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PubMed1982

Cyanide toxicity of sodium nitroprusside in therapeutic use with and without sodium thiosulphate.

Sodium nitroprusside (SNP) as a mono-infusion was administered to 51 patients for periods of a few hours. A further group of 19 patients received SNP for periods of several days as a combination solution of SNP mixed with sodium thiosulphate. The concentrations of cyanide and of thiocyanate in the blood of all patients were measured. In seven of the patients the level of thiosulphate was also measured. Infusion of SNP on its own at levels exceeding 2 microgram/kg/min led to the rising of cyanide levels in the blood being proportional to dosage. Infusion of SNP mixed with thiosulphate showed no such accumulation of cyanide in any patient, irrespective of dosage level and duration. The efficacy at lowering blood pressure was fully maintained in the mixed infusion. The elimination half-life for thiosulphate was 16.5 min. Pharmacokinetic calculation of the rise in cyanide level showed that mono-infusions of 5-10 micrograms SNP/kg/min could within 5-10 h cause a life-threatening cyanide level in the blood. By contrast, mixed infusion of SNP together with thiosulphate, for which light-opaque syringes and tubing must be used, is a procedure free of danger and should become the technique of choice when therapeutically administering SNP in order to lower blood pressure.

Adolescent↗
PubMed1979

A blood cyanide distribution study in the rabbits intoxicated by oral route and by inhalation.

Blood cyanide concentration was determined in rabbits intoxicated orally or by inhalation. Experiments were carried out under urethane anaesthesia. In the inhalation experiments, rabbits inhaled a combustion product containing HCN via the tracheal cannula and in the oral studies animals were administered NaCN solution into the stomach. In addition to the carotid artery and jugular vein blood samples, postmortem samples were obtained from both sides of the heart and the descending vena cava. The arterial cyanide concentration in the inhalation group showed a close relationship with ventilation. After an initial rise, blood levels decreased a little, in some cases with transient apnea. At the last stage it again increased with gasping, reaching its maximal value. After ultimate apnea, the blood cyanide concentration declined. The blood cyanide values were higher in the oral group than in the inhalation group. The difference between the two groups became larger in the inferior order, the left heart blood--the right heart blood--blood in the descending vena cava. The left heart/right heart ratio of the inhalation group was significantly higher than that of the oral group (1.28+/- 0.28 vs. 0.95+/- 0.09). The coefficient of variation (c.v.) of the inhalation group was larger than that of the other group. Within the inhalation group, the left heart blood showed the largest c.v. values and this was probably due to redistribution of the cyanide by bloodstream after attainment of the maximal concentration.

Administration, Oral↗
PubMed1991

Monitoring cyanide and thiocyanate concentrations during infusion of sodium nitroprusside in children.

Over a 19-month period, all requests for blood cyanide and/or serum thiocyanate concentrations to the Clinical Laboratory of The Children's Hospital, Boston, were reviewed in order to determine how physicians screen for nitroprusside-related toxicity. During that period, 52 patients receiving nitroprusside were monitored for cyanide and/or thiocyanate toxicity. Overall, there were 62 cyanide and 86 thiocyanate determinations. None of the thiocyanate determinations and five of the cyanide concentrations were within the toxic range as established by the reference laboratory, and no patient displayed signs or symptoms of toxicity which could not also be explained by their underlying illness. Our findings suggest that while physicians are concerned with nitroprusside toxicity in children, there exists no apparent consensus as to how to monitor for this toxicity. The results also indicate that the relationship between blood cyanide or serum thiocyanate concentrations and clinical evidence of toxicity is not straightforward and requires further delineation.

Adolescent↗
PubMed1998

Recovery and refining of Au by gold-cyanide ion biosorption using animal fibrous proteins.

Animal fibrous proteins (AFPs) such as egg-shell membrane (ESM), chicken feather (CF), wool, silk, or elastin are an intricate network of stable and water-insoluble fibers with high surface area and are abundant bioresources. Every AFP tested was found to accumulate gold-cyanide ion from aqueous solutions in high yield, depending on pH and some other parameters. Gold-cyanide ion is adsorbed by AFP at low pH range, with maximum binding observed at approx pH 2.0. Under the certain conditions, gold-cyanide ion was accumulated up to 8.6, 7.1, 9.8, 2.4, and 3.9% of dry weight on ESM, CF, wool, silk, and elastin, respectively. In the case of ESM, it was found that ESM removed gold-cyanide ion almost quantitatively and almost all the gold uptake by ESM was easily desorbed with 0.1 M NaOH. ESM can be used repeatedly for the process of gold adsorption-desorption. The gold-biosorptive capacity of ESM that was chemically modified with glutaraldehyde was higher than that of control. In column procedure, ESM packed on column removed gold-cyanide ion from the dilute aqueous solution to extremely low concentrations (nondetectable concentration of below 1 ppb).

Adsorption↗
PubMed2004

Cyanide as a copper and quinone-directed inhibitor of amine oxidases from pea seedlings ( Pisum sativum) and Arthrobacter globiformis: evidence for both copper coordination and cyanohydrin derivatization of the quinone cofactor.

The interactions of cyanide with two copper-containing amine oxidases (CuAOs) from pea seedlings (PSAO) and the soil bacterium Arthrobacter globiformis (AGAO) have been investigated by spectroscopic and kinetic techniques. Previously, we rationalized the effects of azide and cyanide for several CuAOs in terms of copper coordination by these exogenous ligands and their effects on the internal redox equilibrium TPQ(amr)-Cu(II) right harpoon over left harpoon TPQ(sq)-Cu(I). The mechanism of cyanide inhibition was proposed to occur through complexation to Cu(I), thereby directly competing with O(2) for reoxidation of TPQ. Although cyanide readily and reversibly reacts with quinones, no direct spectroscopic evidence for cyanohydrin derivatization of TPQ has been previously documented for CuAOs. This work describes the first direct spectroscopic evidence, using both model and enzyme systems, for cyanohydrin derivatization of TPQ. K(d) values for Cu(II)-CN(-) and Cu(I)-CN(-), as well as the K(i) for cyanide inhibition versus substrate amine, are reported for PSAO and AGAO. In spite of cyanohydrin derivatization of the TPQ cofactor in these enzymes, the uncompetitive inhibition of amine oxidation is determined to arise almost exclusively through CN(-) complexation of Cu(I).

Amine Oxidase (Copper-Containing)↗
PubMed2007

Spectrum of cyanide toxicity and allocation in Heliconius erato and Passiflora host plants.

The larvae of three races of Heliconius erato were fed various species of Passiflora containing varying levels of cyanoglucosides. The mortality rate of larvae and pupae rose when larvae were fed species of Passiflora capable of releasing larger quantities of cyanide. When larvae were fed species of Passiflora with these properties, the resulting adult butterflies also released higher levels of cyanide. This may serve as a defense mechanism. The compounds responsible for the release of cyanide were not evenly distributed throughout the adult butterfly's body. The thorax contained the highest concentration of cyanogenic substances, followed by the head, wings, and abdomen. The younger tissues of Passiflora plants had higher levels of cyanide-releasing compounds than stems and mature leaves. Cyanogenic glycoside distribution within the plants is consistent with optimal allocation theory. The levels of cyanide-releasing substances in plants varied depending on the season.

Animals↗
PubMed1979

Cyanide reactivity of cytochrome c derivatives.

The kinetic rates and equilibrium association constants for cyanide binding have been measured for a series of cytochrome c derivatives as a probe of heme accessibility. The series included horse and yeast cytochromes iodinated at Tyr 67 and 74, horse cytochrome formylated at Trp 59 in both a low and high redox potential form, the Met 80 sulfoxide derivative of horse cytochrome and the N-acylisourea heme propionate derivative of tuna cytochrome. Native cytochromes c are well known to bind cyanide slowly in a reaction simply first order both in cytochrome and cyanide up to at least 100 mM in cyanide. The derivative demonstrate markedly different kinetics which indicate the following conclusions. (1) In spite of chemical modification at different loci, all the derivatives have highly similar reactivity, suggesting common ligation structures and mechanisms for reaction. (2) Compared to native cytochromes, reaction rates are 10-20 fold greater. This is in accord with a more accessible heme crevice, but not a completely opened crevice. For the completely opened case, rate increases are expected to be between three and five orders of magnitude. (3) Reaction rates are either independent of cyanide concentration (zero order) or show only slight variation. A mechanism which accounts for the data over four orders of magnitude in concentration postulates a protein conformation step, opening of the heme crevice, as the rate determining step. This conformation change has a limiting rate of 6 . 10(-2) s-1.

Animals↗
PubMed1986

Pathways for the bioactivation of aliphatic nitriles to free cyanide in mice.

Reports from several laboratories agree that many, but not all, aliphatic nitriles undergo hepatic biotransformation in mice and rats to release free cyanide, but the mechanisms at work in these reactions remain in doubt. We have used primarily n-butyronitrile, propionitrile, and their respective alpha-carbon-hydroxylated homologs, propionaldehyde cyanohydrin and lactonitrile, to examine this question in mice. Pretreatment of mice with the hepatic microsomal enzyme inducers, pregnenolone-16 alpha-carbonitrile, troleandomycin, and isosafrole, or with the cytochrome P-450-depleting agent, cobaltous chloride, did not influence the mortality of mice given single doses of nitriles. Repeated injections of aspirin or sodium salicylate in water failed to protect mice against death by the nitriles. Dimethyl sulfoxide, however, was effective in reducing mortality after nitrile administration. Repeated injections of 4-methylpyrazole or disulfiram protected mice against death after nitriles. Most of the treatment regimens successful against the nitriles also protected against death due to the cyanohydrins. The cyanohydrins were more acutely toxic than their parent nitriles, produced death much more rapidly, and resulted in the same toxic signs, suggesting that they are intermediates in the bioactivation pathway leading to free cyanide. The cyanohydrins appeared to serve as weak substrates for yeast alcohol dehydrogenase, however, incubation of them with either yeast or horse liver alcohol dehydrogenase did not increase the rate of cyanide release over that in incubations where the enzymes were absent. The slow rate of cyanide release due to spontaneous hydrolysis interfered with the determinations of alcohol dehydrogenase activity, but it cannot account for the rapid action and high toxicity of the cyanohydrins in vivo, or for the efficacy of the treatment regimens which protected against death. It appears unlikely that prostaglandin synthetase or alcohol dehydrogenase are importantly involved in nitrile bioactivation. The same active process, however, appears to be responsible both for alpha-carbon hydroxylation and for the subsequent degradation of the resulting cyanohydrins to release free cyanide. It is far more efficient in mediating the latter reaction than the former.

Alcohol Dehydrogenase↗
PubMed1990

Cyanide-induced alteration of cytosolic pH: involvement of cellular hydrogen ion handling processes.

Neuronal cells exposed to cyanide rapidly lose the capacity to regulate internal Ca2+ homeostasis, thereby accumulating an excess cytosolic Ca2+ load. The present study was undertaken to examine the effects of KCN on another important ion: hydrogen ion. KCN (1-10 mM) rapidly decreased intracellular pH (pHi) of cultured pheochromocytoma (PC12) cells as indicated by the pH-sensitive fluorescent dye 2',7-bis(carboxyethyl)-5(6)-carboxyfluorescein. Removal of Ca2+ from the media or pretreating the cells with diltiazem (10(-5) M), a calcium channel blocker, delayed the onset and reduced the magnitude of the drop in pHi. Lowering the pH of the incubation medium (pHo) to 6.9 exaggerated the drop in pHi, while raising it to 7.9 attenuated the change in pHi. Removal of Na+ from the media enhanced the cyanide effect. Reintroduction of Na+ or substitution with Li+ reversed the cytosolic acidification, suggesting involvement of the Na+/H+ exchanger in the cyanide action. Pretreatment of cells with amiloride, 0.2 mM, blunted the cytosolic acidification induced by KCN, possibly by decreasing intracellular Na+ accumulation and disrupting H+ efflux. Cyanide thus produces a rapid dysfunction of hydrogen ion handling mechanisms and this may play a role in cyanide neurotoxicity.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Severe hypoxia produced by concomitant intoxication with sublethal doses of carbon monoxide and cyanide.

It has long been known that a number of tissue hypoxicants are generated in the fire scenario. However, until recently few investigators have undertaken to correlate smoke inhalation deaths with the simultaneous exposure to histotoxic hypoxicants. Carbon monoxide and hydrogen cyanide are two histotoxic hypoxicants that are generated in nearly every fire. Prior studies performed in our laboratory have demonstrated that death can result from concomitant exposure to otherwise sublethal concentrations of carbon monoxide and cyanide. Since most smoke inhalation victims exhibit acid/base anomalies, we sought to investigate whether the death associated with simultaneous exposure to these two hypoxicants, at concentrations widely held to be nonlethal, could be explained by acid/base imbalances. Male ICR mice were exposed to 0.35% carbon monoxide immediately after having been injected ip with potassium cyanide solution, or were challenged with either agent alone. Animals challenged with cyanide or carbon monoxide alone demonstrated significant hypoxia. However, animals challenged with both agents demonstrated much greater hypoxia than could be explained by an additive effect alone. Controls demonstrated no alteration in acid/base homeostasis. Blood pH perturbations were found to be due to severe lactic acidosis coupled with inadequate respiratory compensation. Thus, it appears that the synergistic lethal effect of simultaneous administration of carbon monoxide and cyanide are related to a precipitous decrease in blood pH, the tissue hypoxia and its resulting complications.

Animals↗
PubMed1985

1H, 13C NMR, and electronic absorption spectroscopic studies of the interaction of cyanide with aurothiomalate.

The reaction between cyanide and aurothiomalate (Autm) has been studied by 1H and 13C NMR spectroscopy and by uv spectroscopy. At cyanide:Autm ratios greater than or equal to 2, aurocyanide, [Au(CN)2]-, is the sole product but was also produced at lower ratios. Two intermediates were also identified. These were a mixed ligand complex, [tmAuCN]-, which accounted for over 80% of the gold at a ratio of cyanide to Autm of 1, and a bisthiomalato complex, [Autm2]-, which accounted for 6.8% of the total gold at this ratio of cyanide to Autm. The formation of these complexes may be significant in the antiarthritic activity of Autm since cyanide is produced by potential target cells such as polymorphonuclear leukocytes.

Chemical Phenomena↗
PubMed1991

Toxicity of potassium cyanide added to fresh fruit and juice.

To investigate the toxicity of potassium cyanide in fresh fruit and juice, male and female Wistar rats were orally dosed with fruit homogenates or juices containing 3 x LD50 of potassium cyanide. These were given in single doses at various intervals after spiking. The dosing solutions were analysed for cyanide using a cyanide test kit. There was a good correlation between the toxic signs in rats and the cyanide remaining in dosing solutions. The toxicity of spiked apple and honeydew melon diminished with time, while spiked grape and both grape and apple juices maintained their toxicity during the 4-hr studies. The pH of the samples both before and after spiking seemed to be an important factor in determining the toxicity.

Administration, Oral↗
PubMed1979

Effects of low cobalamin diet and chronic cyanide toxicity on cobalamin distribution in baboons.

This paper reports the bodily distribution of total cobalamin and individual cobalamins at the termination of an experiment on the effects of a low cobalamin diet and chronic cyanide or thiocyanate administration in baboons. The results show that the distribution of cobalamins in the tissues of the baboon can be altered by a low cobalamin diet and also by chronic intoxication with cyanide, whether or not the animals are on a low cobalamin diet. All animals on the low cobalamin diet showed a reduction in total and individual cobalamins. In blood plasma and erythrocytes, kidney, spleen, testis and brain, the proportion of methylcobalamin tended to be disproportionately reduced in cobalamin-depleted animals. This reduction was lessened or prevented by the administration of cyanide. Neither cyanide not thiocyanate produced a significant increase in the proportion of cyanocobalamin in plasma, though thiocyanate produced a large increase in cyanocobalamin in erythrocytes. In liver, cyanocobalamin was more than doubled by the administration of cyanide to cobalamin-depleted animals.

Animals↗
PubMed1996

Preventive effect of melatonin against cyanide-induced seizures and lipid peroxidation in mice.

Subcutaneous injection of potassium cyanide (6, 8, and 9 mg/kg) caused a severe tonic seizure in a dose-dependent manner. However, the incidence of seizures induced by potassium cyanide was significantly inhibited by preadministration of melatonin (20 mg/kg, s.c.) Lipid peroxidation in homogenates from whole brain of mice was significantly increased (39%, 106% and 132%, respectively) by the exposure to potassium cyanide (0.01, 0.05, and 0.1 mM). The potassium cyanide (0.1 mM)-induced lipid peroxidation was prevented by melatonin (0.1, 0.5, 1.0, or 2 mM) in a concentration-dependent manner. These results suggest that free radicals formation and subsequent lipid peroxidation may contribute in part to the development of seizures induced by cyanide in mice.

Animals↗
PubMed1989

The cyanide-metabolizing enzyme rhodanese in rat nasal respiratory and olfactory mucosa.

Hydrogen cyanide is a commonly occurring and highly toxic air pollutant. Inhalation of hydrogen cyanide would expose the nasal tissues to its toxic affects unless a detoxicating mechanism were available. Experiments with rat nasal tissues showed that the cyanide-metabolizing enzyme, rhodanese, is present in high concentrations, particularly in the olfactory region. The olfactory tissues had nearly 7-fold more rhodanese on a per mg mitochondrial protein basis than did the liver. These experiments show that nasal metabolism of cyanide may have an important influence on the toxicity of inhaled cyanide and cyanogenic materials.

Animals↗
PubMed1995

Modification of cyanide toxicodynamics: mechanistic based antidote development.

Cyanide's actions are complex and cannot be attributed solely to inhibition of oxygen utilization. Recent mechanistic studies show that cyanide inhibits multiple enzymes and alters several vital intracellular processes to produce the intoxication syndrome. By understanding the intracellular targets and the mechanisms underlying the toxicity, it is proposed that more effective antidotal regimens can be achieved. A mechanistic based, multi-step in vitro model was developed for screening potential cyanide antidotes. A series of compounds was screened for their ability to reverse the effect of cyanide on six neurochemical markers in the PC12 cell line (neuronal cell model). Each compound was assigned a composite score based on the six assays; several compounds were identified which then exhibited efficacy in animal testing. Additional mechanistic based studies show that antioxidants and nitric oxide generators have promise as anti-cyanide agents. It is concluded that mechanistic based antidote design can be used to identify new compounds for testing in animal models.

Animals↗
PubMed1989

The role of hydrogen cyanide and carbon monoxide in fire casualties: a prospective study.

Determinations of blood cyanide and carboxyhemoglobin concentrations were performed in 18 victims found dead in buildings after fires during a 2-year period. The results indicated that 50% of the victims had been exposed to toxic levels of hydrogen cyanide and 90% to toxic levels of carbon monoxide. Lethal concentrations of carbon monoxide were found in 83% of the victims. In one case a lethal blood cyanide but a non-toxic blood carboxyhemoglobin value was found. It is concluded that carbon monoxide appears to be more important than hydrogen cyanide as a toxic agent in the fire atmosphere, but cyanide poisoning without carbon monoxide poisoning may, under certain circumstances, be the cause of death in fire victims.

Adolescent↗
PubMed1991

High cyanide level in a homicide victim burned after death: evidence of post-mortem diffusion.

Elevated levels of carbon monoxide and cyanide serve as evidence of intravital burning in fire victims. Hydrogen cyanide is released by combustion of nitrogen-containing organic material such as plastics and wool. We present a case of a man who died of haemopneumothorax caused by a stab wound. According to several eye witnesses the body was wrapped in a plastic sheet and burned 2 days after death with the aid of gasoline. No coal pigment was observed in the mucosa of the upper airways at autopsy. The blood sample taken from the pulmonary vessels 6 days after death disclosed a level of blood carboxyhaemoglobin of 4% and of blood cyanide of 10 mg/l. The low carboxy-haemoglobin level was consistent with the smoking habits of the victim. The thoracic cavity had been opened by burning of the intercostal soft tissue. This allowed hydrogen cyanide gas to enter the thoracic cavity and diffuse into the blood probably causing the high blood-cyanide level.

Adult↗