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PubMed1989

Metabolism of organonitriles to cyanide by rat nasal tissue enzymes.

1. A method for determination of cyanide release during microsomal metabolism of organonitriles was developed. 2. Vmax values for cyanide release from acetonitrile, propionitrile, butyronitrile, isobutyronitrile, acrylonitrile, benzyl cyanide and succinonitrile were determined for rat nasal and liver microsomal metabolism. 3. Km and Vmax values were determined for nasal and liver microsomal metabolism of benzyl cyanide to cyanide. 4. Vmax values were all greater in nasal microsomes than in liver microsomes. Except for acrylonitrile, butyronitrile and isobutyronitrile metabolism, the ethmoturbinate microsomes had higher activities than the maxilloturbinate microsomes. 5. Two methods for determining Vmax values indicate that rat liver, but not the nose, contains at least two cytochrome P-450 isozymes involved in metabolism of benzyl cyanide to cyanide. 6. These results, and previously reported nasal rhodanese activity data, indicate that inhaled organonitriles are substantially detoxicated in the nasal cavity.

Animals↗
PubMed1996

Predictors of carbon monoxide and hydrogen cyanide exposure in smoke inhalation patients.

OBJECTIVE: A prospective study of civilian (nonfirefighter) smoke inhalation patients was carried out to test the hypotheses that: 1) absorption of carbon monoxide and hydrogen cyanide from smoke can be predicted by clinical examination and historical data; and, more specifically 2) a history of exposure to burning synthetic polymers is an important predictor of systemic cyanide levels. METHODS: The study was conducted over a three-year period at six urban hospitals. Patients with or without burns who were exposed to smoke within five hours of hospital arrival were sampled for carboxyhemoglobin, whole blood cyanide, urine cotinine and urine creatinine. Controls consisted of a smaller group of smoking status-matched, nonsmoke-exposed burn patients. ANALYSIS: Historical information was obtained on SMOKING status, FIRETYPE (structural vs other), MATERIAL burned (natural vs synthetic) and LAGTIME (from exposure to sampling). A smoke inhalation SCORE (0-10) was assigned to each case, based on physical examination findings and changes on chest X ray, and carboxyhemoglobin and cyanide levels were entered into various multivariate linear regression models. RESULTS: A total of 40 cases and 9 controls were recruited, ranging in age from 15 to 92 years. Thirty-four cases were discharged alive and six expired in-hospital. Observed carboxyhemoglobin levels ranged from 1.2% to 41.6% in cases (mean 8.6%), and from 0.5 to 7.3% in controls (mean 2.9%). Observed cyanide levels ranged from nondetectable (< 0.05 micrograms/mL) to 2.79 micrograms/mL in cases (mean 0.25 micrograms/mL), and from nondetectable to 0.11 micrograms/mL in controls (mean 0.03 micrograms/mL). Among cases, linear regression models explained up to 35% of the observed variance in carboxyhemoglobin levels (p < 0.001) and up to 48% of the variance in cyanide levels (p = 0.0001). CONCLUSIONS: SCORE was the strongest predictor of both carboxyhemoglobin and cyanide levels; LAGTIME also explained significant variance for [log-transformed] carboxyhemoglobin. Historical factors, such as FIRETYPE, MATERIAL, and SMOKING status, did not explain significant variance in most of the statistical models employed.

Adolescent↗
PubMedDate not supplied

[Conditions for the manifestation of cyanide-resistant respiration in Pseudomonas aeruginosa].

Conditions for manifestation of cyanide-resistant respiration were studied in Pseudomonas aeruginosa. Transition of the culture from the logarithmic to the stationary phase of growth, once the source of carbon (hexadecane, glucose, citrate, succinate) or nitrogen was exhausted, was accompanied with a decrease in the sensitivity of bacterial respiration to cyanide. As soon as the limiting factor was added, the culture started to grow again and its respiration became more sensitive to the inhibitor. Changes in the sensitivity of respiration to cyanide were observed when the bacterial growth was not limited with oxygen, and cyanide was not accumulated in the cultural broth. The manifestation of cyanide-resistant respiration was caused by changes in the physiological state of the bacterium induced by the cessation of growth. The culture formed phenazine pigments while growing on all of the studied substrates. However, no correlation was established between the resistance of respiration to cyanide and the concentration of the pigments in the medium. Therefore, the resistance of respiration of Ps. aeruginosa to cyanide should be attributed to changes in the electron transport chain.

Culture Media↗
PubMed1990

Transient spectroscopy of the reaction of cyanide with ferrous myoglobin. Effect of distal side residues.

The reaction of cyanide metmyoglobin with dithionite conforms to a two-step sequential mechanism with formation of an unstable intermediate, identified as cyanide bound ferrous myoglobin. This reaction was investigated by stopped-flow time resolved spectroscopy using different myoglobins, i.e. those from horse heart, Aplysia limacina buccal muscle, and three recombinant derivatives of sperm whale skeletal muscle myoglobin (Mb) (the wild type and two mutants). The myoglobins from horse and sperm whale (wild type) have in the distal position (E7) a histidyl residue, which is missing in A. limacina Mb as well as the two sperm whale mutants (E7 His----Gly and E7 His----Val). All these proteins in the reduced form display an extremely low affinity for cyanide at pH less than 10. The differences in spectroscopy and kinetics of the ferrous cyanide complex of these myoglobins indicate a role of the distal pocket on the properties of the complex. The two mutants of sperm whale Mb are characterized by a rate constant for the decay of the unstable intermediate much faster than that of the wild type, at all pH values explored. Therefore, we envisage a specific role of the distal His (E7) in controlling the rate of cyanide dissociation and also find that this effect depends on the protonation of a single ionizable group, with pK = 7.2, attributed to the E7 imidazole ring. The results on A. limacina Mb, which displays the slowest rate of cyanide dissociation, suggests that a considerable stabilizing effect can be exerted by Arg E10 which, according to Bolognesi et al. (Bolognesi, M., Coda, A., Frigerio, F., Gatti, C., Ascenzi, P., and Brunori, M. (1990) J. Mol. Biol. 213, 621-625), interacts inside the pocket with fluoride bound to the ferric heme iron. A mechanism of control for the rate of dissociation of cyanide from ferrous myoglobin, involving protonation of the bound anion, is discussed.

Animals↗
PubMed1990

[Plasma and red blood cell cyanide concentrations during hypotension induced by sodium nitroprusside or by a nitroprusside-trimetaphan mixture in rabbits].

Plasma and red blood cells cyanide concentrations during hypotension induced by sodium nitroprusside and a nitroprusside-trimetaphan mixture were studied in 29 male rabbits under halothane anesthesia. They were randomly divided into three groups; Nitroprusside (group N; n = 10), A nitroprusside-trimetaphan mixture (group M; n = 10), Controls (group C; n = 9). No changes were noted in plasma and red blood cells cyanide concentrations in group C throughout the experiment. During and after induced hypotension, in group N, plasma cyanide concentration was significantly higher than the control value. The maximum increase occurred 60min after induction of hypotension and the highest concentration of plasma cyanide was six times the control value. In contrast, in group M, plasma cyanide concentration was unchanged from the control value. However, during and after induced hypotension, red blood cells cyanide concentrations of group N and group M were significantly higher compared with the control values. Red blood cells concentrations of cyanide increased for 30 and 60 min during induced hypotension in group N (27.11 +/- 3.9 micrograms.ml-1, P less than 0.001, 46, 73 +/- 4.7 micrograms.ml-1, P less than 0.001, respectively) and in group M (0.31 +/- 0.05 micrograms.ml-1, P less than 0.05, 0.29 +/- 0.03 micrograms.ml-1, P less than 0.05, respectively). In conclusion, the data suggest that a nitroprusside-trimetaphan mixture is a safe method for hypotensive anesthesia.

Animals↗
PubMed1987

Cyanide concentrations in blood after cigarette smoking, as determined by a sensitive fluorimetric method.

Using the sensitive fluorimetric method described here, we evaluated the determination of blood cyanide as a method for monitoring exposure to tobacco smoke. The mean concentration of cyanide in blood from eight nonsmokers was 0.098 (SD 0.036) mumol/L. The concentration of cyanide in blood of smokers who had refrained from smoking for at least 2 h before sampling peaked immediately after the subjects smoked a cigarette, then rapidly declined, with a half-life of about 4 min. Its rapid disappearance from blood makes cyanide an unsuitable marker of exposure to tobacco smoke. Because the ability of patients with hepatic dysfunction to detoxify cyanide has been presumed to be impaired, we monitored the concentrations of cyanide in the blood of four patients with severe hepatic insufficiency who smoked a cigarette. The rate of elimination of cyanide from blood after smoking was only slightly less in these patients than in the controls, and the difference was not statistically significant.

Adult↗
PubMedDate not supplied

[Respiratory cyanide resistance in Candida lipolytica and the supersynthesis of citric acids].

The interrelationship between the cyanide resistance of respiratio and the process of citric acid synthesis was studied with various strains of Candida lipolytica. When the synthesis of citric acids was intensive, the respiration of cells was almost entirely inhibited by cyanide. The respiration became cyanide resistant only when the biosynthesis of citric acids was over. Induction of the cyanide resistance of respiration with antimycin A stopped the biosynthesis of citric acids. The cyanide resistance of respiration in yeast cultures incapable of considerable production of citric acids was displayed when the growth ceased. There was a strong direct correlation between the rate of citric acid synthesis and the degree of inhibition of the respiration by cyanide. It was concluded therefore that the process of citric acid overproduction could reset the reduction equivalents, thus making unnecessary the cyanide resistant pathway of electron transport.

Antimycin A↗
PubMed1982

[Effect of glutamic acid oversynthesis on the development of cyanide-resistant respiration in the bacterium Corynebacterium glutamicum].

The composition of the respiratory chains of the wild stain Corynebacterium glutamicum and of its mutant differing in their ability for the glutamic acid oversynthesis in a medium with melassa was studied. Under excess of biotine and the parent strain is incapable of acid oversynthesis, while the mutant forms and excretes the acid. Both bacterial strains contain menaquinone and equal sets of cytochromes C550, b556, b563, and a600. The membrane-bound dehydrogenases of the parent strain are represented by NADH-, NADPH- and succinate dehydrogenases. Unlike the parent strain, the mutant membrane preparation does not oxidize NADPH. Both strains do not practically differ in their menaquinone content. The cyanide-resistant oxidase of a non-cytochrome nature appears in the wild strain during its transfer to the stationary growth phase. Induction of glutamic acid oversnythesis by addition of penicilline prevents the formation of the cyanide-resistant oxidase. On the contrary, the mutant transfer to the stationary growth phase is not accompanied by a formation of cyanide-resistant oxidase, which appears only after cessation of glutamic acid oversynthesis. Induction of the cyanide-resistant respiration by addition of cyanide inhibits the acid oversynthesis. Oxidation of substrates by membrane preparations of both bacterial strains in the absence and presence of cyanide is not followed by the hydrogen peroxide formation. It is assumed that there exist competitive interactions between the supersynthesis of glutamic acid and the cyanide-resistant respiration. The possible structure of the respiratory chain of Cor. glutamicum is discussed.

Corynebacterium↗
PubMed1995

The effects of cyanide on the extracellular levels of dopamine, 3,4-dihydroxyphenylacetic acid, homovanillic acid, 5-hydroxyindoleacetic acid and inositol phospholipid breakdown in the brain.

The effects of sodium cyanide on the extracellular levels of dopamine and the main brain metabolites of dopamine and 5-hydroxytryptamine were studied in awake, freely moving rats using microdialysis technique. Already 20 min after the administration of cyanide (2 mg/kg; ip) the extracellular level of striatal dopamine was increased and after 40 min an enhancement of the homovanillic acid level was observed. Slight but significant decreases of 3,4-dihydroxyphenylacetic acid and 5-hydroxyindoleacetic acid were also observed. The increased extracellular levels of dopamine and homovanillic acid could indicate an increased release of dopamine. An alternative explanation could be an extracellular leakage of dopamine due to neuronal damage caused by cyanide. Cyanide has also been reported to induce marked changes in cytosolic brain Ca2+. We examined the effect of cyanide on inositol phospholipid breakdown in rat cerebral cortex and pig striatum in vitro. This breakdown was not affected by sodium cyanide and appears therefore not to be responsible for the reported changes of cytosolic Ca2+ induced by sodium cyanide.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1988

Toxicology and hazard evaluation of cyanide fumigation powders.

Studies were conducted to assess potential handling hazards from the pesticidal use of HCN-liberating "cyanide fumigation powders". Simulations were conducted in enclosed chambers on the release of HCN vapor from wetted powder containing 40% NaCN/60% kaolin at application rates of 1 g powder/m3 of space (usual rate) and 5 g/m3 (overuse condition). With the overuse situation, HCN vapor concentrations may be rapidly attained that produce serious or lethal toxicity; with the lower application rate minor signs and symptoms of HCN vapor exposure toxicity may develop. The acute peroral LD50 (rat and rabbit) of fumigant formulation is reduced in proportion to the kaolin content, but kaolin does not modify the inherent toxicity of NaCN. A typical cyanide hazard exists from swallowing cyanide fumigant powder formulations. Lethal systemic toxicity was produced by contamination of the eye (rabbit) with powder formulation, which also caused a rapid onset of moderately severe conjunctivitis and keratitis. Applied to dry intact skin (rabbit) neither NaCN nor its kaolin formulation produced systemic toxicity. However, on moistened intact skin lethal amounts of cyanide were absorbed; but the kaolin content reduced the hazard in comparison with NaCN-alone applied to moist skin. With abraded dry skin there was no difference in lethal toxicity between NaCN-alone and its formulation; also, the toxicity of the formulation on abraded skin was three times that on intact moist skin. These finds indicate that the use of cyanide fumigant powder formulations may be hazardous by contact of powder with moist or abraded skin, contamination of the eye, swallowing, and inhalation of evolved HCN. There is a clear need for respiratory, cutaneous, and ocular protection when handling cyanide fumigant powder formulations.

Administration, Cutaneous↗
PubMed2006

Application of hydrocyanic acid vapor generation via focused microwave radiation to the preparation of industrial effluent samples prior to free and total cyanide determinations by spectrophotometric flow injection analysis.

A sample preparation procedure for the quantitative determination of free and total cyanides in industrial effluents has been developed that involves hydrocyanic acid vapor generation via focused microwave radiation. Hydrocyanic acid vapor was generated from free cyanides using only 5 min of irradiation time (90 W power) and a purge time of 5 min. The HCN generated was absorbed into an accepting NaOH solution using very simple glassware apparatus that was appropriate for the microwave oven cavity. After that, the cyanide concentration was determined within 90 s using a well-known spectrophotometric flow injection analysis system. Total cyanide analysis required 15 min irradiation time (90 W power), as well as chemical conditions such as the presence of EDTA-acetate buffer solution or ascorbic acid, depending on the effluent to be analyzed (petroleum refinery or electroplating effluents, respectively). The detection limit was 0.018 mg CN l(-1) (quantification limit of 0.05 mg CN l(-1)), and the measured RSD was better than 8% for ten independent analyses of effluent samples (1.4 mg l(-1) cyanide). The accuracy of the procedure was assessed via analyte spiking (with free and complex cyanides) and by performing an independent sample analysis based on the standard methodology recommended by the APHA for comparison. The sample preparation procedure takes only 10 min for free and 20 min for total cyanide, making this procedure much faster than traditional methodologies (conventional heating and distillation), which are time-consuming (they require at least 1 h). Samples from oil (sour and stripping tower bottom waters) and electroplating effluents were analyzed successfully.

Journal Article↗
PubMed2006

Chromogenic oxazines for cyanide detection.

[reaction: see text] We have designed two heterocyclic compounds for the colorimetric detection of cyanide. The skeleton of both molecules fuses a benzooxazine ring to an indoline fragment and can be assembled efficiently in three synthetic steps starting from commercial precursors. The two compounds differ in the nature of the substituent on the carbon atom at the junction of the fused heterocycles, which can be either a methyl or a phenyl group. In the presence of cyanide, both molecules are converted quantitatively into cyanoamines with the concomitant appearance of an intense band in the visible region of the absorption spectrum. The developing absorption is a result of the opening of the benzooxazine ring with the formation of a 4-nitrophenylazophenolate chromophore. Nuclear magnetic resonance spectroscopy and X-ray crystallographic analyses demonstrate that the covalent attachment of a cyanide anion to the indoline fragment is responsible for these transformations. The chromogenic process is particularly fast for the methyl-substituted oxazine and can be exploited to detect micromolar concentrations of cyanide in water. Furthermore, the colorimetric response of this compound to cyanide does not suffer the interference of the halide anions, which instead are known to complicate the detection of cyanide in conventional sensing protocols. Thus, our mechanism and compounds for the colorimetric identification of cyanide can lead to the development of practical strategies for the convenient determination of this toxic anion in aqueous environments.

Journal Article↗
PubMed1978

Relative Contribution of Cytochrome-mediated and Cyanide-resistant Electron Transport in Fresh and Aged Potato Slices.

The respiration of fresh potato (Solanum tuberosum, var. Russet Burbank) slices is predominantly cyanide-sensitive whether in the presence or absence of uncoupler. By contrast, the wound-induced respiration which develops in thin slices with aging is cyanide-resistant, and in the presence of cyanide, sensitive to chlorobenzhydroxamic acid, a selective inhibitor of the cyanide-resistant respiration. Titration of the alternate path in coupled slices with chlorobenzhydroxamic acid, in the presence and absence of cyanide, shows that the contribution of the cyanide-resistant pathway to the wound-induced respiration is zero. Similar titrations with uncoupled slices reveal that the alternate path is engaged and utilized extensively.The maximal capacity of the cytochrome path (V(cyt)) has been estimated in fresh and aged slices in the presence of the uncoupler carbonyl-cyanide m-chlorophenyl hydrazone. It has been found that V(cyt) of aged slices is but 30 to 40% higher than that of fresh slices. The results suggest that the bulk of the wound-induced respiration is mediated through the cytochrome pathway which exists in fresh slices in suppressed form, and which is fully expressed by slice aging. The engagement of the alternate path by uncouplers in aged slices is attributed to an increase in substrate mobilization, with the result that the electron transport capacity of the cytochrome chain is exceeded.

Journal Article↗
PubMed1980

Malate Oxidation in Plant Mitochondria via Malic Enzyme and the Cyanide-insensitive Electron Transport Pathway.

MALATE OXIDATION IN PLANT MITOCHONDRIA PROCEEDS THROUGH THE ACTIVITIES OF TWO ENZYMES: a malate dehydrogenase and a NAD(+)-dependent malic enzyme. In cauliflower, mitochondria malate oxidation via malate dehydrogenase is rotenone- and cyanide-sensitive. Addition of exogenous NAD(+) stimulates the oxidation of malate via malic enzyme and generates an electron flux that is both rotenone- and cyanide-insensitive. The same effects of exogenous NAD(+) are also observed with highly cyanide-sensitive mitochondria from white potato tubers or with mitochondria from spinach leaves. Both enzymes are located in the matrix, but some experimental data also suggest that part of malate dehydrogenase activity is also present outside the matrix compartment (adsorbed cytosolic malate dehydrogenase?). It is concluded that malic enzyme and a specific pool of NAD(+)/NADH are connected to the cyanide-insensitive alternative pathway by a specific rotenone-insensitive NADH dehydrogenase located on the inner face of the inner membrane. Similarly, malate dehydrogenase and another specific pool of NAD(+)/NADH are connected to the cyanide- (and antimycin-) sensitive pathway by a rotenone-sensitive NADH dehydrogenase located on the inner face of the inner membrane. A general scheme of electron transport in plant mitochondria for the oxidation of malate and NADH can be given, assuming that different pools of ubiquinone act as a branch point between various dehydrogenases, the cyanide-sensitive cytochrome pathway and the cyanide-insensitive alternative pathway.

Journal Article↗
PubMed1982

Cyanide-insensitive respiration in relation to growth of a low-temperature basidiomycete.

The cyanogenic low-temperature basidiomycete (Coprinus psychromorbidus Redhead and Traquair), unlike other cyanide-tolerant fungi, does not detoxify cyanide via formamide hydro-lyase. Instead, tolerance apparently depends on cyanide-insensitive respiration involving activity of the mitochondrial alternative oxidase. Respiration and growth of young mycelium that lacks alternative oxidase activity are blocked both by cyanide and 1 mum antimycin. When activity of the alternative oxidase is elicited in young mycelium by 0.05 mm cyanide, subsequent treatment with antimycin stimulates respiration and fails to halt growth. Older mycelium becomes tolerant coincidentally with the release of cyanide by the mycelium. Tolerant older mycelium in medium containing 0.05 to 1.0 mum antimycin grows at 30 to 45% of the control rate. Cyanide- and antimycin-tolerant growth and respiration are blocked by salicyl hydroxamic acid, an inhibitor of the alternative oxidase, and by rotenone, which inhibits ATP synthesis at site I.

Journal Article↗
PubMed1983

Changes of cyanide content and linamarase activity in wounded cassava roots.

When cassava (Manihot esculenta Crantz) root was cut into blocks and incubated under laboratory conditions, the blocks showed more widespread and more even symptoms of physiological deterioration than those under natural conditions. Thus, the tissue block system has potential for biochemical studies of natural deterioration of cassava root. The changes in cyanide content and linamarase (linamarin beta-d-glucoside glucohydrolase; EC 3.2.1.21) activity in various tissues during physiological deterioration were investigated. Total cyanide content increased in all parts of block tissue after 3-day incubation. The degree of increase in cyanide was most pronounced in white parenchymal tissue, 2 to 3 millimeters thick, next to the cortex (A-part tissue), where no physiological symptoms appeared. On the other hand, linamarase activity was decreased in all parts of block tissue after a 3-day incubation. A time course analysis of A-part tissue indicated a clear reciprocal relationship between changes in total cyanide and linamarase activity; total cyanide increased, while linamarase activity decreased. Free cyanide constituted a very small portion of the total cyanide and did not change markedly.

Journal Article↗
PubMed1980

Aerobic electron transport in Propionibacterium shermanii. Effects of cyanide.

Cyanide inhibited D- and L-lactate and NADH oxidase activities of membrane particles from Propionibacterium shermanii but only at relatively high concentrations. Inhibition occurred at two different sites in the electron transport pathway. One site, with a half-maximal inhibition concentration (I0.5) of 2 to 3 mM KCN, is located at the terminal oxidase involved in cytochrome b oxidation; the evidence is consistent with cytochrome d being the major oxidase involved. At high concentrations, cyanide inhibited reduction of cytochrome b by D-lactate (I0.5 value 20-25 mM cyanide). A proportion of the oxygen-uptake remained uninhibited even by 100 mM cyanide; this proportion was about 80% for succinate, 30% for L-lactate, 15% for D-lactate and 10% for NADH. The oxygen uptake per mol of substrate oxidised increased with increasing cyanide concentration and was accompanied by the formation of hydrogen peroxide as a product of a cyanide-insensitive oxidase system.

Aerobiosis↗
PubMed1988

The possible role of the closed-open transition in proton pumping by cytochrome c oxidase: the pH dependence of cyanide inhibition.

The rate of oxidation of reduced cytochrome c catalyzed by cytochrome oxidase in the presence and absence of cyanide has been measured spectrophotometrically at pH 5.5, 6.4, 7.4 and 8.3. At the cytochrome c concentration used (272 microM), the uninhibited rate is maximal at pH 6.4 and drops to a value about one sixth of this maximum at pH 8.3. In the presence of cyanide, the rate initially drops rapidly, but with the cyanide concentration used (5.5 microM) there is still a measurable rate of oxidation when maximal inhibition has been reached. This inhibited rate decreases as the pH increases, whereas the apparent rate constant for cyanide binding is almost independent of pH. The results have been analyzed on the basis of a model in which two-electron reduction of the oxidized enzyme triggers a transition from a closed to an open conformation. It is assumed that cyanide can only bind to the open conformation and, furthermore, that rapid internal electron transfer to the dioxygen-reducing site occurs in this state alone. The analysis shows that the true constant for cyanide binding decreases with decreasing pH to a constant value at low pH. It also indicates that the increase in the catalytic constant with decreasing pH is associated with an increase in the rate of the closed-open conformational transition on protonation of the enzyme, and it is proposed that this transition is operative in electron gating in the proton-pump function of the enzyme.

Animals↗