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PubMed1985

Different effects of cyanide on the activities of 7-ethoxycoumarin O-deethylation catalyzed by two forms of cytochrome P-450 purified from 3-methylcholanthrene-treated rats.

The effect of cyanide on 7-ethoxycoumarin O-deethylation by two cytochrome P-450 isozymes obtained from 3-methylcholanthrene treated rat liver microsomes was investigated. 7-Ethoxycoumarin O-deethylation was stimulated by the addition of cyanide to a reconstituted monooxygenase system consisting of NADPH, dilauroyl 3-L-phosphatidylcholine, NADPH-cytochrome P-450 reductase and MC P-448(2) (low spin form of cytochrome). In contrast, a weak inhibitory effect of cyanide on 7-ethoxycoumarin O-deethylation was observed when MC P-448(1) (high spin form of cytochrome) was used in the reconstituted system. Cyanide did not influence the apparent Km for 7-ethoxycoumarin when either form of cytochrome P-450 was used in the reconstituted system and did not stimulate the cumene hydroperoxide dependent O-deethylation by MC P-448(2). The stimulatory effect of cyanide on O-deethylation by MC P-448(2) was decreased with increasing the concentration of the reductase added to the reconstituted system. On the other hand, the effect of cyanide on O-deethylation by MC P-448(1) was virtually independent on the amount of the reductase added.

7-Alkoxycoumarin O-Dealkylase↗
PubMed1990

Cyanide-induced neurotoxicity: calcium mediation of morphological changes in neuronal cells.

Calcium channel blockade decreases the elevation of brain calcium as well as the tremors produced by cyanide in mice. To determine if cyanide-induced morphological changes could also be inhibited by calcium channel blockade, the effect of diltiazem was studied in cultured rat pheochromocytoma (PC12) cells, a neuronal model. Incubation with KCN (1 to 10 mM for 1 to 2 hr) caused depletion of secretory granules, alignment of remaining granules along the plasma membrane, and mitochondrial swelling. All these effects were inhibited by pretreatment with 0.01 mM diltiazem. Scanning electron microscopy revealed that cyanide (1 to 10 mM for 1 to 2 hr) produced loss of microvilli and bleb formation in PC12 cells. These changes were partially inhibited by preincubation with 0.01 mM diltiazem. Incubation of cells with 10 mM cyanide increased release of lactic dehydrogenase (LDH) into the culture media at 60 and 120 min. A decrease in cell viability, as determined by trypan blue dye exclusion, paralleled the release of LDH. At 120 min of cyanide incubation, 24% of the cells excluded dye. Both the release of LDH and decreased cell viability were attenuated by pretreatment with diltiazem. The results indicate that the influx of extracellular calcium is an important factor mediating cyanide-induced morphologic changes in neuronal cells.

Animals↗
PubMed1984

Changes in glucose metabolism and cyanide sensitivity in Schistosoma mansoni during development.

Schistosoma mansoni was studied by biochemical and electrophysiological techniques to follow the physiological changes occurring during transformation in the mammalian host. Volume conducted electrical potentials and measurement of CO2 evolution indicate that 3 h post-transformational schistosomula are highly sensitive to cyanide. By 24 h after transformation, evolution of CO2 under control conditions is reduced by 77% from 3 h levels, while lactate excretion rises by 84%. Cyanide does not affect the frequency or magnitude of endogenous electrical transients, but does eliminate 83% of the already reduced levels of CO2 evolved in 24 schistosomula. Electrophysiological analyses indicate that the timecourse of metabolic changes in skin- and mechanically transformed schistosomula are similar, and incubation of schistosomula in 200 micrograms ml-1 puromycin does not alter the onset of cyanide insensitivity. The adult parasite evolves a low level of CO2 which is reduced by 88% in the presence of 1 mM cyanide. No significant Pasteur effect is detected, however, and endogenous electrical activity as well as mechanical responses of the adult musculature are unaffected by cyanide exposure. Our results indicate that schistosomula continue to rely on cyanide-sensitive respiratory components for at least 3 h after transformation; by 24 h, however, the parasites are metabolically similar to the adult stage, i.e., they depend on lactate fermentation for most of their energy requirements.

Aerobiosis↗
PubMed1989

Brain lipid peroxidation and antioxidant protectant mechanisms following acute cyanide intoxication.

The status of brain antioxidant enzymes and glutathione levels in mice intoxicated with KCN were correlated with lipid peroxidation in brain membranes. KCN (7 mg/kg, s.c.) rapidly increased conjugated dienes in brain lipids, with peak levels observed 30 min after cyanide treatment. At 60 min post cyanide, conjugated diene levels were only slightly elevated above controls. Temporal changes in activity of most antioxidant enzymes corresponded with the observed time course of cyanide-induced membrane lipid peroxidation. Thirty minutes after KCN, brain catalase (CA), glutathione peroxidase (GPX) and glutathione reductase (GR) activities were significantly reduced (percent inhibition compared to control: CA 44%, GPX 30%, and GR 41%). At 60 min, CA and GPX enzyme activity returned to control levels, whereas GR was elevated 34% above control activity. Superoxide dismutase was not significantly inhibited 30 min after KCN, but declined to 71% of control activity at 60 min. Brain levels of reduced glutathione declined 42% below control 30 min after cyanide and returned to within 9.4% of control at 60 min. At 30 and 60 min after cyanide, oxidize glutathione levels were not significantly changed from control levels. These studies suggest that membrane lipid peroxidation and subsequent membrane dysfunction observed in cyanide intoxication is related in part to a compromised antioxidant defense.

Animals↗
PubMedDate not supplied

Chronic cyanide exposure--A biochemical and industrial hygiene study.

A study was undertaken to assess the health status of workers exposed to cyanide fumes and cyanide aerosols in one of the local factories. Cyanide levels in the breathing zone and the working atmosphere were measured. Cyanide and thiocyanate concentrations in blood and urine were determined colorimetrically. The cyanide and thiocyanate concentrations in blood and urine of exposed workers were much higher than those of control workers. Smokers had higher concentrations than nonsmokers. The highest values of cyanide were found to be 0.8 and 0.2 mg/m3 in the breathing zone and general workroom atmosphere respectively. In spite of such low values, the workers complained of typical HCN poisoning. It is suggested that MAC values of 5 mg/m3 (in terms of CN) should be reviewed in respect to conditions in India.

Adult↗
PubMed1983

The effects of cyanide on the growth and respiration of Enterobacter aerogenes in continuous culture.

The effect of cyanide on the physiology of lactate- and oxygen-limited Enterobacter aerogenes NCTC 10336 was studied in chemostat culture (D = 0.1 h-1). In the absence of cyanide, the molar growth yield from oxygen (YO2) under oxygen limitation was 60% of the carbon-limited value. A similar decrease in yield was observed in a lactate-limited culture (excess oxygen) which was continuously fed low concentrations of potassium cyanide. The cultures with the lower growth yields possessed respiratory systems less sensitive to inhibition by cyanide. This was particularly marked in cultures grown in the presence of cyanide. Increased cyanide resistance was associated with an increase in the concentration of a cytochrome oxidase tentatively identified as a d-type and the appearance of additional cytochromes tentatively identified as b-type.

Cyanides↗
PubMed1978

Red cell cyanide.

The amount of cyanide released on acidifying whole blood was much greater than the total from the plasma and red cells assayed separately, and varied directly with plasma thiocyanate concentrations. This artifactual formation of cyanide by whole blood was reduced by exposure to carbon monoxide. Incubation of haemolysates of washed red blood cells showed that optimum cyanide production from thiocyanate occurred at pH 4.5 with none at pH 7.4; spectrophotometric study confirmed the involvement of haemoglobin. It is doubtful whether this activity of haemoglobin is of normal physiological importance and it is probable that the evidence for the enzyme, 'thiocyanate oxidase' was based on this artifact of assay. Plasma cyanide is probably the metabolically relevant measurement, since the red blood cells act as a 'cyanide sink'. Where values for whole blood cyanide are required we recommend separate assay of plasma and saline washed red blood cells.

Cyanides↗
PubMed1999

Biodegradation of cyanide compounds by a Pseudomonas species (S1).

A Pseudomonas sp. (S1), isolated from soil by an enrichment technique was tested for its potential to degrade different cyanide compounds. Further, biodegradation/biotransformation of binary mixtures of the cyanide compounds by the culture was also studied. The results indicated that the culture could grow on the following nitriles by using them as carbon and nitrogen sources: acetonitrile, butyronitrile, acrylonitrile, adiponitrile, benzonitrile, glutaronitrile, phenylacetonitrile, and succinonitrile. Studies on the biodegradation of these cyanide compounds in binary mixtures showed that the presence of acrylonitrile or KCN delayed the degradation of acetonitrile in a mixture, while none of the other cyanide compounds affected the degradation of one another. The transformation products of the nitriles were their corresponding acids, and similarly, KCN was also directly transformed to formic acid. Studies on the transformation of these cyanide compounds showed that the rate of transformation of nitriles to their corresponding carboxylic acids was acrylonitrile > acetonitrile > adiponitrile > benzonitrile > KCN. This culture has the unique characteristic of transforming representatives of saturated aliphatic, aliphatic olefinic, aromatic, and aralkyl nitriles, as well as alkali cyanide, to their corresponding carboxylic acids.

Acetonitriles↗
PubMed1989

Sodium cyanide and its rapid detoxification by grape juice.

Recently media attention has been focused on minute traces of cyanide found in grapes supposedly injected with cyanide. No more than minute traces of cyanide are likely to be found within a few hours of cyanide ion injection into grapes. Free cyanide ion in grape juice is quickly converted to ammonia upon spontaneous saponification of the cyanohydrins rapidly formed from the reaction of cyanide with sugars. Mice offered 10-fold diluted grape juice 24 hr after the addition of 2 g NaCN/100 ml juice showed no evident signs of illness for a period of 1 week during which access to all other fluids was denied.

Animals↗
PubMed1985

Studies of cyanide poisoning.

The use of amyl nitrite and phenoxybenzamine in the treatment of acute cyanide poisoning was evaluated. Sixty anesthetized beagle dogs were injected i.v. with sodium cyanide (2.5 mg/kg) and were followed for changes in the heart rate, electrocardiogram, respiration, blood pressure and methemoglobin concentration. Twenty control dogs died within 5 to 7 min, showing severe bradycardia, a sharp drop in arterial blood pressure, and respiratory paralysis. Pretreatment with phenoxybenzamine (0.5 mg/kg) prevented these changes in 8 of 10 dogs; however, this drug was ineffective if given after the cyanide. In contrast, amyl nitrite given after cyanide administration reversed both the cardiovascular changes and the respiratory paralysis in 24 of the 30 dogs studied. These changes occurred before the formation of significant amounts of methemoglobin and indicate that early death caused by cyanide may be due in part to cardiovascular-respiratory failure in addition to the classic poisoning of the cytochrome oxidase system. These studies indicate that phenoxybenzamine prevents and amyl nitrite reverses the otherwise lethal effects of cyanide.

Amyl Nitrite↗
PubMedDate not supplied

Interaction of carbon monoxide and cyanide on cerebral circulation and metabolism.

Significant elevations of carboxyhemoglobin and blood cyanide have been found in fire victims. The nature of the interaction of acute exposures to these agents is unclear. This study was undertaken to describe the of cyanide and carbon monoxide--alone and in combination--on the circulation and metabolism of the brain in anesthetized dogs. Cerebral blood flow increased to 130 and 200% of control with elevations in carboxyhemoglobin to 30 and 51% or with elevations in blood cyanide to 1.0 and 1.5 microgram/ml, respectively. Cerebral oxygen consumption remained unchanged until the higher level of carbon monoxide or cyanide was reached. When carbon monoxide and cyanide were administered simultaneously, cerebral blood flow increased in an additive manner, but significant decreases in cerebral oxygen consumption occurred at the combination of the lower concentrations. These data suggest that carbon monoxide and cyanide are physiologically additive on producing changes in cerebral blood flow, but may act synergistically on cerebral metabolism.

Animals↗
PubMed1988

Mammalian cyanide detoxification with sulphane sulphur.

It has been understood for nearly a century that most of the cyanide entering mammals by either ingestion or inhalation of sublethal quantities is detoxified by combination with cyanide-reactive sulphur. The detoxifying reaction is primarily enzymic, and the enzymes that catalyse it, as well as those that catalyse reactions which generate the cyanide-reactive sulphane sulphur, have been isolated and studied extensively. However, analytical methods suitable for quantitative characterization of the physiological pool of sulphur available for this detoxification have only recently come under development. A new method is based on the evaluation of cyanide depletion under controlled, mild reaction conditions in the presence of a sulphurtransferase and cofactor. The use of differential pulse polarography with nested internal standards makes this a practical procedure for samples containing as little as a few nanomoles of cyanide-reactive material. As measured by this method, the sulphane sulphur concentration in mammalian liver tissue is in the fractional millimolar range, with even less in the bloodstream. Nevertheless, the specific binding of sulphane sulphur by serum albumin, and the rapid cyanolysis of the albumin-bound sulphur, may yet indicate a significant role for the sulphurtransferase capability of serum albumin in cyanide detoxification.

Animals↗
PubMed2006

Headspace single-drop microextraction with in-drop derivatization and capillary electrophoretic determination for free cyanide analysis.

A new method involving headspace single-drop microextraction (SDME) with in-drop derivatization and CE is developed for the preconcentration and determination of free cyanide. An aqueous microdrop (5 microL) containing Ni(II)-NH(3) (as derivatization agent), sodium carbonate and ammonium pyromellitate (as internal standard) was used as the acceptor phase. The extracted cyanide forms a stable Ni(CN)(4) (2-) complex which is then determined by CE. Common experimental parameters (sample and acceptor phase pH, extraction temperature, extraction time and sample ionic strength) affecting the extraction efficiency were investigated. Using headspace SDME, free cyanide can be effectively extracted from the neutral solutions, i.e. without the acidification of the sample which often is prone to errors due to incomplete liberation and artefactual cyanide production. Proposed SDME-CE method provided about 58-fold enrichment in 20 min. The calibration curve was linear for concentrations of CN(-) in the range from 0.25 to 20 micromol/L (R(2) = 0.997). The LOD (S/N = 3) was estimated to be 0.08 micromol/L of CN(-). Such a detection sensitivity is high enough for free cyanide determination in common environmental and physiological samples. Finally, headspace SDME was applied to determine free cyanide in human saliva and urine samples with spiked recoveries in the range of 91.7-105.6%. The main advantage of this method is that sample clean-up, preconcentration and derivatization procedures can be completed in a single step. In addition, the proposed technique does not require any sample pretreatment and thus is much less susceptible to interferences compared to existing methods.

Cyanides↗
PubMed1985

Attempts to use cyanide ion to trap imine intermediates in the microsomal N-dealkylation of propranolol: formation of alpha-aminonitriles as artifacts when using ether for extraction.

Cyanide anion was used to attempt to trap possible imine intermediates in the oxidative N-dealkylation of propranolol (1). Reaction of 3-(1-naphthoxy)-1-amino-2-propanol (desisopropylpropranolol, 2) with acetone provided this expected intermediate in an approximately 7:1 ratio of oxazolidine 6 to imine 5, as determined by 1H NMR. The mixture when treated with sodium cyanide gave the expected alpha-aminonitrile 7. Microsomal oxidation of propranolol in the presence of sodium cyanide gave two cyanide-containing adducts as shown by GC-MS (12a and 12b). Using specifically deuterated propranolols (8, 9, 10, and 11) as substrates showed both of these cyanide-containing adducts to have lost the N-isopropyl group. Compounds 12a and 12b were shown to be diastereomeric alpha-aminonitriles arising from the reaction of 2 with propionaldehyde, a contaminant from the ether used for extraction, and cyanide anion. Authentic 7, stable to derivatization and GC-MS conditions, rapidly decomposed under the conditions of the metabolic experiments.

Animals↗
PubMed1999

2,6-Dichloro-phenol indophenol prevents switch-over of electrons between the cyanide-sensitive and -insensitive pathway of the mitochondrial electron transport chain in the presence of inhibitors.

To evolve a simple oxygen electrode-based method to estimate alternative respiration, one needs to develop a procedure to prevent switch-over of electrons to either pathway upon inhibition by cyanide or salicylhydroxamic acid. It was hypothesized that the inclusion of appropriate electron acceptor, possessing redox potential close to one of the electron transport carriers in between ubiquinone (branch point) and cytochrome a-a3, should be able to stop switch-over of electrons to either pathway by working as an electron sink. To test the hypothesis, 2,6-dichloro-phenol indophenol (DCPIP; redox potential +0.217 V), an artificial electron acceptor having a redox potential quite similar to the site near cytochrome c1 (redox potential +0.22 V) on the cyanide-sensitive pathway, was used with isolated mitochondria and leaf discs in the absence and presence of inhibitors (potassium cyanide, antimycin A, and salicylhydroxamic acid). Polarographic data confirmed electron acceptance by DCPIP only from the inhibited (by cyanide or salicylhydroxamic acid) mitochondrial electron transport chain, hence preventing switch-over of electrons between the cyanide-sensitive and cyanide-insensitive pathway of respiration. Results with antimycin A and reduction status of DCPIP further confirmed electron acceptance by DCPIP from the mitochondrial electron transport chain. Possible implications of the results have been discussed.

2,6-Dichloroindophenol↗
PubMed2002

Cyanide binding to cd(1) nitrite reductase from Pseudomonas aeruginosa: role of the active-site His369 in ligand stabilization.

Cyanide binding to fully reduced Pseudomonas aeruginosa cd(1) nitrite reductase (Pa cd(1) NiR) has been investigated for the wild-type enzyme and a site-directed mutant in which the active-site His369 was replaced by Ala. This mutation reduces the affinity toward cyanide (by approximately 13-fold) and especially decreases the rate of binding of cyanide to the reduced d(1) heme (by approximately 100-fold). The crystal structure of wild-type reduced Pa cd(1) NiR saturated with cyanide was determined to a resolution of 2.7 A. Cyanide binds to the iron of the d(1) heme, with an Fe-C-N angle of 168 degrees for both subunits of the dimer and only His369 is within hydrogen bonding distance of the nitrogen atom of the ligand. These results suggest that in Pa cd(1) NiR the invariant distal residue His369 plays a dominant role in controlling the binding of anionic ligands and allow the discussion of the mechanism of cyanide binding to the wild-type enzyme.

Amino Acid Substitution↗
PubMed1997

Plasmodium falciparum: cyanide-resistant oxygen consumption.

It has been hypothesized that Plasmodium parasites utilize a branched chain respiratory pathway, consisting of a classical cyanide-sensitive branch and an alternative cyanide-resistant branch. To further explore this hypothesis, the effect of cyanide on Plasmodium falciparum was determined using a polarographic assay. The rate of oxygen consumption by saponin-freed parasites was approximately 5% that of control human white blood cells or of Toxoplasma gondii, consistent with an anabolic role for P. falciparum respiration. However, while all of the oxygen consumption of the control white blood cells and of T. gondii could be inhibited by cyanide, 25% of the oxygen consumption of the P. falciparum parasites was found to be insensitive to high concentrations of cyanide. The cyanide-resistant portion of the parasite oxygen consumption was completely inhibited by two inhibitors of alternative oxidase activities in other systems, propyl gallate and salicyclhydroxamic acid. These studies provide the first direct evidence for a branched chain respiratory pathway in P. falciparum. Furthermore, salicyclhydroxamic acid, propyl gallate, and related inhibitors of alternative oxidase activities were shown to inhibit the growth of P. falciparum in vitro. These results support the need for further investigation of alternative oxidase activity as an antimalarial chemotherapeutic target.

Animals↗
PubMed1994

Antagonism of the lethal effects of cyanide by a synthetic water-soluble cobalt(III) porphyrin compound.

Efficacy of hydroxocobalamin (vitamin B12) as a cyanide antidote is limited by its high molecular weight (1355 g/mol) and by the competitive binding of the cobalamin dimethylbenzimidazole. The present study describes experiments with a lower molecular weight cobalt porphyrin that has a high affinity for cyanide, Co(III)-5,10,15,20-tetrakis(4-sulfonatophenyl) porphyrin (CoTPPS), which was prepared by the method of Herrmann et al. (1978). CoTPPS was synthesized and its efficacy as an antidote to the lethal effects of cyanide either alone or in various combinations with NaNO2 and/or Na2S2O3 was determined. The LD50 value for CoTPPS was found to be 334 mg/kg. These studies were conducted using the CoTPPS LD01, 200 mg/kg. The cyanide antagonists NaNO2 (0.1 g/kg, sc), Na2S2O3 (1.0 g/kg, ip), and CoTPPS (0.2 g/kg, ip) were administered at 45, 15, and 10 min respectively prior to graded doses of KCN (sc). The LD50 values for KCN in male Swiss-Webster mice were calculated by probit analysis at the 95% confidence level and the various treatments were compared by potency ratios. These results indicated that the administration of CoTPPS alone protects against the lethal effects of cyanide. Moreover, CoTPPS adds to the protection provided by Na2S2O3 and/or NaNO2. Efficacy of this antidote is probably related to the binding equilibrium between CoTPPS and cyanide.

Animals↗