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PubMed2004

Ferrate(VI) oxidation of cyanide in water.

Experiments were conducted to test removal of cyanide (free cyanide and several cyanide complexes) in water, under alkaline medium (pH > or = 11), by a new potassium ferrate salt. The removal rate of free cyanide by oxidation with Fe(VI) was greater at pH 11.0 than at pH 12.0. A complete oxidation was obtained with a 2.67 Fe(VI)/CN ratio at pH 11.0. In these conditions, the rate of cyanide oxidation by Fe(VI) was slow, with a reaction rate constant estimated at 0.95 +/- 0.10 s(-1) l mol(-1) at pH 11.0 and 19.6 degrees C in this study. This study revealed that Fe(VI) did not decompose all cyanide complexes. Copper, cadmium and zinc complexes were removed efficiently by Fe(VI). Moreover, these metals were also removed from the solution by coagulation effect of Fe(OH)3, the Fe(VI) product of reaction. A particular behaviour was reported with copper, as a rapid oxidation of cyanide was observed in the presence of this metal. On the contrary, oxidation of nickel and silver complexes was incomplete.

Cyanides↗
PubMed2006

Development of a plant uptake model for cyanide.

A model for cyanide species uptake by willow (Salix eriocephala L. var. Michaux) was developed to interpret data from hydroponic experiments quantitatively. While the potential for cyanide phytoremediation has been demonstrated modeling will aid in determining plant processes that contribute to cyanide transport and metabolism in willow and will target specific physiological parameters for field-scale phytoremediation design and optimization. The objective of the model development was to gain insight into the relative role of different processes with respect to dissolved free and iron-complexed cyanide transport and assimilation in plants and to determine rates at which these processes occur within the willow plant under the experimental conditions. A physiologically-based model describing plant uptake, transport, and metabolism of cyanide species was developed to reflect the processes that influence the movement of cyanide into and throughout the plant. Plant compartmentalization (root, stem, and leaf) corresponded to the level of detail in the data collected via hydroponic experiments. Inclusion of more detailed intra- and intercellular processes would create a model inconsistent with the macroscale nature of the data. Mass balances around each compartment were developed via kinetic representations for the mass transfer processes and were combined to form a model describing the fate of cyanide species within plant-water systems.

Biodegradation, Environmental↗
PubMed1957

Experimentally induced chromosome abberrations in plants. II. The effect of cyanide and other heavy metal complexing agents on the production of chromosome aberrations by x-rays.

The discovery of Lilly and Thoday, that the presence of potassium cyanide (KCN) increases the production of chromosome aberrations by x-rays in anoxia, but has no effect on the production of chromosome aberrations by x-rays in air, was confirmed. In the presence of cyanide, the effect of a given dose of x-rays in nitrogen was found to be even greater than the effect of the same dose of x-rays in air. The cyanide effect on x-ray breakage in nitrogen was obtained at cyanide concentrations as low as 2 x 10(-5)M. The breakage obtained after the combined x-ray-cyanide treatments was of the x-ray type, as evidenced by the distribution of breaks within and between the chromosomes. A number of other heavy metal complexing agents as well as some other compounds were tested for their ability to increase x-ray breakage in nitrogen and air. Of these compounds only cupferron proved to be effective. The results are discussed and it is concluded that the increased x-ray breakage in the presence of cyanide or cupferron cannot be due to an accumulation of peroxides. Instead it is suggested that the cyanide effect may be due to a complex formation between the active agents and heavy metals, presumably iron, within the chromosomes. The consequences of this hypothesis on the concept of the "oxygen effect," are discussed.

Chromosome Aberrations↗
PubMedDate not supplied

Rapid determination of cyanide and azide in beverages by microdiffusion spectrophotometric method.

A rapid screening method was developed for the determination of the toxic volatile anions, cyanide and azide, in beverages. This method consisted of a microdiffusion extraction combined with spectrophotometry using the Konig cyanide reaction and ferric azide complex formation in conjugation with cerium azide oxido-reduction. The time required to achieve full recovery in the extraction of hydrogen cyanide and hydrazoic acid from samples was considerably shortened by increasing the diffusion temperature from 25 degrees C to 40 degrees C. The time required to achieve saturated color development in the Konig cyanide reaction was also shortened by increasing incubation temperature to 40 degrees C. The interference in both azide color reactions was examined for volatile compounds. Cyanide interfered only in the case of ferric azide complex formation. Sulfide, sulfate, nitrite, and acetic acid interfered in both the color reactions. The established method gave a detection limit of 6 microM for cyanide and 0.5mM for azide, and it required only 1 h to determine both anions. Cyanide and azide disappeared by evaporation from beverages during 25 degrees C storage under open conditions in a pH-dependent manner as a function of their respective pKa values of 9.2 and 4.6.

Azides↗
PubMed2000

Various nitric oxide donors protect chick embryonic neurons from cyanide-induced apoptosis.

The discovery of numerous biochemical effects of cyanide not directly related to the inhibition of the respiratory chain, including the involvement of apoptosis, has challenged the basis of traditional antidote treatment, which primarily depends on nitrite-induced conversion of hemoglobin into methemoglobin, releasing the blockade of cytochrome c oxidase by high-affinity binding of cyanide as cyanmethemoglobin. The fact that amyl nitrite has antidotal effects not related to methemoglobin formation has unfolded new mechanism of actions of nitrites including release of nitric oxide (NO). In this study, we characterized the effect of various NO donor compounds on cyanide-induced cell death in cultured chick embryonic neurons. Apoptosis was induced by treating the neuronal cultures with 1 mM NaCN for 1 h, followed by a cyanide-free incubation period of 23 h. Using this treatment protocol, we showed that cyanide-induced apoptosis was blocked in the presence of the different NO donors sodium nitroprusside, S-nitrosoglutathione, S-nitroso-N-acetylpenicillamin, nitroglycerin, 3-morpholinosydnonimine, and diethylamine nitric oxide, indicating independence of the redox-related species of NO released. The effect was confirmed to be mediated by NO, since exhausted NO donors did not afford protection, and the mechanism likely involved chemical modification of thiol groups, since the effect was completely reversed by dithiothreitol. Furthermore, NMDA antagonists protected against cyanide-induced cell death, whereas inhibitors of nitric oxide synthase increased cyanide-induced apoptotic damage, indicating a protective effect of endogenously generated NO, at least in cell cultures.

Animals↗
PubMed1997

Prevention of fetal and maternal cyanide toxicity from nitroprusside with coinfusion of sodium thiosulfate in gravid ewes.

Coadministration of sodium thiosulfate with sodium nitroprusside (SNP) to children and adults prevents increases in cyanide concentrations during anesthesia or long-term SNP infusions. We wondered whether maternally administered sodium thiosulfate would prevent increases in fetal red cell cyanide concentrations in gravid ewes receiving SNP infusions. Under anesthesia, the fetal head was delivered through a lateral hysterotomy for catheterization of the jugular vein; the fetus was left in utero. Six control ewes near term received SNP at 25 micrograms.kg-1.min-1 for 4 h. Norepinephrine was used to maintain maternal mean arterial pressure at 80% baseline values. Six experimental ewes received the same treatment except that sodium thiosulfate was infused with SNP (1 g sodium thiosulfate per 100 mg SNP). Serial red cell cyanide concentrations in ewes and fetuses were followed. One control fetal death resulted from abruptio placenta, and this ewe and fetus were excluded from analysis. An additional control ewe and fetus died from apparent cyanide poisoning late during the course of the experiment. While control ewes and fetuses suffered progressive increases in red cell cyanide concentrations into the toxic range, experimental ewes and fetuses never developed toxic red cell cyanide levels (ewes P < .003, fetuses P < .004). These data, if applicable to humans, suggest that coadministration of sodium thiosulfate with SNP to pregnant women at doses currently in use for nonpregnant patients will prevent fetal, as well as maternal, cyanide toxicity.

Animals↗
PubMed1990

Measurement of blood cyanide with a microdiffusion method and an ion-specific electrode.

The use of a cyanide ion-specific electrode in combination with the Conway microdiffusion method was modified for the measurement of cyanide concentration in human red blood cells and plasma. With our modified method, the optimal pH of cyanide isolation from red blood cells and plasma was investigated. Cyanide recovery from red blood cells increased with decreasing pH. The maximal recovery of 96.9 +/- 2.6% was obtained at a pH of less than 1. Cyanide recovery from plasma, however, peaked at a pH between 7 and 8, and further changes in pH reduced the recovery rate. The maximal recovery rate from plasma was 74.1 +/- 1.5%. In previous studies, cyanide isolations from both plasma and red blood cells were carried out at a pH of less than 1. This study shows that cyanide isolation from plasma should be performed at a pH between 7 and 8.

Blood Chemical Analysis↗
PubMed2000

Cyanide inhibits respiration yet stimulates aerobic growth of Zymomonas mobilis.

Potassium cyanide at submillimolar concentrations (20-500 microM) inhibited the high respiration rates of aerobic cultures of Zymomonas mobilis but, remarkably, stimulated culture growth. In batch culture, after an extended lag phase, exponential growth persisted longer, resulting in higher biomass densities. In aerobic chemostat cultures, elevated biomass concentration was observed in the presence of cyanide. This growth stimulation effect is attributed to decreased production of the inhibitory metabolite acetaldehyde at lowered respiration rates, when more reducing equivalents are channelled to alcohol dehydrogenase. Growth in the presence of cyanide did not alter the membrane cytochrome content. In non-growing cyanide-preincubated cells, with ethanol as the respiratory substrate, cyanide increased ATP levels; in such cells, a large part of the cyanide-sensitive respiration was inhibited within a few seconds after ethanol addition, while inhibition of the rest of respiration took several minutes. The more cyanide-sensitive respiration was apparently energy-nongenerating, and was absent in membrane preparations. Pelleting of membranes from cell-free extracts produced 'soluble' fractions in which a b-type haem was detectable by reduced minus oxidized difference spectroscopy. The function of the Z. mobilis respiratory chain in cell growth and respiratory protection, and the possible physiological role of aerobic generation of inhibitory metabolites, are discussed.

Acetaldehyde↗
PubMed1981

Mechanism of the effect of cyanide on cell membrane potentials in Necturus gall-bladder epithelium.

1. Addition of sodium cyanide to the mucosal or the serosal medium bathing the isolated gall-bladder of Necturus maculosus causes hyperpolarization of both apical and basolateral membrane of the epithelial cells. The effect of cyanide is practically immediate, reversible (if exposure is brief), and long-lasting (greater than 30 min). 2. The hyperpolarization is accompanied by: (a) reduction of the equivalent resistance of the cell membranes, as shown by cable analysis and input resistance measurements, and (b) increase of the potassium selectivity of both cell membranes, as evidenced by the effects of external substitutions of potassium for sodium on cell membrane potentials. We conclude that the cyanide-induced hyperpolarization is caused mainly or exclusively by an increase of the potassium permeability of the cell membranes. 3. Addition of the calcium ionophore A23187 (5 microM) to the mucosal medium in the presence of 1 mM-calcium caused similar effects to those produced by cyanide. After either cyanide or A23187, addition of the other agent did not cause further membrane potential changes. 4. Quinine (100 microM, mucosal medium) reduced the potassium permeability of the apical membrane both under control conditions and during exposure to cyanide. 5. We suggest that the cyanide-induced increase of the potassium permeability of the cell membrane is mediated by an elevation of intracellular calcium ion activity, attributable to release from mitochondrial sources.

Absorption↗
PubMed2000

Cyanide increases reduction but decreases sequestration of methylene blue by endothelial cells.

The mechanisms of endothelial cell transplasma membrane electron transport (TMET) have not been completely identified. Redox probes such as methylene blue (MB) can be useful tools, but the complexity of their disposition upon exposure to the cells can hinder interpretation. For example, MB is reduced on the cell surface by TMET, but after entering the cell in reduced form, it is reoxidized and sequestered within the cell. We developed a method to separately quantify the reduction and reoxidation rates such that it can be determined whether a metabolic inhibitor such as cyanide affects the reduction or oxidation process. MB was introduced at the inlet to a column filled with endothelial cell covered beads either as a short 12 s injection (bolus) or a long 45 min infusion (pulse), and its effluent concentration was measured as a function of time. The cells extracted 56% of the MB from the bolus, but only 41% during the pulse steady state. In the presence of cyanide, these extractions increased to 70% and decreased to 4%, respectively. Mathematical model results support the interpretation that these paradoxical effects on bolus and pulse extractions reflect the differential effects of cyanide on extracellular reduction and intracellular oxidation, i.e., cyanide increased the reduction rate from 7.3 to 13.0 cm s-1 X 10(-5) and decreased the oxidation rate from 1.09 to 0.02 cm s-1 X 10(-3). Cyanide also increased intracellular NADH by almost eight times, suggesting that TMET is sensitive to the cell redox status, i.e., NADH is a direct or indirect electron source. The cyanide-induced decrease in sequestration indicates a cyanide-sensitive intracellular oxidation mechanism. The results also demonstrate the potential utility of this approach for further evaluation of these endothelial redox mechanisms.

Animals↗
PubMed2005

Up-regulation of uncoupling protein 2 by cyanide is linked with cytotoxicity in mesencephalic cells.

Uncoupling protein 2 (UCP-2) regulates mitochondrial function by increasing proton leak across the inner membrane to dissociate respiration from ATP synthesis and reduce reactive oxygen species generation. A number of studies have shown that UCP-2 expression protects cells from oxidative stress mediated injuries. In the current study, we show UCP-2-mediated reduction in mitochondrial function contributes to the mitochondrial dysfunction and the necrotic death of primary cultured mesencephalic cells (MCs) after exposure to cyanide, a complex IV inhibitor. The necrotic cell death was directly related to the level of mitochondrial dysfunction, as shown by reduction in ATP levels and decreased mitochondrial membrane potential. Treatment with cyanide for 6 h or longer upregulated UCP-2 expression. Blockade of up-regulation with a transcription or a translational inhibitor reduced the response to cyanide. Knockdown with RNAi or transfection with a UCP-2 dominant-negative interfering mutant reduced the cyanide-induced mitochondrial dysfunction and cell death, showing that constitutive expression of UCP-2 plays a role in the response to cyanide. Overexpression of UCP-2 by transfection with human full-length cDNA potentiated the cyanide toxicity. These findings indicate that UCP-2 can serve as a regulator of mitochondria-mediated necrotic cell death, in which enhanced expression can increase the vulnerability of primary MCs to injury due to complex IV-mediated inhibition by cyanide.

Adenosine Triphosphate↗
PubMed2004

Enzymatic assimilation of cyanide via pterin-dependent oxygenolytic cleavage to ammonia and formate in Pseudomonas fluorescens NCIMB 11764.

Utilization of cyanide as a nitrogen source by Pseudomonas fluorescens NCIMB 11764 occurs via oxidative conversion to carbon dioxide and ammonia, with the latter compound satisfying the nitrogen requirement. Substrate attack is initiated by cyanide oxygenase (CNO), which has been shown previously to have properties of a pterin-dependent hydroxylase. CNO was purified 71-fold and catalyzed the quantitative conversion of cyanide supplied at micromolar concentrations (10 to 50 micro M) to formate and ammonia. The specific activity of the partially purified enzyme was approximately 500 mU/mg of protein. The pterin requirement for activity could be satisfied by supplying either the fully (tetrahydro) or partially (dihydro) reduced forms of various pterin compounds at catalytic concentrations (0.5 micro M). These compounds included, for example, biopterin, monapterin, and neopterin, all of which were also identified in cell extracts. Substrate conversion was accompanied by the consumption of 1 and 2 molar equivalents of molecular oxygen and NADH, respectively. When coupled with formate dehydrogenase, the complete enzymatic system for cyanide oxidation to carbon dioxide and ammonia was reconstituted and displayed an overall reaction stoichiometry of 1:1:1 for cyanide, O(2), and NADH consumed. Cyanide was also attacked by CNO at a higher concentration (1 mM), but in this case formamide accumulated as the major reaction product (formamide/formate ratio, 0.6:0.3) and was not further degraded. A complex reaction mechanism involving the production of isocyanate as a potential CNO monooxygenation product is proposed. Subsequent reduction of isocyanate to formamide, whose hydrolysis occurs as a CNO-bound intermediate, is further envisioned. To our knowledge, this is the first report of enzymatic conversion of cyanide to formate and ammonia by a pterin-dependent oxygenative mechanism.

Ammonia↗
PubMed2001

Pseudomonas aeruginosa PAO1 kills Caenorhabditis elegans by cyanide poisoning.

In this report we describe experiments to investigate a simple virulence model in which Pseudomonas aeruginosa PAO1 rapidly paralyzes and kills the nematode Caenorhabditis elegans. Our results imply that hydrogen cyanide is the sole or primary toxic factor produced by P. aeruginosa that is responsible for killing of the nematode. Four lines of evidence support this conclusion. First, a transposon insertion mutation in a gene encoding a subunit of hydrogen cyanide synthase (hcnC) eliminated nematode killing. Second, the 17 avirulent mutants examined all exhibited reduced cyanide synthesis, and the residual production levels correlated with killing efficiency. Third, exposure to exogenous cyanide alone at levels comparable to the level produced by PAO1 killed nematodes with kinetics similar to those observed with bacteria. The killing was not enhanced if hcnC mutant bacteria were present during cyanide exposure. And fourth, a nematode mutant (egl-9) resistant to P. aeruginosa was also resistant to killing by exogenous cyanide in the absence of bacteria. A model for nematode killing based on inhibition of mitochondrial cytochrome oxidase is presented. The action of cyanide helps account for the unusually broad host range of virulence of P. aeruginosa and may contribute to the pathogenesis in opportunistic human infections due to the bacterium.

Animals↗
PubMed1993

Protection against cyanide poisoning by the co-administration of sodium nitrite and hydroxylamine in rats.

1. The protectiveness of combined treatment with sodium nitrite (SN) and hydroxylamine (HA) in cyanide intoxication was investigated in male rats. 2. Pretreatment with equimolar dose of SN or HA produced a significant protection against cyanide poisoning as shown by the protection index (LD50 of cyanide in protected rats/LD50 of cyanide in saline-treated rats). 3. The co-administration of SN and HA as a split dose produced an optimal and sustained methaemoglobinaemia. 4. Pretreatment with combined SN and HA administration at different time intervals offered sustained protection against cyanide and resultant cytochrome oxidase inhibition. 5. Adjunction of sodium thiosulphate (STS) in the SN+HA regimen further augmented the protection against cyanide poisoning. 6. The results suggest that pretreatment with SN+HA co-administration could significantly reduce the toxic manifestation of cyanide.

Animals↗
PubMed1992

Cyanide toxicity from sodium nitroprusside: risks and management.

OBJECTIVE: To review the risks, manifestations, and treatment of cyanide toxicity from nitroprusside therapy. DATA SOURCES: All English case reports identified in Index Medicus (MEDLINE) of cyanide intoxication related to nitroprusside from 1970 to the present were reviewed. In addition, literature regarding the incidence, risks, and treatment of cyanide toxicity from nitroprusside is presented. CONCLUSIONS: Numerous cases of cyanide toxicity associated with nitroprusside have been reported. The overall incidence appears to be infrequent; however, certain patients may be at high risk. Risk factors may include hypoalbuminemia, cardiopulmonary bypass procedures, or the administration of moderate to high doses of nitroprusside. Treatment of cyanide toxicity requires the cessation of nitroprusside and, for severe toxicity, use of the cyanide antidote kit. Cyanide toxicity from nitroprusside may be prevented by concomitant administration of sodium thiosulfate infusions.

Adolescent↗
PubMed1977

Hepatic aminopyrine N-demethylase system: effect of cyanide on microsomal N-demethylase activity.

Cyanide, an inhibitor of many hemoproteins, was shown to affect a number of microsomal drug-metabolizing activities catalyzed by cytochrome P-450. The N-demethylation reaction of aminopyrine was inhibited noncompetitively by this inhibitor in microsomal preparations from rats. The binding reaction of aminopyrine with microsomal cytochrome P-450 was also modified by cyanide, and an abnormal aminopyrine-induced difference spectrum of microsomes by cyanide, and an abnormal aminopyrine-induced difference spectrum of microsomes appeared when cyanide was added to the reaction mixture. Partial dissociation of cytochrome P-450. Cyanide complex by aminopyrine was observed by spectrophotometrical and epr spectroscopic methods. These results suggest that aminopyrine and cyanide reciprocally affect binding with cytochrome P-450 and modification by cyanide of aminopyrine binding reaction with the hemoprotein produces an inhibition of N-demethylase activity.

Aminopyrine↗
PubMedDate not supplied

The occurrence of cyanide formation in six full-scale publicly owned treatment works.

This paper presents results from an intensive monitoring program implemented at six full-scale publicly owned treatment works (POTWs) to investigate the fate and formation of cyanide in wastewater treatment processes, with a focus on chlorination and dechlorination processes. A review of historical monitoring data for cyanide species in these POTWs was also conducted. This POTW monitoring program provided a database for the investigation of cyanide formation in wastewater secondary treatment. Data from participating POTWs showed evidence of cyanide formation in this 1-year monitoring effort, although the cyanide formation pattern varied significantly from one plant to another and among seasons. Generally, the chlorination of thiocyanate (SCN-) seems to be the most important mechanism for the formation of cyanide in wastewater treatment processes, especially in chlorination and dechlorination. This hypothesis is supported by the findings of a related laboratory study of mechanisms of cyanide formation in POTWs. It is recommended that POTWs monitor SCN in influent and secondary effluent to identify its presence and adjust chlorine dose appropriately.

Chlorine Compounds↗
PubMedDate not supplied

Insights to false positive total cyanide measurements in wastewater plant effluents.

Many publicly owned treatment works in North America are exceeding permitted limits for total cyanide in their wastewater treatment effluents. A recently introduced rapid, segmented, flow-injection analysis procedure using UV digestion and amperometric detection of the membrane-separated cyanide was used to investigate the various scenarios by which elevated cyanide levels might be present in wastewater treatment plant effluent. A number of significant interferences can produce false positive bias during sample analysis with the traditional acid distillation technique, but are minimized or absent with the new analytical method. However, increased levels of cyanide were found in some chlorinated wastewaters compared to the levels before chlorination, suggesting a fast reaction mechanism associated with the disinfectant and some precursor in the wastewater. In particular, the contact of chlorine with nitrite in the presence of a carbon precursor appears to contribute to cyanide formation during wastewater treatment and sample handling. This paper explores the scenarios under which cyanide can form during wastewater treatment as well as those in which a false bias for total cyanide can be obtained during sample processing and provides guidance for appropriate sample handling, screening, and processing to ensure valid analytical results.

Chemistry Techniques, Analytical↗