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PubMed1983

Steady-state kinetics of the catalase reaction in the presence of cyanide.

Under carefully controlled experimental conditions, the Michaelis constant for H2O2 was measured to be 1.39 and 1.29 M in the reactions of beef erythrocyte and liver catalases, respectively. These values remained unchanged at temperatures between 1 and 26 degrees C. The turnover number of the Michaelis complex was about 2.25 X 10(7) s-1 for either enzyme at 26 degrees C. The cyanide inhibition in the catalase reaction has been reported to be noncompetitive in spite of the fact that cyanide and H2O2 compete for the same site on the catalase molecule. At high concentrations of H2O2, however, the inhibition became clearly competitive. The existence of the Michaelis complex and the anomalous features of cyanide inhibition were clearly accounted for on the basis of simple kinetic models. At H2O2 concentrations below 100 mM, the catalase reaction obeyed first order kinetics with respect to H2O2 and its apparent second order rate constant was measured to be 7.6 X 10(6) and 7.9 X 10(6) M-1 . S-1 for erythrocyte and liver catalases, respectively.

Animals↗
PubMed2005

Enhancement of cyanide-induced mitochondrial dysfunction and cortical cell necrosis by uncoupling protein-2.

Uncoupling protein 2 (UCP-2) is expressed in the inner mitochondrial membrane and modulates mitochondrial function by partially uncoupling oxidative phosphorylation, and it has been reported to modulate cell death. Cyanide is a potent neurotoxin that inhibits complex IV to alter mitochondrial function to induce neuronal death. In primary rat cortical cells KCN produced an apoptotic death at 200-400 microM. Higher concentrations of potassium cyanide (KCN) (500-600 microM) switched the mode of death from apoptosis to necrosis. In necrotic cells, ATP levels were severely depleted as compared to cortical cells undergoing apoptosis. To determine if UCP-2 expression could alter KCN-induced cell death, cells were transiently transfected with full-length human UCP-2 cDNA (UCP-2+). Overexpression switched the mode of death produced by KCN (400 microM) from apoptosis to necrosis. The change in cell death was mediated by impaired mitochondrial function as reflected by a marked decrease of ATP levels and reduction in mitochondrial membrane potential. RNA interference or transfection with a dominant interfering mutant blocked the necrotic response observed in UCP-2+ cells. Additionally, treatment of UCP-2+ cells with cyclosporin A blocked necrosis, indicating the involvement of mitochondrial permeability pore transition in the necrotic death. These results show that increased expression of UCP-2 alters the response to a potent mitochondrial toxin by switching the mode of cell death from apoptosis to necrosis. It is concluded that UCP-2 levels influence cellular responses to cyanide-induced mitochondrial dysfunction.

Animals↗
PubMed1982

Nitroprusside increases cyclic guanylate monophosphate concentrations during relaxation of rabbit aortic strips and both effects are antagonized by cyanide.

The authors have confirmed previous observations that sodium cyanide (CN-) partially reverses the vasodilator effects of sodium nitroprusside (SNP) on vascular smooth muscle. As tested on rabbit aortic strips contracted by norepinephrine (NE), the final tension is independent of the order of addition of reagents. In the same concentration, CN- alone had no effect on tension also as reported by others. The ED50 values for relaxation of aortic strips for a series of directly acting agonists ("nitric oxide vasodilators") were: sodium azide (N-3) 2.1 X 10(-7) M; SNP 2.7 X 10(-7) M; hydroxylamine (H2NOH) hydrochloride 2.5 X 10(-6) M; human nitric oxide hemoglobin (HbNO) 3.5 X 10(-6) M; and sodium nitrite (NO-2) 1.2 X 10(-4) M. In addition to SNP, CN- antagonized the vasodilator effects of N-3 and H2NOH, but it failed to reverse relaxation by HbNO, NO gas, NO-2 (as observed by us), glyceryl trinitrate, adenosine, or papaverine (as observed by others). The only change noted in cyclic-adenosine monophosphate (c-AMP) concentrations in aortic strips exposed to 1) NE, 2) NE + NO-2 or SNP, or 3) NE + NO-2 or SNP + CN- was an increase due to NE. The only statistically significant change noted in cyclic-guanosine monophosphate (c-GMP) concentrations exposed to 1) NE, 2) NE + NO-2 or 3) NE + NO-2 + CN- was also an increase due to NE. In contrast, SNP resulted in further increases in c-GMP after NE, and when cyanide was added, a significant decrease in c-GMP followed. These results are only partially consistent with a role for c-GMP in relaxation of vascular smooth muscle, but cyanide may become a useful tool for the study of mechanisms of action of the nitric oxide vasodilators.

Animals↗
PubMedDate not supplied

Cyanide ingestion: preventing the cascade.

Patients with cyanide exposure present a rare and unique challenge to the critical care nurse. The following article assists the critical care nurse and advanced practice nurse in understanding the pathophysiology of cyanide exposure, assessment of signs and symptoms, and antidotal and supportive therapies. In addition, a case review of nursing care for a patient exposed to cyanide is discussed.

Antidotes↗
PubMed1978

Occupational exposures to cyanide in Baltimore fire fighters.

A group of 479 fire fighters were investigated for routine exposure to hydrogen cyanide in the fire atmosphere using measurements of serum thiocyanate (SCN-). Our findings indicate that fire fighters were exposed to levels of hydrogen cyanide sufficient to raise their mean serum thiocyanate (SCN-) levels above that of controls. This elevation of serum SCN- occurred independently of smoking habits. Exposure to cyanide occurred much less frequently than previously studied exposures to carbon monoxide. Difficulties of correlating acute symptoms and the effectiveness of mask use with serum thiocyanate are discussed.

Air Pollutants↗
PubMed1997

Evaluation of cyanide exposure and its effect on thyroid function of workers in a cable industry.

A thyroid-hormone evaluation of workers dealing with cyanide compounds in an electroplating process of a cable industry was carried out. Serum thiocyanate (SCN) levels of 35 nonsmoking copper-ply employees were assayed by a ferric-chloride color test. The mean SCN concentration of these employees was 316 +/- 15 mumol/L, which was significantly (P < 0.01) higher than that of control subjects (90.8 +/- 9.02 mumol/L). Serum thyroxine (T4), triiodothyronine (T3), and thyroid-stimulating hormone (TSH) concentrations of exposed workers were compared with those of 35 control subjects. Cyanide exposure resulted in a decrease in T4 and T3 concentrations (P < 0.05) and an increase in TSH concentration (P < 0.05), compared with the control subjects. The serum T4 level was found to be negatively correlated (r = -0.363, P < 0.05), whereas the TSH level was positively correlated (r = 0.354, P < 0.05), with SCN concentration in the exposed group. The study suggests that occupational cyanide exposure in the industry impairs thyroid function.

Adult↗
PubMed1970

The respiratory chain of plant mitochondria. IV. Oxidation rates of the respiratory carriers of mung bean mitochondria in the presence of cyanide.

The half-time for oxidation of cytochrome b(557) in mitochondria from etiolated mung bean (Phaseolus aureus) hypocotyls is 5.8 milliseconds at 24 Celsius in the absence or presence of 0.3 mm KCN, when the oxidation is carried out by injecting a small amount of oxygenated medium into a suspension of mitochondria made anaerobic in the presence of succinate plus malonate. Since oxygen is consumed by the alternate, cyanide-insensitive respiratory pathway of these mitochondria, cycles of oxidation and reduction can be obtained with the oxygen pulses when cyanide is present. Reduced cytochromes (a + a(3)) also become oxidized at nearly the uninhibited rate under these conditions, a(3) completely and a partially. The half-time for oxidation of c(547) is also unaffected by 0.3 mm KCN, but c(549) has a half-time equal to that of c(547) in the presence of KCN, compared to the shorter one observed in the absence of inhibitor. The maximum extent of oxidation of the cytochromes c is about 70% in the presence of 0.3 mm KCN; this oxidation is rapidly followed by an extensive reduction which is synchronous with the reduction of cytochrome a observed under the same conditions. In the presence of cyanide, it appears likely that the cytochromes c and b(557) are oxidized by cytochrome oxidase in oxygen pulse experiments, rather than by the alternate oxidase. The oxidation of cytochrome b(553) is partially inhibited by KCN, but complete oxidation is attained in the aerobic steady state with excess oxygen. If the oxygen pulse experiment is carried out in the presence of sufficient malonate so that entry of reducing equivalents into the respiratory chain occurs at a rate negligible compared to inter-carrier electron transport, the half-time for flavoprotein oxidation is unaffected by 0.3 mm KCN while that for ubiquinone oxidation is but 2-fold larger. The observed net oxidation rate of these two carriers in mung bean mitochondria is more sensitive to the entry rate of reducing equivalents, as set by succinate concentration and malonate to succinate ratio, then it is in skunk cabbage (Symplocarpus foetidus) mitochondria. These observations are interpreted in terms of a respiratory carrier Y, placed between flavoprotein plus ubiquinone and the cytochromes, which is the fork in the split respiratory pathway to the two terminal oxidases and which has lower electron transport capacity in mung bean mitochondria than in skunk cabbage mitochondria.

Cyanides↗
PubMed2007

Yam bean seed poisoning mimicking cyanide intoxication.

BACKGROUND: Yam bean is a common food in southern Taiwan. However, its seeds are rarely consumed. We describe five patients of yam bean seed poisoning in Taiwan, one of them life-threatening. CLINICAL PRESENTATION: The five patients presented with perioral numbness, nausea and vomiting after eating a same soup made from yam bean seeds. One of them, a 54-year-old woman, had difficulty breathing and lost consciousness. Physical examination showed dilated pupils and coma with no focal neurological signs. The initial blood pressure was normal. Laboratory data showed a severe anion gap metabolic acidosis, with a serum lactate level of 185 mg/dL. An initial diagnosis of cyanide intoxication was considered and she was given sodium nitrite and sodium thiosulfate i.v. Hypotension ensued shortly afterwards and pulmonary artery catheterization showed a decreased cardiac index. Aggressive fluid and inotropic therapy were given and the patient eventually recovered. The other four patients suffered only minor gastrointestinal and neurological symptoms and received supportive treatment. Cyanide levels were negative in all five patients. CONCLUSION: Yam bean seed poisoning can cause acute metabolic acidosis and altered mental status, which could be confused with acute cyanide intoxication from a cyanogenic glycoside-containing plant. To our knowledge, this is the first outbreak of yam bean seed poisoning reported in the English published work.

Cyanides↗
PubMed1969

Cyanide stimulation of the systemic arterial chemoreceptors in foetal lambs.

1. In foetal lambs, delivered by Caesarean section under light chloralose anaesthesia, injection of sodium cyanide into the left atrium or ascending aorta caused a rise of arterial pressure and femoral vasoconstriction. The response to 0.77 mg/kg was barely present at 0.6 of term; by 0.8 of term there was a large response to one third of this dose.2. The cardiovascular response to cyanide injection into the left atrium or ascending aorta was diminished either by section of the vagi or by carotid denervation, and was abolished by cutting both sets of nerves.3. Injection of sodium cyanide into both common carotids simultaneously caused a substantial cardiovascular response and often a respiratory effort, abolished by carotid denervation, whereas injection into a single carotid rarely caused an effect.4. It is concluded that the carotid chemoreceptors in mature foetal lambs can be excited by a stimulus of sufficient intensity, even though they do not respond to moderate hypoxaemia.

Animals↗
PubMed1966

Cyanide intoxication: protection with oxygen.

Prophylactic protection against cyanide intoxication in mice can be enhanced by the administration of oxygen, especially when it is used in combination with the conventional cyanide antidotes, sodium nitrite and sodium thiosulfate. The LD(50) values were compared in groups of mice premedicated with sodium thiosulfate or sodium nitrite, or both, in air and in oxygen. These results indicate that oxygen alone provides only minimal protection. Although oxygen enhances the protective effect of sodium thiosulfate to a minor degree, it does not enhance the protection of sodium nitrite at all; and yet, it potentiates the effectiveness of a combination of these two antagonists against cyanide intoxication.

Animals↗
PubMed2006

Oxygen reactivity of both respiratory oxidases in Campylobacter jejuni: the cydAB genes encode a cyanide-resistant, low-affinity oxidase that is not of the cytochrome bd type.

The microaerophilic bacterium Campylobacter jejuni is a significant food-borne pathogen and is predicted to possess two terminal respiratory oxidases with unknown properties. Inspection of the genome reveals an operon (cydAB) apparently encoding a cytochrome bd-like oxidase homologous to oxidases in Escherichia coli and Azotobacter vinelandii. However, C. jejuni cells lacked all spectral signals characteristic of the high-spin hemes b and d of these oxidases. Mutation of the cydAB operon of C. jejuni did not have a significant effect on growth, but the mutation reduced formate respiration and the viability of cells cultured in 5% oxygen. Since cyanide resistance of respiration was diminished in the mutant, we propose that C. jejuni CydAB be renamed CioAB (cyanide-insensitive oxidase), as in Pseudomonas aeruginosa. We measured the oxygen affinity of each oxidase, using a highly sensitive assay that exploits globin deoxygenation during respiration-catalyzed oxygen uptake. The CioAB-type oxidase exhibited a relatively low affinity for oxygen (K(m) = 0.8 microM) and a V(max) of >20 nmol/mg/s. Expression of cioAB was elevated fivefold in cells grown at higher rates of oxygen provision. The alternative, ccoNOQP-encoded cyanide-sensitive oxidase, expected to encode a cytochrome cb'-type enzyme, plays a major role in the microaerobic respiration of C. jejuni, since it appeared to be essential for viability and exhibited a much higher oxygen affinity, with a K(m) value of 40 nM and a V(max) of 6 to 9 nmol/mg/s. Low-temperature photodissociation spectrophotometry revealed that neither oxidase has ligand-binding activity typical of the heme-copper oxidase family. These data are consistent with cytochrome oxidation during photolysis at low temperatures.

Campylobacter jejuni↗
PubMed1978

Cyanide- and hydroxamate-resistant respiration in Neurospora crassa.

Strain inl-89601 of Neurospora crassa respires exclusively by means of the mitochondrial cytochrome chain. The respiration of this strain is entirely inhibited by cyanide or antimycin A, the classical inhibitors of cytochrome chain respiration. When this strain was grown in the presence of chloramphenicol, however, two additional terminal oxidases were detected. One of these oxidases is inhibited by substituted hydroxamic acids and has been described previously. The second oxidase was not inhibited by cyanide or hydroxamic acid but was inhibited by azide in the presence of both cyanide and hydroxamic acid. This azide-sensitive respiration was due to a single respiratory pathway with a Ki for azide of 200 micrometer. A small amount of azide-sensitive respiration was detected in mitochondrial fractions obtained from chloramphenicol-treated cells, and it is likely that the azide-sensitive oxidase is localized in the mitochondrion. The determinants for the azide-sensitive and hydroxamate-sensitive oxidases segregate in a Mendelian manner in crosses and are either unlinked or not closely linked to each other.

Azides↗
PubMed1983

Carbonyl cyanide-m-chlorophenyl hydrazone-resistant Escherichia coli mutant that exhibits a temperature-sensitive unc phenotype.

Two spontaneous Escherichia coli mutant strains which are resistant to an oxidative phosphorylation uncoupler, carbonyl cyanide-m-chlorophenyl hydrazone, were isolated. Strain CM22 (ccr-2) was resistant to another uncoupler, pentachlorophenol, and to the inhibitors of proton-translocating ATPase, namely tributyltin and sodium azide. Carbonyl cyanide-m-chlorophenyl hydrazone or pentachlorophenol administered to cell suspensions of strain CM22 did not cause a pH change induced by H+ influx, and a similar result was obtained with everted particles. The respiratory rate of strain CM22 with succinate was twice that of wild-type strain KH434. When carbonyl cyanide-m-chlorophenyl hydrazone was administered, a stimulation of O2 uptake was observed in wild-type strain KH434 but not in the mutant strain CM22. Strain CM22 did not grow on succinate at 42 degrees C. Isolation of a true revertant at a frequency of 10(-8) demonstrated that the pleiotropic phenotype was induced by a single mutation. P1 transduction indicated that the mutant allele, ccr-2, was cotransduced with the ilv genes at a frequency of about 55%.

Adenosine Triphosphatases↗
PubMed2005

Acute cyanide poisoning by subcutaneous injection.

A 30 year old woman with a history of depression and previous suicide attempts was brought to the emergency department in coma. She had injected herself with cyanide subcutaneously and had severe metabolic acidosis. She underwent sustained haemodialysis in the intensive care unit (ICU) before laboratory confirmation of cyanide poisoning. The serum cyanide concentration was 4.6 microg/ml. After 48 hours the patient, now asymptomatic, was discharged from the ICU.

Acute Disease↗
PubMed2000

Fatal methane and cyanide poisoning as a result of handling industrial fish: a case report and review of the literature.

The potential health hazards of handling industrial fish are well documented. Wet fish in storage consume oxygen and produce poisonous gases as they spoil. In addition to oxygen depletion, various noxious agents have been demonstrated in association with spoilage including carbon dioxide, sulphur dioxide, and ammonia. A fatal case of methane and cyanide poisoning among a group of deep sea trawler men is described. Subsequent independent investigation as a result of this case led to the discovery of cyanides as a further potential noxious agent. This is thus the first case in which cyanide poisoning has been recognised as a potentially fatal complication of handling spoiled fish. The previous literature is reviewed and the implications of the current case are discussed.

Animals↗
PubMed1975

Chronic cyanide exposure: a clinical, radioisotope, and laboratory study.

The effect of chronic cyanide exposure in the electroplating sections of three factories employing 36 workers was studied and compared with a control group. The concentration of cyanides to which the workers were exposed was measured. The regression line showing the relationship between thiocyanates in urine and the concentration of cyanides in the air was plotted. Increased percentages of haemoglobin and lymphocyte count were present in all exposed workers, in addition to punctate basophilia in 28 workers. Cyanmethaemoglobin was found to be characteristic. Apart from other complaints, two men with psychosis similar to one case reported in therapeutic thiocyanate intoxication were found. Twenty of the workers had thyroid enlargements to a variable degree and consistency, in two of whom it resembled lymphadenoid goitre. Thyroid 131I uptakes at 4 and 24 hours were significantly higher than in the controls, while 131PBI was unchanged. The reason for this iodine deficiency-like action is discussed.

Adult↗
PubMedDate not supplied

Cyanide binding to canine myeloperoxidase.

Equilibria and kinetics of cyanide binding to canine myeloperoxidase were studied. Spectral results support the presence of two heme binding sites; an isosbestic point at 444 nm and a linear Scatchard plot suggest that the binding affinity of cyanide to the two subunits of the enzyme is the same. The dissociation constant is 0.53 microM. The pH dependence of the apparent second order rate constant indicates the presence of an acid-base group on the enzyme with a pKa of 3.8 +/- 0.1. The protonated form of cyanide binds to the basic enzyme with a rate constant of (4.3 +/- 0.3) x 10(6) M-1 s-1.

Animals↗
PubMed2003

Stimulation of the cyanide-resistant alternative respiratory pathway by oxygen in Acremonium chrysogenum correlates with the size of the intracellular peroxide pool.

The relationship between oxygen input and activity of the cyanide-resistant alternative respiration of submerged cultures of Acremonium crysogenum was investigated. The volumetric oxygen transfer coefficient of the respective cultures correlated positively within almost two ranges of magnitude with the size of the intracellular peroxide pool, which in turn, correlated with the activity of the cyanide-resistant alternative respiratory pathway. Increased aeration also stimulated the glucose uptake rate but had no effect on the total respiration rate or the growth rate. Addition of the lipid peroxyl radical scavenger DL-alpha-tocopherol to A. chrysogenum cultures decreased the rate of intracellular peroxide production as well as glucose uptake. An increase in the cyanide-resistant fraction of total respiration was observed, while growth and the total respiratory activity remained unchanged. We conclude that intracellular peroxides may stimulate the alternative respiration in A. chrysogenum.

Acremonium↗