not be determined whether these changes resulted from histotoxic anoxia or an alteration of oligodendroglial myelin metabolism.

Animals↗
PubMed1994

Antagonism of cyanide intoxication with murine carrier erythrocytes containing bovine rhodanese and sodium thiosulfate.

Murine carrier erythrocytes containing bovine rhodanese and sodium thiosulfate are being explored as a new approach to antagonize the lethal effects of potassium cyanide in mice. Prior studies indicated that these carrier erythrocytes persist in the vascular system for the same length of time as normal erythrocytes and can enhance metabolism of cyanide to thiocyanate. The present studies demonstrate the ability of these carrier red blood cells containing rhodanese and thiosulfate to antagonize the lethal effects of cyanide either alone or in various combinations with sodium nitrite and/or sodium thiosulfate. Potency ratios are compared in groups of mice treated with sodium nitrite, sodium thiosulfate, and carrier erythrocytes containing rhodanese and sodium thiosulfate either alone or in various combinations prior to the administration of potassium cyanide. These results indicate that the administration of carrier erythrocytes containing rhodanese and thiosulfate alone can provide significant protection against the lethal effects of cyanide. These carrier erythrocytes potentiate the antidotal effect of sodium thiosulfate alone or the combination of sodium nitrite and sodium thiosulfate. The mechanisms of cyanide antagonism by these carrier erythrocytes and their broader conceptual significance to the antagonism of other chemical toxicants are discussed.

Animals↗
PubMed2004

Rapid cyanide detection using the Cyantesmo kit.

BACKGROUND: Sources of cyanide exposure are many, including combustion of plastic and vinyl, such as in a house fire, laboratory or industrial exposures including exposure in the electroplating industry both of printed circuit boards and in jewelry work. Rapid and definitive diagnosis of cyanide poisoning is unavailable in the emergency department setting. It is desirable to make a definitive diagnosis in order to prevent potential complications of empiric treatment of presumptive cyanide poisoning from the cyanide antidote kit currently approved by the US Food and Drug Administration (FDA). We investigated a technique to detect cyanide currently utilized by water treatment facilities to determine if it can be applied to rapidly detect concentrations of cyanide in the clinically important range. METHODS: Varying standardized dilutions of KCN ranging from 0.25 microg/mL to 30 microg/mL were acidified with a drop of sulphuric acid in a closed system under a ventilation hood. Cyantesmo test strips were placed into the test tubes above the fluid level where liberated HCN gas interacted with the test strip to effect a color change. Color changes were compared to negative controls and to each other. RESULTS: The test strips demonstrated an incrementally increasing deep blue color change over a progressively longer portion of the test strip in less than 5 minutes for each concentration of KCN including 1, 3, 10, and 30 microg/mL. The concentrations of 0.25, 0.5, and 0.75 required more than 2 hours to begin demonstration of any color change. CONCLUSION: The Cyantesmo test strips accurately and rapidly detected, in a semi-quantifiable manner, concentrations of CN greater than 1 microg/mL contained in each test sample. Future work to validate this test in blood and in clinical specimens is planned.

Cyanides↗
PubMed2002

Removal of cyanide from dilute solution using a cell with three-phase three-dimensional electrode.

The removal of cyanide from dilute solutions containing free cyanide or cuprocyanide was experimentally investigated using a new electrochemical reactor, three-phase three-dimensional electrode cell. The experimental results were assessed in term of removal efficiency of cyanide. The results showed that the reactor could efficiently remove cyanide from the two solutions. The removal efficiency reached as high as about 93% for the two solutions by electrolysis for 10 min at 20 V cell voltage and 0.16 m3/h airflow. It was also observed that the removal efficiency depended on the applied cell voltage, airflow, interelectrode and initial pH value of the containing-cyanide solution. The former two factors have a positive effect while the latter two have a negative effect on cyanide removal in the experimental range.

Cyanides↗
PubMed1976

Cyanide and thiocyanate concentrations following sodium nitroprusside infusion in man.

Twenty-six patients, receiving an infusion of sodium nitroprusside (SNP) during surgery, had considerable increases in both red cell and plasma cyanide concentration, but only small changes in plasma thiocyanate concentration. There was a linear relationship between both plasma and RBC cyanide concentrations and the total dose of SNP. The expired cyanide concentration followed the changes in the plasma. We believe that the development of metabolic acidosis, and the recent fatalities involving SNP, are attributable to histotoxic hypoxia as a result of excessive plasma concentrations of cyanide. On the basis of our results, we recommend that the total dose of SNP should not exceed 1.5 mg/kg during short-term infusions and that the plasma cyanide should not exceed 300 nmol%. Plasma thiocyanate concentrations are, in general, an unreliable indication of extent of exposure to cyanide, although they may become important during long-term infusions.

Adolescent↗
PubMedDate not supplied

Specific determination of cyanide in blood by headspace gas chromatography.

An improved method has been developed for the quantitative determination of cyanide in human blood by headspace gas chromatography with electron-capture detection. In this novel method, cyanide was detected after conversion of hydrogen cyanide into cyanogen chloride by a reaction with chloramine T. The advantage of this new procedure lies in the fact that hydrogen cyanide formation and chlorination are carried out in a single step and in the same reaction medium. This method is simple, rapid, and specific for cyanide and does not suffer from any interference by cyanate and thiocyanate. The detection limit is 5 micrograms/L. The detection response is linear from 5 to 1000 micrograms/L, and the within-run coefficient of variation in this range is 8% or less. This method is particularly useful for routine diagnostic analysis of biological samples in case of acute cyanide poisoning.

Chromatography, Gas↗
PubMed1985

Effects of protein-free diet and food deprivation on hepatic rhodanese activity, serum proteins and acute cyanide lethality in mice.

This study was undertaken to evaluate changes in hepatic and extra-hepatic cyanide detoxication resulting from nutritional deficits and any parallel changes in cyanide sensitivity. Male CD-1 mice were fed control diet, control diet in reduced quantities or protein-free diet. After 14 d body weight and relative liver size were lower in the protein-free diet and the food-deprived groups than in the control group. Hepatic and serum protein and albumin concentrations were lower in the protein-free diet group and hepatic protein and albumin concentrations were higher in the food-deprived group than in the control group. Hepatic rhodanese activity was higher in the protein-free diet group than in either of the other two groups. Compared to controls lethality was higher in the protein-free diet group when cyanide was administered in doses of 4 mg/kg body weight alone and 10.7 and 16.0 mg/kg body weight after thiosulfate pretreatment; but only higher in the food-deprived group at the higher dose cyanide given together with thiosulfate. These data suggest that hepatic rhodanese is not principally involved in the detoxication of cyanide even when exogenous thiosulfate is provided, nor does thiosulfate appear to exert its antidotal action by increasing the available cyanide-labile albumin-bound sulfane-sulfur.

Animals↗
PubMed1999

Azide- and cyanide-binding to the Escherichia coli bd-type ubiquinol oxidase studied by visible absorption, EPR and FTIR spectroscopies.

Cytochrome bd-type ubiquinol oxidase contains two hemes b (b(558) and b(595)) and one heme d as the redox metal centers. To clarify the structure of the reaction center, we analyzed Escherichia coli cytochrome bd by visible absorption, EPR and FTIR spectroscopies using azide and cyanide as monitoring probes for the exogenous ligand binding site. Azide-binding caused the appearance of a new EPR low-spin signal characteristic of ferric iron-chlorin-azide species and a new visible absorption band at 647 nm. However, the bound azide ((14)N(3)) anti-symmetric stretching infrared band (2, 010.5 cm(-1)) showed anomalies upon (15)N-substitutions, indicating interactions with surrounding protein residues or heme b(595) in close proximity. The spectral changes upon cyanide-binding in the visible region were typical of those observed for ferric iron-chlorin species with diol substituents in macrocycles. However, we found no indication of a low-spin EPR signal corresponding to the ferric iron-chlorin-cyanide complexes. Instead, derivative-shaped signals at g = 3.19 and g = 7.15, which could arise from the heme d(Fe(3+))-CN-heme b(595)(Fe(3+)) moiety, were observed. Further, after the addition of cyanide, a part of ferric heme d showed the rhombic high-spin signal that coexisted with the g(z) = 2.85 signal ascribed to the minor heme b(595)-CN species. This indicates strong steric hindrance of cyanide-binding to ferric heme d with the bound cyanide at ferric heme b(595).

Azides↗
PubMed2001

Effects of respiratory acidosis and alkalosis on the distribution of cyanide into the rat brain.

The aim of this study was to determine whether respiratory acidosis favors the cerebral distribution of cyanide, and conversely, if respiratory alkalosis limits its distribution. The pharmacokinetics of a nontoxic dose of cyanide were first studied in a group of 7 rats in order to determine the distribution phase. The pharmacokinetics were found to best fit a 3-compartment model with very rapid distribution (whole blood T(1/2)alpha = 21.6 +/- 3.3 s). Then the effects of the modulation of arterial pH on the distribution of a nontoxic dose of intravenously administered cyanide into the brains of rats were studied by means of the determination of the permeability-area product (PA). The modulation of arterial blood pH was performed by variation of arterial carbon dioxide tension (PaCO2) in 3 groups of 8 anesthetized mechanically ventilated rats. The mean arterial pH measured 20 min after the start of mechanical ventilation in the acidotic, physiologic, and alkalotic groups were 7.07 +/- 0.03, 7.41 +/- 0.01, and 7.58 +/- 0.01, respectively. The mean PAs in the acidotic, physiologic, and alkalotic groups, determined 30 s after the intravenous administration of cyanide, were 0.015 +/- 0.002, 0.011 +/- 0.001, and 0.008 +/- 0.001 s(-1), respectively (one-way ANOVA; p < 0.0087). At alkalotic pH the mean permeability-area product was 43% of that measured at acidotic pH. This effect of pH on the rapidity of cyanide distribution does not appear to be limited to specific areas of the brain. We conclude that modulation of arterial pH by altering PaCO2 may induce significant effects on the brain uptake of cyanide.

Acidosis, Respiratory↗