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Cyanide is a toxic compound which inhibits the cellular utilization of oxygen. A number of substances can give rise to cyanide intoxication, which in some cases may have a delayed onset. The symptoms are non-specific and reflect cellular hypoxia. Several strategies may be employed in the treatment. Hydroxycobalamine is an effective and non-toxic antidote. On the basis of a case story, the toxicology, symptoms and treatment of cyanide poisoning are discussed.
The present paper deals with the wastewater pond accident in Nagybánya (Romania) in 2000 of which the result was an about 100 tons of highly toxic cyanide spill into the River Tisza. Measurements and laboratory tests were performed during the toxic wave transport. On the basis of this data set mass balance calculations were performed by hydraulic and transport models to investigate and better understand the effect of the accident and to calculate the possible heavy metal sedimentation process in Tisza River bed. This paper deals with calculations for cyanide and copper which are mostly associated to cyanide pollution.
Quaternary ammonium salt has strong affinity with gold in cyanide solutions, but it is not readily stripped. Stripping with acidic thiourea solutions and air sparging shows promise. There are some reports on the process of thiourea stripping, but little about its mechanism. In this paper, the stripping mechanism of N263/sulphuric thiourea/alkaline cyanide gold solution is studied by EXAFS. According to the experiments, sulphuric acid, thiourea and gold-thiourea complex can be extracted by N263 as a neutral molecule, and the stripping process can be described as following: (1) Sulphuric acid and thiourea are extracted by N263; (2) In organic phase, gold-cyanide complex is converted to gold-thiourea complex, which exists as Au[SC(NH2)2]2HSO4, and CN- forms HCN with acid at the same time; (3) HCN is removed by air sparging, and Au[SC(NH2)2]2HSO4 is distributed between organic phase and liquor phase, most of which transfers to liquor phase and is stripped.
The teratogenic effect of maternal cyanide consumption on the gross morphology of the post-natal phase of the developing rat cerebellum was studied. Twenty pregnant female rats weighing between 170 g and 190 g were separated into control and experimental groups. The control animals were fed a standard diet of mice cubes, while the experimental animals were fed 500 ppm potassium cyanide, mixed with the standard diet. The diets were fed to the animals and their litters in separate cages and water provided ad libitum during gestation and to the offspring after birth. After birth, the offspring (five per group) of days 1, 9, 14, 21, 28 and 50 were weighed, killed by cervical dislocation and the gross parameters studied. In the experimental animals, no significant differences were observed in the studied parameters between the control and experimental animals on day 1. A significant reduction in body weight was observed on day 14 (P < 0.05). The brain weight was significantly reduced on day 9 (P < 0.05). Similarly, the cerebellar weight was significantly reduced on days 14,21 and 28 (P < 0.05). The maximum vermal length was significantly reduced on day 50 (P < 0.05), and the maximum side-to-side dimension of the cerebellum was also reduced on day 28 (P < 0.05). There was no reduction in the thickness (anteroposterior dimension) of the cerebellum in the experimental group (P > 0.05). From the result, it is inferred that maternal consumption of 500 ppm cyanide causes reduction in the cerebellar weight, vermal length and side-to-side dimension of the developing cerebellum in postnatal life in rats.
The authors present the results of toxicological examination of blood of fatal victims of fires in "closed" spaces. Hydrogen cyanide was present in 26 out of 64 postmortem blood samples. COHb was found in 52 cases. The hydrogen cyanide levels ranged from 0.8 to 39.2 microg/l, the COHb levels ranged from 16.0 to 85.0%. The level of hydrogen cyanide was determined by the pyrazolopyridine method modified by Nedoma, and the COHb level was determined by the Wolff method.
Rats were intoxicated with LD50 of potassium cyanide and some nitriles. Content of glutathione in brain and liver tissues and activity of cytochrome oxidase in brain were studied. Activity of brain cytochrome oxidase was inhibited in rats intoxicated with cyanide, acrylonitrile and valeronitrile. All the nitriles studied reduced the tissue glutathione content. Cyanides did not exhibit any effects on glutathione concentration.
OBJECTIVE: To investigate the biochemical changes in rat brain and liver following acute exposure to a lethal dose of cyanide, and its response to treatment of alpha-ketoglutarate (alpha-KG) in the absence or presence of sodium thiosulfate (STS). METHODS: Female rats were administered 2.0 LD50 potassium cyanide (KCN; oral) in the absence or presence of pre-treatment (-10 min), simultaneous treatment (0 min) or post-treatment (+2-3 min) of alpha-KG (2.0 g/kg, oral) and/or STS (1.0 g/kg, intraperitoneal, -15 min, 0 min or + 2-3 min). At the time of onset of signs and symptoms of KCN toxicity (2-4 min) and at the time of death (5-15 min), various parameters particularly akin to oxidative stress viz. cytochrome oxidase (CYTOX), superoxide dismutase (SOD), glutathione peroxidase (GPx), reduced glutathione (GSH) and oxidized glutathione (GSSG) in brain, and CYTOX, sorbitol dehydrogenase (SDH), alkaline phosphatase (ALP), GSH and GSSG in liver homogenate were measured. RESULTS: At both time intervals brain CYTOX, SOD, GPx, and GSH significantly reduced (percent inhibition compared to control) to 24%, 56%, 77%, and 65%, and 44%, 46%, 78%, and 57%, respectively. At the corresponding time points liver CYTOX and GSH reduced to 74% and 63%, and 44% and 68%, respectively. The levels of GSSG in the brain and liver, and hepatic ALP and SDH were unchanged. Pre-treatment and simultaneous treatment of a-KG alone or with STS conferred significant protection on above variables. Post-treatment was effective in restoring the changes in liver but failed to normalize the changes in the brain. CONCLUSIONS: Oral treatment with alpha-KG alone or in combination with STS has protective effects on cyanide-induced biochemical alterations in rat brain and liver.
On treatment of rat cardiac myocytes with potassium cyanide, ATP content significantly and rapidly decreased in all experimental groups as compared to untreated cells. Contrary to that, the level of muscarinic cholinergic receptors increased significantly, depending on the cyanide concentration. Twenty four hours after removal of cyanide, myocytes exhibited normal levels of both the receptor expression and ATP content.
Levels of steam-volatile phenol, hydrogen cyanide and benzo(a)pyrene in various types of tobacco smoking products marketed in the country have been determined for the first time. Steam-volatile phenol levels in six popular brands of Indian cigarettes varied from 118 to 226 micrograms, and in six popular brands of bidis, from 129 to 273 micrograms. Cheroot and cigarillos yielded 400 micrograms and 333 micrograms steam-volatile phenol respectively. The hydrogen cyanide levels in the mainstream smoke of five popular brands of Indian cigarettes varied from 366 to 638 micrograms and in the mainstream smoke of four popular brands of bidis from 688 to 904 micrograms. Cheroot and cigarillos yielded 588 micrograms and 1119 micrograms hydrogen cyanide respectively. The values of benzo(a)pyrene content in Indian cigarettes varied from 85 to 114 ng and in bidis from 108 to 144 ng. Herbal bidi and cheroot had 1315 ng and 2519 ng benzo(a)pyrene respectively. Cigarettes were smoked as per international standard smoking conditions and the levels of noxious agent were found to be higher than in currently marketed western cigarettes. However, these levels in all the indigenous products including bidis cannot be directly compared with those of cigarettes as they were smoked under modified conditions.
A set of mitochondrial antibiotic-resistant mutants of Paramecium have been analyzed with respect to their growth-rates, cytochromic content and respiratory properties. The mutants could be arranged in a continuous series ranging from strains equivalent to wild-type to severely affected ones; affected strains display longer generation times, reduced amount of cytochrome oxidase and very high levels of cyanideinsensitive respiration. Perfect phenocopies of the mutants were obtained by treating wild-type cells with low concentrations of erythromycin suggesting that the mutations exert their pleiotropic effect by perturbating mitochondria protein synthesis in agreement with the idea that these mutations affect the mitochondrial ribosomes. In the mitochondria of some of the mutants, electrons can be channelled with equal efficiency into the "classical" cyanide-sensitive pathway and the alternate cyanide insensitive (and SHAM-sensitive) one, providing direct demonstration of the branching of these two respiratory pathways. In the absence of any added inhibitor, however, electrons tend to be channelled in the cyanide-sensitive pathway. All the physiological data fit perfectly the genetic data concerning the "stability" of the various mutations in "mixed mitochondrial populations", i.e., markers that were known to be strongly counter-selected with respect to wild-type in such populations correspond to severely affected strains, while markers that were known to be "stable" correspond to "healthy" strains. A more quantitative analysis of the data shows that that there is little or no "complementation" between wild-type and mutated mitochondria in mixed cells indicating a high extent of functional autonomy of mitochondria in Paramecium.
Three cases of suspected cyanide poisoning due to plant ingestion are described. The basis of cyanide toxicity and antagonism are briefly reviewed. Currently recommended management of suspected cyanide intoxication is outlined.
Ninety-seven people died from a fire that occurred in the Dupont Plaza Hotel in Puerto Rico on 31 Dec. 1986. All, except four who died later in the hospital, were found dead at the scene. All of the fatalities at the hotel (except for eight) were burned beyond recognition. Blood from seventy-eight of the victims was screened for carboxyhemoglobin at the Institute for Forensic Sciences in Puerto Rico and was then sent to the National Institute of Standards and Technology, Gaithersburg, Maryland, for analysis of carboxyhemoglobin and cyanide concentrations. The blood data indicated that carbon monoxide and hydrogen cyanide, singly or combined, were probably not responsible for the majority of the deaths that occurred in the badly burned victims. On the other hand, the significantly higher carboxyhemoglobin in the nonburned victims indicated that carbon monoxide alone or combined with hydrogen cyanide probably played a major role in the cause of their deaths.
Two head-space gas chromatographic methods for the determination of hydrogen cyanide (HCN) in blood were demonstrated using electron capture detector (ECD). One was the double head-space gas sampling technique and the other used the reaction pre-column packed with Chloramine-T for the conversion of HCN into cyanogen chloride (CNC1). In the former method, HCN in blood was firstly released by acidification, and then the HCN gas was replaced into the another vial in which Chloramine-T solution had been placed. The head-space gas in the second vial was analyzed by gas chromatograph (GC). In the latter, HCN gas released was directly injected into the GC pre-connected the reaction column. The conversion of HCN into CNC1 was easily achieved by both methods. The use of dichloromethane as an internal standard and PTFE-faced septum for the sealing of vial greatly improved the precision and reliability of these analytical methods. The calibration curves by these methods gave good linearity and the lower detection limit taken from these plots was ca. 0.05 micrograms/ml. In particular, the reaction pre-column method, by which blood cyanide can be analyzed rapidly and accurately with only simple alteration of apparatus, is superior in the routine analysis of blood cyanide.
The effect of potassium cyanide on the desaturase activity for stearyl-CoA in microsomes of various mammalian tissues has been investigated. Potassium cyanide inhibited the desaturase activities in microsomes from livers of rat, hen, guinea pig and rat lung, but not the activities in microsomes from rabbit liver, pig thyroid and bovine adrenocortex, It is concluded that the so-called "cyanide-sensitive factor" does not seem to be common to all the desaturase activities of stearyl-CoA in the microsomes of mammalian tissues.
Two cases of pediatric accidental ingestion of an acetonitrile-containing cosmetic are reported. One of the children, a 16-month-old boy, was found dead in bed the morning after ingesting the product. No therapy had been undertaken, as the product was mistakenly assumed to be an acetone-containing nail polish remover. The second child, a 2-year-old boy, experienced signs of severe cyanide poisoning, but survived with vigorous supportive care. Both children had blood cyanide levels in the potentially lethal range. The observed delayed onset of severe toxic reactions supports the proposed mechanism of acetonitrile conversion to inorganic cyanide via hepatic microsomal enzymes. Physicians and poison centers should be alerted to the existence of this highly toxic product, sold for removal of sculptured nails and likely to be confused with the less toxic acetone-containing nail polish removers. We urge regulatory agencies to reconsider the wisdom of marketing a cosmetic that poses such an extreme health hazard.
Effects of various classes of drugs on complete ischemia (gasping) induced by decapitation and cyanide intoxication in mice were investigated. The average gasping duration in complete ischemia and survival time in potassium cyanide injection of control mice were 21.0 +/- 0.1 and 26.1 +/- 0.4 sec (mean +/- SEM), respectively. Some antidepressants, neuroleptics and tranquilizers significantly and dose-dependently prolonged the duration of gasping and survival time, and decreased locomotor activity. Vincamine and its analogues are markedly effective for treating cyanide intoxication. It is conceivable that this is a characteristic phenomenon for vincamine. Xanthine analogues significantly and dose-dependently shortened the duration of gasping and survival time and increased locomotor activity. These results suggest that the cerebral protecting effect primarily relates to the cerebral energy demand.
The phosphorylation of fructose-1,6-bisphosphatase is preceded by a transient increase in the intracellular level of cyclic AMP which activates a cyclic AMP-dependent protein kinase (Pohlig, G., and Holzer, H. (1985) J. Biol. Chem. 260, 13818-13823). Possible mechanisms by which sugars or ionophores might activate adenylate cyclase and thereby lead to an increase in cyclic AMP concentrations were studied. Studies with permeabilized yeast cells demonstrated that neither sugar intermediates nor carbonyl cyanide m-chlorophenylhydrazone are able to increase adenylate cyclase activity. In the light of striking differences of the effects of fermentable sugars and of carbonyl cyanide m-chlorophenylhydrazone on parameters characterizing the membrane potential, it seems not reasonable that the activity of adenylate is under control of the membrane potential. Rapid quenching of 9-aminoacridine fluorescence after addition of fermentable sugars to starved yeast cells indicated an intracellular acidification. The 31P NMR technique showed a fast drop of the intracellular pH from 6.9 to 6.55 or 6.4 immediately after addition of glucose or carbonyl cyanide m-chlorophenylhydrazone. The time course of the decrease of the cytosolic pH coincides with the transient increase of cyclic AMP concentration and the 50% inactivation of fructose-1,6-bisphosphatase under the conditions of the NMR experiments. Kinetic studies of adenylate cyclase activity showed an approximately 2-fold increase of activity when the pH was decreased from 7.0 to 6.5, which is the result of a decrease in the apparent Km for ATP with no change in Vmax. These studies suggest that activation of adenylate cyclase by decrease in the cytosolic pH starts a chain of events leading to accumulation of cyclic AMP and phosphorylation of fructose-1,6-bisphosphatase.
It was shown that hydrophilic benzo- and naphthoquinones stimulate the cyanide-resistant respiration in liver and muscle mitochondria when succinate or NADH and glutamate or malate are used as oxidation substrates. The substrate-dependent oxygen uptake in the presence of cyanide is initiated by menadione, vicasol, 1.2-naphthoquinone, coenzyme Q0 and duroquinone. Rotenone and antimycin A do not inhibit the cyanide-resistant respiration. Oxidation of glutamate and malate in the course of CN-resistant respiration is inhibited by ortho- and bathophenanthroline and p-chloromercurybenzoate, whereas succinate oxidation by tenoyltrifluoroacetone, carboxin and pentachlorophenol. Superoxide dismutase, Cu2+ and catalase inhibit the CN-resistant respiration in the presence of quinones. Addition of catalase to the experimental cell causes O2 release.