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PubMed1981

[Membrane potential of Pseudomonas aeruginosa spheroplasts having a cyanide-resistant respiration].

The membrane potential (delta psi) of Ps. aeruginosa spheroplasts was measured by a hydrophobic cation--tetraphenylphosphonium (TPP+) under conditions of simultaneous and separate action of the main respiratory chain and cyanide-resistant oxidase. In all cases, oxidation of endogenous substrates by spheroplasts was followed by generation of a membrane potential of the value of 127--156 mv. An addition of 1 mM cyanide did not practically affect the potential value. The discharge of the potential was attained by further addition of dicyclohexylcarbodiimide (DCCD) or valinomycin. The oxidation of the substrates added by the main respiratory chain was accompanied by an additional increase in the potential by 20--30 mv. In this case, an addition of cyanide decreased the potential by the same value. Oxidation of all substrates, except for TMPD+ ascorbate under conditions of functioning of cyanide-resistant oxidase also increased the potential by 15--50 mv. However, in this case cyanide did not practically affect the increase of the potential. The gain in the potential under TMPD + ascorbate oxidation by cyanide-resistant spheroplasts is prevented by cyanide. A question is discussed as to whether the transfer of reducing equivalents directly via cyanide-resistant oxidase is associated with the generation of a membrane potential or its functioning is not connected with the accumulation of energy in the form available for the cell.

Cyanides↗
PubMed1977

Interaction between ethyl methylene blue and cyanide-induced increases in blood lactate.

Previous workers have reported that ethyl methylene blue (EMB) diminishes cyanide-induced increases in blood lactate (CIL); the present study investigates the mechanism underlying this interaction. Accordingly, sodium cyanide (1.2 mg./Kg.) was infused into the abdominal aorta of anesthetized, spontaneously breathing dogs. Following cyanide infusion, arterial lactate concentration increased 5.4 +/- 1.1 mmol./L. and arterial PCO2 decreased 22 +/- 3 mm. Hg. A second group of dogs was pretreated with EMB (8 to 15 mg./Kg.); this dose of EMB elicited twofold increments in oxygen consumption and induced the formation in vivo of methemoglobin (0.8 +/- 0.1 gm./100 ml.). Following cyanide infusion, the increase in lactate in EMB animals was only 0.6 +/- 0.2 mmol./L.; the decrease in arterial PCO2 was limited to 5 +/- 1 mm. Hg. In order to clarify the relationship between cyanide-induced hypocapnia and CIL, cyanide was infused into a third group of dogs that were maintained isocapneic via mechanical ventilation; despite constancy of arterial PCO2, lactate increased 6.0 +/- 0.7 mmol./L. To determine the effect of EMB-induced tissue hypermetabolism on CIL, twofold increments in oxygen consumption were produced in a fourth group of dogs by pretreatment with sodium salicylate. Following cyanide infusion, salicylate-pretreated animals increased lactate 7.2 +/- 1.2 mmol./L. In order to assess the relationship between EMB-induced methemoglobinemia and the decrease in CIL, similar concentrations of methemoglobin were produced in two subsequent groups of dogs by two different techniques (i.e., by aniline pretreatment or by infusion of methemoglobinemic blood that had been prepared in vitro by addition of sodium nitrite). CIL in these animals was again markedly diminished (i.e., increments of only 0.6 +/- 0.3 mmol./L.) It is concluded that EMB diminishes CIL by a mechanism other than elimination of cyanide-induced hypocapnia or induction of tissue hypermetabolism. The results suggest that methemoglobin formation may completely account for the ability of EMB to effect a decrement in CIL.

Aniline Compounds↗
PubMed1996

Acute cyanide poisoning: clinical spectrum, diagnosis, and treatment.

Cyanide poisoning presents in many forms. Industrial intoxications occur due to extensive use of cyanide compounds as reaction products. Smoke inhalation, a polyintoxication, is most often responsible for domestic cyanide poisonings. Suicidal poisonings are rare. Cyanogenic compounds may produce acute or subacute toxicity. Signs of cyanide poisoning include headache, vertigo, agitation, confusion, coma, convulsions and death. Definitive laboratory confirmation is generally delayed. Elevated plasma lactate, associated with cardiovascular collapse, should suggest cyanide intoxication. Immediate treatment includes 100% oxygen, assisted ventilation, decontamination, correction of acidosis and blood pressure support. Antidotes include oxygen, hydroxocobalamin, di-cobalt EDTA and methaemoglobin-inducers. Hydroxocobalamin is an attractive antidote due to its rapid cyanide binding and its lack of serious side-effects, even in the absence of cyanide intoxication. Sodium thiosulphate acts more slowly than other antidotes and is indicated in subacute cyanogen poisoning and as an adjunct to acute cyanide poisoning. Initial evaluation of antidotal efficacy is based on correction of hypotension and lactic acidosis; the final analysis rests on the degree of permanent central nervous system injury.

Acute Disease↗
PubMed2002

Simultaneous determination of cyanide and carbonyls in cyanogenic plants by gas chromatography-electron capture/photoionization detection.

A new method to simultaneously detect cyanide and carbonyl compounds arising from cyanogenic glycosides in plants is described. A portable gas chromatograph.housing two detectors using a single carrier gas is employed to measure the carbonyl compounds (photoionization detector) and cyanide as its cyanogen chloride derivative (electron capture detector) from the headspace of a plant sample. This method affords in-field, rapid screening of plants to determine cyanogenicity. Good agreement was seen between this method for cyanide determination and two traditional field cyanide test kits. Detection of both the cyanide and the carbonyl compound(s) allows for confirmation of the presence of cyanogenic glycosides and eliminates the problem of false positives often seen in traditional cyanide test kits. Gas phase limits of detection for cyanide, acetone, butanone, and benzaldehyde were 69, 41, 105, and 0.39 parts per billion by volume (ppbv), respectively, allowing sensitive detection of cyanogenic glycoside breakdown products. The method's utility for screening cyanogenic plants is demonstrated, and it should be useful for screening cyanogenic foodstuffs to determine suitability for consumption.

Carbonyl Cyanide m-Chlorophenyl Hydrazone↗
PubMed1996

Nitrosyl cyanide, a putative metabolic oxidation product of the alcohol-deterrent agent cyanamide.

When incubated with catalase/glucose-glucose oxidase, 13C-labeled cyanamide gave rise not only to 13C-labeled cyanide, but also to 13C-labeled CO2. Moreover, a time-dependent formation of nitrite was observed when cyanamide was oxidized in this system. These results suggested that the initial product of cyanamide oxidation, viz. N-hydroxycyanamide, was being further oxidized by catalase/H2O2 to nitrosyl cyanide (O = N-C = N). Theoretically, nitrosyl cyanide can hydrolyze to the four end-products detected in the oxidative metabolism of cyanamide in vitro, viz. nitroxyl, cyanide, nitrite, and CO2. Accordingly, both unlabeled and 13C-labeled nitrosyl cyanide were synthesized by the low temperature (-40 to -50 degrees) nitrosylation of K-(18-crown-6)cyanide with nitrosyl tetrafluoroborate. The product, a faint blue liquid at this temperature, was transferred as a gas to phosphate-buffered solution, pH 7.4, where it was solvolyzed. Analysis of the headspace by gas chromatography showed the presence of N2O, the dimerization/dehydration product of nitroxyl, while cyanide was detected in the aqueous solution, as measured colorimetrically. [13C]CO2 was analyzed by GC/MS. An oxidative biotransformation pathway for cyanamide that accounts for all the products detected and involving both N-hydroxycyanamide and nitrosyl cyanide as tandem intermediates is proposed.

Alcohol Deterrents↗
PubMed2004

Recovery of cyanide in gold leach waste solution by volatilization and absorption.

In this study, the effects of pH, time and temperature in regeneration of cyanide in the leaching waste solution of gold production from disseminated gold ore by cyanidation process were investigated and the optimum conditions, consumptions and cyanide recovery values were determined. The sample of waste solution containing 156 mg/l free CN- and 358 mg/l total CN-, that was obtained from Gümüşhane-Mastra/Turkey disseminated gold ores by cyanidation and carbon-in-pulp (CIP) process under laboratory conditions was used in the experiments. Acidification with H2SO4, volatilization of hydrogen cyanide (HCN) with air stripping and absorption of HCN in a basic solution stages were applied and under optimum conditions, 100% of free cyanide and 48% of complex cyanide and consequently 70% of the total cyanide in the liquid phase of gold leach effluent are recovered.

Adsorption↗
PubMed1993

Purification and properties of cyanide hydratase from Fusarium lateritium and analysis of the corresponding chy1 gene.

The filamentous fungus Fusarium lateritium is cyanide tolerant, due, at least in part, to the induction by cyanide of the enzyme formamide hydrolyase (EC 4.2.1.66). This enzyme, more commonly known as cyanide hydratase, catalyses the hydration of cyanide to formamide. The enzyme was purified from F. lateritium and showed a subunit molecular mass of 43 kDa (as judged by SDS-PAGE), while the native protein appeared to form aggregates of up to 1217 kDa (as judged by gel-filtration and non-denaturing PAGE). mRNA samples from cultures grown with and without cyanide were in vitro translated and immunoprecipitated. This demonstrated that, in this species, the gene encoding the enzyme designated chy1, is cyanide inducible. Differential screening was used to isolate a cyanide hydratase cDNA clone which was subsequently used to obtain the corresponding genomic clone. A fragment of the cDNA clone encoding all but the first seven amino acids of the protein was expressed in E. coli using the expression vector pGEX-2T. Features of F. lateritium cyanide hydratase together with an analysis of the nucleotide sequence encoding this enzyme are presented.

Amino Acid Sequence↗
PubMed1992

Salicylic Acid induces cyanide-resistant respiration in tobacco cell-suspension cultures.

Cyanide-resistant, alternative respiration in Nicotiana tabacum L. cv Xanthi-nc was analyzed in liquid suspension cultures using O(2) uptake and calorimetric measurements. In young cultures (4-8 d after transfer), cyanide inhibited O(2) uptake by up to 40% as compared to controls. Application of 20 mum salicylic acid (SA) to young cells increased cyanide-resistant O(2) uptake within 2 h. Development of KCN resistance did not affect total O(2) uptake, but was accompanied by a 60% increase in the rate of heat evolution from cells as measured by calorimetry. This stimulation of heat evolution by SA was not significantly affected by 1 mm cyanide, but was reduced by 10 mm salicylhydroxamic acid (SHAM), an inhibitor of cyanide-resistant respiration. Treatment of SA-induced or uninduced cells with a combination of cyanide and SHAM blocked most of the O(2) consumption and heat evolution. Fifty percent of the applied SA was taken up within 10 min, with most of the intracellular SA metabolized in 2 h. 2,6-Dihydroxybenzoic and 4-hydroxybenzoic acids also induced cyanide-resistant respiration. These data indicate that in tobacco cell-suspension culture, SA induces the activity and the capacity of cyanide-resistant respiration without affecting the capacity of the cytochrome c respiration pathway.

Journal Article↗
PubMed1977

Contribution of a Cyanide-insensitive Alternate Respiratory System to Increases in Formamide Hydro-lyase Activity and to Growth in Stemphylium loti in Vitro.

Stemphylium loti, a pathogen of a cyanogenic plant, possesses a cyanide-insensitive alternate respiratory pathway. In the absence of cytochrome inhibitors, the alternate system had only a minor role in respiration. When S. loti was grown in medium amended with antimycin to block the cytochrome chain, the alternate system accounted for the total oxygen consumption associated with respiration.The contribution of the alternate respiratory system to increases in formamide hydro-lyase (FHL) activity and to growth in S. loti in vitro was assessed. FHL, induced by cyanide, converts cyanide to nontoxic formamide and is partially responsible for the tolerance of S. loti to high concentrations of cyanide in vitro. When the cytochromes were blocked and the cyanide-insensitive respiratory pathway accounted for 100% of the oxygen uptake associated with respiration, FHL activity, but not changes in dry weight, was positively correlated with activity of the alternate pathway. As the alternate pathway activity decreased with increasing concentrations of salicylhydroxamic acid, the level of FHL activity correspondingly decreased. The alternate respiratory system may provide for increases in FHL activity but not for growth. S. loti appears to have two mechanisms for cyanide tolerance in vitro: cyanide-insensitive respiration and FHL activity. The initial activity of FHL for detoxification of cyanide may depend on the alternate respiratory pathway when the cytochromes of the electron transport chain are blocked.

Journal Article↗
PubMed1983

Respiration of Gametangia of the Aquatic Phycomycete Allomyces macrogynus: Inhibition by Cyanide or Antimycin and Salicylhydroxamic Acid or Propyl Gallate.

Gametangia of the aquatic phycomycete Allomyces macrogynus have a cyanide- and antimycin A-insensitive respiration, which is sensitive to salicylhydroxamic acid (alternative respiration). Propyl gallate is also an inhibitor of this alternative pathway, and propyl gallate is more efficient than hydroxamic acid. Gametangial respiration is insensitive to propyl gallate, but propyl gallate sensitivity is gradually established when the gametangia are titrated with cyanide. Carbonyl cyanide m-chlorophenyl hydrazone stimulates the cyanide-sensitive respiration and engages the alternative sensitive respiration. Sodium azide inhibits both the alternative and the cyanide-sensitive respiration, but the cyanide-sensitive respiration is inhibited 10 times more efficiently than the alternative respiration. Rotenone inhibits the total respiration and the propyl gallate-insensitive respiration by 33% and the cyanide-insensitive respiration by 43%.The kinetic results reported here are discussed with respect to the models of de Troostembergh and Nyns (1977 Arch Int Physiol Biochem 85:404-406; 1978 Eur J Biochem 53:423-432) and of Bahr and Bonner (1973 J Biol Chem 248:3446-3450) for the partitioning of electrons between cyanide-insensitive and propyl gallate-insensitive respiration. The results reported here do not agree with the model of de Troostembergh and Nyns.

Journal Article↗
PubMed2002

Cytochrome P450 2E1 (CYP2E1) is essential for acrylonitrile metabolism to cyanide: comparative studies using CYP2E1-null and wild-type mice.

Acrylonitrile (AN) is a rodent carcinogen and suspected human carcinogen. Metabolism of AN proceeds via conjugation with glutathione or epoxidation via cytochrome P4502E1 (CYP2E1) to cyanoethylene oxide (CEO). It was hypothesized that CEO metabolism via epoxide hydrolase (EH) is the primary pathway for cyanide formation. The objective of this work is to assess the enzymatic basis of metabolism to cyanide. Male wild-type and CYP2E1-null mice received 0, 2.5, 10, 20, or 40 mg of AN/kg by gavage, and cyanide was measured in blood and tissues. CYP2E1 and EH expression were assessed using Western blot analyses. Present results demonstrated that cyanide concentrations in blood and tissues of AN-treated wild-type mice were higher at 1 versus 3 h, increased in a dose-dependent manner, and were significantly higher in AN-treated versus vehicle-treated mice. In contrast, cyanide concentrations in the blood and tissues of AN-treated CYP2E1-null mice were not statistically different from those of vehicle-treated mice. Furthermore, this work showed that EH is expressed in CYP2E1-null and wild-type mice. In conclusion, under the current experimental conditions using CYP2E1-null mice, current work demonstrated for the first time that CYP2E1-mediated oxidation is a prerequisite for AN metabolism to cyanide. Since earlier studies showed that CYP2E1 is the only enzyme responsible for AN epoxidation, it is concluded that AN metabolism to CEO is a prerequisite for cyanide formation, and this pathway is exclusively catalyzed by CYP2E1. Finally, this work confirmed that cyanide plays an essential role in the causation of the acute toxicity/mortality of AN.

Acrylonitrile↗
PubMed1987

The active site of aromatase cytochrome P-450. Differential effects of cyanide provide evidence for proximity of heme-iron and carbon-19 in the enzyme-substrate complex.

19-Norandrostenedione and androstenedione are shown to be metabolized by purified, reconstituted human placental aromatase cytochrome P-450. Kinetic evidence indicates that both steroids share a common catalytic site: 19-norandrostenedione is a competitive inhibitor of androstenedione aromatization, and the Ki value for its inhibition (120 nM) is similar to the Km value for its metabolism (132 nM). The two substrates differ, however, in their sensitivity to inhibition by the heme-iron ligand cyanide; 19-norandrostenedione is approximately 3-fold more sensitive to cyanide inhibition. Spectroscopic studies show that this differential inhibition by cyanide occurs because androstenedione competes with cyanide, whereas 19-norandrostenedione promotes cyanide binding to the heme-iron. It is proposed that these opposite effects on cyanide-iron coordination are due to the proximity of the heme-iron and C-19 of androstenedione in the enzyme-substrate complex, which results in steric exclusion of cyanide from the active site by the C-19 methyl group of androstenedione. Dioxygen is not excluded from binding to the heme-iron during catalysis, presumably because it bonds at an angle, in contrast to the linear bond of iron-cyanide complexes. A model for the active site of aromatase cytochrome P-450 is presented.

Aromatase↗
PubMed1994

Archean geochemistry of formaldehyde and cyanide and the oligomerization of cyanohydrin.

The sources and speciation of reduced carbon and nitrogen inferred for the early Archean are reviewed in terms of current observations and models, and known chemical reactions. Within this framework hydrogen cyanide and cyanide ion in significant concentration would have been eliminated by reaction with excess formaldehyde to form cyanohydrin (glycolonitrile), and with ferrous ion to form ferrocyanide. Natural reactions of these molecules would under such conditions deserve special consideration in modeling of primordial organochemical processes. As a step in this direction, transformation reactions have been investigated involving glycolonitrile in the presence of water. We find that glycolonitrile, formed from formaldehyde and hydrogen cyanide or cyanide ion, spontaneously cyclodimerizes to 4-amino-2-hydroxymethyloxazole. The crystalline dimer is the major product at low temperature (approximately 0 degrees C); the yield diminishes with increasing temperature at the expense of polymerization and hydrolysis products. Hydrolysis of glycolonitrile and of oxazole yields a number of simpler organic molecules, including ammonia and glycolamide. The spontaneous polymerization of glycolonitrile and its dimer gives rise to soluble, cationic oligomers of as yet unknown structure, and, unless arrested, to a viscous liquid, insoluble in water. A loss of cyanide by reaction with formaldehyde, inferred for the early terrestrial hydrosphere and cryosphere would present a dilemma for hypotheses invoking cyanide and related compounds as concentrated reactants capable of forming biomolecular precursor species. Attempts to escape from its horns may take advantage of the efficient concentration and separation of cyanide as solid ferriferrocyanide, and most directly of reactions of glycolonitrile and its derivatives.

Acetonitriles↗
PubMed1986

The efficacy of alpha-ketoglutaric acid in the antagonism of cyanide intoxication.

It has been reported that compounds containing carbonyl groups can readily react with cyanide. Pyruvic acid, an alpha-ketocarboxylic acid, has been shown to antagonize the lethal effects of cyanide. It is suggested that its mechanism of action rests in its ability to react with or "bind" cyanide. In this study, alpha-ketoglutaric acid, also an alpha-ketocarboxylic acid, was evaluated for its ability to counteract the lethal effects of cyanide. alpha-Ketoglutaric acid increased the LD50 value of cyanide (6.7 mg/kg) by a factor of five, a value statistically equivalent to that ascertained in mice pretreated with sodium thiosulfate and sodium nitrite. The combination of alpha-ketoglutaric acid and sodium thiosulfate increased the LD50 value of cyanide to 101 mg/kg. Addition of sodium nitrite to the alpha-ketoglutaric acid/sodium thiosulfate regimen increased the LD50 value of cyanide to 119 mg/kg. Unlike sodium nitrite, no induction of methemoglobin formation was observed with alpha-ketoglutaric acid pretreatment. It is apparent from these studies that the administration of alpha-ketoglutaric acid in conjunction with sodium thiosulfate resulted in fewer animal deaths than sodium nitrite and sodium thiosulfate without the dangerous formation of methemoglobin.

Animals↗
PubMedDate not supplied

Effect of cyanide binding on the copper sites of cytochrome c oxidase: an X-ray absorption spectroscopic study.

Cu x-ray absorption spectroscopy (XAS) has been used to investigate the effect of cyanide treatment on the structures of the copper sites in beef heart cytochrome c oxidase. The Cu K-edge spectrum changes significantly upon cyanide binding to resting state enzyme, as does the Cu extended x-ray absorption fine structure (EXAFS) spectrum. The Cu EXAFS Fourier transfer (FT) exhibits an enhanced peak for the cyanide-treated enzyme in the region containing the Cu...Fe peak in the resting state FT (at R' approximately equal to 2.6-2.7 A). This peak in the cyanide-treated sample is hypothesized to arise from "outer shell" scattering from a linear Cu-cyanide moiety, suggesting cyanide binding to CuB only (CuB 2+-CN-) or cyanide bridging between the Fe of heme a3 and CuB (Fe3+-(CN-)-CuB 2+).

Binding Sites↗
PubMed1990

Protection against cyanide-induced convulsions with alpha-ketoglutarate.

Protection against convulsions induced by cyanide was observed after treatment with alpha-ketoglutarate, either alone or in combination with sodium thiosulfate, a classical antagonist for cyanide intoxication. However, sodium thiosulfate alone did not protect against cyanide (30 mg/kg)-induced convulsions. gamma-Aminobutyric acid (GABA) levels in brain were decreased by 31% in KCN-treated mice exhibiting convulsions. The combined administration of alpha-ketoglutarate and sodium thiosulfate completely abolished the decrease of GABA levels induced by cyanide. Furthermore, sodium thiosulfate alone also completely abolished the decrease of GABA levels. These results suggest that the depletion of brain GABA levels may not directly contribute to the development of convulsions induced by cyanide. On the other hand, cyanide increased calcium levels by 32% in brain crude mitochondrial fractions in mice with convulsions. The increased calcium levels were completely abolished by the combined administration of alpha-ketoglutarate and sodium thiosulfate, but not affected by sodium thiosulfate alone. These findings support the hypothesis proposed by Johnson et al. (Toxicol. Appl. Pharmacol., 84 (1986) 464) and Robinson et al. (Toxicology, 35 (1985) 59) that calcium may play an important role in mediating cyanide neurotoxicity.

Animals↗
PubMed1995

Effect of atropine on cyanide-induced acute lethality in mice.

The effects of atropine on acute lethality induced by cyanide were investigated in mice. The LD50 value of cyanide (s.c. injection) was 8.4 (7.6-9.3) mg/kg. However, the LD50 value of cyanide (s.c.) was significantly increased by 1.5-fold when atropine (32 mg/kg) was injected s.c. in mice. Furthermore, the combined administration of atropine (32 mg/kg), Ca2+ (500 mg/kg) and sodium thiosulfate (1 g/kg) tremendously increased the LD50 value by 5.6-fold in mice although sodium thiosulfate or Ca2+ alone increased the LD50 2.5- or 1.5-fold. On the other hand, although the LD50 value of cyanide (intracerebroventricular injection (i.v.t.)) was 52.0 (47.4-57.0) micrograms/brain, the LD50 value of cyanide (i.v.t.) was significantly increased by 1.3- or 1.61-fold in mice 10 min after s.c. injection of atropine (32 mg/kg) or Ca2+ (500 mg/kg). Furthermore, the combined administration of atropine and Ca2+ increased the LD50 value of cyanide by 2.1-fold. These results suggest that atropine inhibits cyanide-induced acute lethality and promotes the antagonistic effect of thiosulfate and Ca2+ in mice.

Animals↗
PubMed1985

Influence of temperature and cyanide on electrical and mechanical activities of isoproterenol-damaged frog heart.

The electrical and mechanical activities of myocardial strips from Rana pipiens treated with isoproterenol (ISO) were studied during cyanide hypoxia at different bath temperatures (12, 25 and 35 degrees C). In normal myocardium at 12 degrees C, the action potential duration (APD) was almost unchanged but the isometric force (P) was reduced to about 60% after 30 min in 3 mmol/l NaCN. At 25 degrees C, APD and P decreased to about 80 and 60%, respectively, after exposure to cyanide for 30 min. At 35 degrees C, a fast decrease of APD (to about 30%) and P (to about 10%) was seen within 30 min. In all cases, washout of cyanide interactions was possible. Large effects occurred when ISO-damaged myocardium was exposed to cyanide. During the initial 30 min of CN-treatment, APD and P were significantly reduced in the whole temperature range between 12 and 35 degrees C, when compared with controls. When the cyanide exposure times were long enough, all preparations developed contracture. Increase of the temperature and/or ISO-pretreatment shortened the time-course for resting tension increase. The effects of cyanide on APD and resting tension (RT) were strongly correlated and presumably a result of a cyanide-induced rise of the intracellular free calcium concentration (Ca2+i).

Action Potentials↗