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PubMed1998

Assessment of cyanogenic glucoside (cyanide) residues in Mbege: an opaque traditional Tanzanian beer.

Levels of cyanide in two varieties of malted millet, spent grain (Machicha) and opaque beer (Mbege) were determined. Protein content and amino acid composition of the malt, Mbege and Machicha were determined. Mbege was made in the laboratory using an improved method. The cyanide content of millet, malt, spent grain and Mbege were 40.6, 513.4, 18.9 and 8.1 ppm, respectively for the Moshi local millet variety. For Sumbawanga-2 millet variety the cyanide content was found to be 41.2, 489.2, 17.8 and 6.8 ppm for the millet, malt, spent grain and Mbege, respectively. The cyanide content increased linearly as the number of days of germination of the millet grain increased and the highest values of cyanide were attained on the third day of germination. Cyanogenic glucosides in the millet were enzymetically hydrolysed to respective cyanohydrins and volatile hydrogen cyanide due to low pH level of the Mbege which was 4. Malting of the millet increased the protein content by 5%. Lysine, the most limiting amino acid in millet, increased by 20%. It was concluded that the fermentation process of the millet malt into Mbege is efficient in reducing the levels of cyanogenic glucosides below levels considered toxic and therefore rendering the product safe.

Amino Acids↗
PubMed2004

First case of illegal euthanasia in Spain: fatal oral potassium cyanide poisoning.

A fatal case of intentional oral cyanide poisoning in a tetraplegic patient whose repeated legal requests to be allowed to perform euthanasia had been refused, is reported. The postmortem provided no specific findings and the diagnosis was based on the toxicological analysis of the different samples available. Cyanide was determined in all biological (blood, vitreous humour, bile, urine and viscera) and non-biological samples_received (liquid found in a glass beside the body in the scene of the crime). The high cyanide concentrations in blood (21.5 mg/L) are consistent with death through cyanide poisoning. Also, the cyanide concentration in the water held in the glass from which the casualty presumably drank 81900 mg/L), and the high levels of potassium ion found (186 mEq/L), allowed us to conclude that the death was due to the intake of an amount of potassium cyanide between 500 and 1000 mg.

Humans↗
PubMed1991

Protection against cyanide toxicity by oral alpha-ketoglutaric acid.

The efficacy of orally administered alpha-ketoglutarate (AKG), alone and in combination with n-acetyl-cysteine (NAC), in reducing the lethal effects of injected potassium cyanide was examined in the mouse. A behavioral scoring system was developed to monitor and measure the signs of toxicity associated with cyanide exposure. AKG significantly reduced the lethality of KCN (6.7 mg/kg ip) in a dose-related manner. The protective effect of AKG was observed if given between 10 and 30 min prior to cyanide exposure. NAC increased the protective effect of AKG but did not alter the time course of protection. AKG alone or in combination with NAC significantly reduced the duration of the toxicity associated with cyanide exposure. This study identifies AKG as an orally effective cyanide antagonist. The protective effect of AKG is enhanced by concomitant administration of NAC. Our work also describes a scoring system which quantifies the signs of toxicity associated with cyanide poisoning.

Acetylcysteine↗
PubMed1991

[Cyanide with vitamin B12 deficiency as the cause of experimental tobacco amblyopia].

The visual toxicity of tobacco smoke was studied and demyelination change of retrobulbar portion of the rat's optic nerve with an elongation of a peak latency time of visual evoked potentials (VEP) was demonstrated. Cyanide detoxication incapacity and deficiency of vitamin B12 (B12) have been considered as possible causes of tobacco amblyopia. In order to elucidate an influence of cyanide poisoning and B12 deficiency on the visual system, 12 male Wistar rats were subjected to 5 hour's daily inhalation of cyanide gas for 52 weeks, the concentration of which was adjusted to that of tobacco smoke. Six rats of these 12 were fed with a lacking B12 diet. Another 12 male Wistar rats were controls which did not undergo inhalation of cyanide gas, and half of them were fed a diet without B12. In 2 out of 6 rats with cyanide and inhalation and B12 deficiency, demyelination change could be recognized in the central portion of the retrobulbar optic nerve. The histological change was segmental and significant elongation of the peak latency time of VEP was not recognized. Cyanide gas inhalation at a low concentration was proved to be harmful to the optic nerve under the condition of B12 deficiency, but other toxic elements such as nicotine and carbon monoxide may be important factors to cause the more severe changes of the optic nerve with an abnormal VEP response recognized in the experimental tobacco amblyopia.

Amblyopia↗
PubMed1989

Rapid determination of toxic cyanide concentrations in blood.

This method for the rapid colorimetry of cyanide in blood, applicable to patients exposed to toxic levels of cyanide, is based on the König reaction, which produces a chromophore from cyanide as well as thiocyanate. The latter compound, normally present in blood, is confined to plasma. Thus, its interference with determination of cyanide was eliminated by performing the assay on the erythrocytes, which contain most of the blood cyanide. Furthermore, cyanide was trapped in the erythrocytes and stabilized during the initial washing steps by conversion of hemoglobin to methemoglobin with inorganic nitrite.

Colorimetry↗
PubMed1989

The biohazard potential of cyanide poisoning during postmortem examination.

A case of suicide by ingestion of cyanide salts provided an opportunity to determine whether personnel involved in postmortem examination of such cases are exposed to any significant degree of biohazard from cyanide remaining in body cavities or tissues of the decedent or both. It was found that potentially toxic concentrations of cyanide can develop in personnel so exposed. These findings have implications not only for the safety of pathologists and pathology assistants, but also for first responders (for example, police, firemen, emergency medical technicians [EMTs], paramedics, R.N.s) and emergency room personnel who may be involved in resuscitation efforts or removal of gastric contents or both in cyanide poisoning victims. Symptoms of cyanide toxicity and recommendations for reducing the potential for clinically significant cyanide exposure in medical settings are briefly reviewed.

Adolescent↗
PubMed1987

Metabolism of cyanamide to cyanide and an inhibitor of aldehyde dehydrogenase (ALDH) by rat liver microsomes.

Rat liver microsomes, as well as purified catalase, convert the alcohol deterrent agent, cyanamide, to an active inhibitor of AlDH. Whether this enzymatic activation of cyanamide is mediated primarily by catalase present in the microsomes or involves the cytochrome P-450 enzymes is not known. We now report that cyanide is also a product of the microsomal oxidation of cyanamide. Formation of cyanide from cyanamide and rat liver microsomes was time dependent, reaching maximal levels within 5-10 min. Induction of the cytochrome P-450 enzymes by phenobarbital (PB) pretreatment doubled the yield of cyanide, while SKF-525A blocked this PB-induced increase. Administration of 3-aminotriazole (3-AT) to PB-treated rats inhibited the catalatic activity of their microsomes by 98% and substantially reduced cyanide formation. These results suggest that while catalase is responsible in major part for the oxidation of cyanamide to cyanide by uninduced microsomes, the participation of the hepatic cytochrome P-450 enzymes cannot be ruled out in PB-induced microsomes. We propose a metabolic scheme wherein N-hydroxycyanamide is the intermediate product of cyanamide oxidation, which then decomposes to yield the observed product, cyanide. By deduction, the second product of this decomposition is postulated to be nitroxyl (HNO), which may be the active AlDH inhibitor.

Aldehyde Dehydrogenase↗
PubMedDate not supplied

[Effect of limitation of bacterial growth with carbon, sulfur and iron on the synthesis of cytochromes, development of cyanide-resistant respiration and super-synthesis of metabolites].

The work is concerned with the effect produced by limiting the growth of various bacteria with carbon, sulfur and iron on cytochrome synthesis, development of cyanide-resistant respiration and oversynthesis of metabolites. The cessation of bacterial growth due to the exhaustion of a carbon source was shown to be accompanied with the development of cyanide-resistant respiration though the oversynthesis of metabolites did not occur. If the growth was limited by a sulfur or iron source, the concentration of cytochromes a, b and c fell down as compared with that when the growth was limited by a carbon source, and metabolites were produced and accumulated in the medium. In that case, the respiration of virtually all the bacteria was inhibited by cyanide to a great extent. As was demonstrated for Pseudomonas aeruginosa, the development of cyanide-resistant respiration was inhibited when metabolites accumulated and then the respiration became completely resistant to cyanide as soon as the oversynthesis ceased. Apparently, whatever limits the bacterial growth, the process of oversynthesis inhibits cyanide-resistant oxidase.

Bacteriological Techniques↗
PubMed1985

Determination of cyanide in whole blood, erythrocytes, and plasma.

We describe a method for determination of cyanide in whole blood, erythrocytes, and plasma after stabilization of cyanide by addition of silver ions. The cyanide is then transferred from the acidified sample, by aeration, into sodium hydroxide and quantified by the König reaction, with sodium hypochlorite as the chlorinating agent. A rapid loss of measurable cyanide found when cyanide was added to plasma in the absence of silver ions was attributed to a reaction with serum albumin. Cyanide added to whole blood was bound to a saturable component in erythrocytes, which we identified as methemoglobin.

Cyanides↗
PubMed1985

The role of cyanide in fires.

Cyanide is a potent and rapidly lethal poison whose clinical and laboratory diagnosis is difficult. Cyanide is released in fire settings involving wool, silk and many synthetic polymers posing a definite risk. Interactions of carbon monoxide released in a fire and cyanide have important physiological consequences. Although the classic mechanisms for the toxicology and antagonism of cyanide have been studied for many years, recent studies have cast doubt as to the mechanism of some of these antagonists. In the fire setting it is not clinically acceptable to administer nitrites to create methemoglobinemia. Cobalt salts are currently too toxic. Oxygen should be administered but there is no proven benefit of hyperbaric oxygen. Oxygen, thiosulfate and hydroxycobalamin are probably the best and safest currently available antidotes to manage this difficult setting. In the future, encapsulated rhodanese enzyme may provide additional rapid therapeutic intervention. It is anticipated that oxygen, thiosulfate and hydroxycobalamin are a safer and more clinically acceptable antidotal combination in the management of cyanide exposure in the fire setting. Our current understanding of combustion toxicology should provide an opportunity to remove building materials and furnishings which pose a cyanide hazard in a fire setting.

Animals↗
PubMed1980

Cyanides and their toxicity: a literature review.

Cyanide is a potent and rapidly-acting asphyxiant which prevents tissue utilization of oxygen by inhibition of the cellular respiratory enzyme, cytochrome oxidase. Inhalation or ingestion of cyanide produces reactions within a few seconds and death within minutes. Cyanide toxicity of dietary origin has been implicated in acute animal deaths and as major etiologic factors in toxic ataxic neuropathy in man and as a cause of vision failure in humans suffering from tobacco amblyopia and leber's hereditary optic atrophy. Diagnosis of cyanide toxicity may be confirmed by a variety of laboratory procedures, but accurate assay is essential for proper conclusions from analysis of animal tissues several hours after death or from human samples in instances of chronic dietary exposure. Biological detoxification of cyanide is available through several routes, and the application of sodium nitrite with sodium thiosulfate or administration of methylene blue are effective treatment procedure. The environmental availability of cyanide in its various forms necessitates an understanding of its pathophysiology and responsible management of hazardous situations.

Absorption↗
PubMed1983

Cyanide-resistant respiration in Streptomyces citreofluorescens.

The capacity of Streptomycetes to carry out cyanide-resistant respiration was investigated. With the model strain, Streptomyces citreofluorescens, it was shown that deprivation of glucose followed by transition from exponential to stationary growth was coupled with declining sensitivity of cellular respiration to cyanide ions. Cyanide-resistant oxidase is located within the cytoplasmic membrane. The occurrence of the cyanide-resistant oxidase did not correspond to qualitative changes of cytochrome spectrum. Cytochrome d is involved neither in cyanide-sensitive nor in cyanide-resistant respiratory chain.

Carbon Monoxide↗
PubMed1984

Alternate substrates of dopamine beta-hydroxylase. II. Inhibition by benzyl cyanides and reactivation of inhibited enzyme.

Several ring-substituted benzyl cyanides lead to inactivation of dopamine beta-hydroxylase during catalysis. With m-hydroxybenzyl cyanide, maximal inactivation occurs when an enzyme group with a pK alpha of 6.0 +/- 0.2 is ionized (Colombo, G., Rajashekhar, B., Giedroc, D. P., and Villafranca, J.J. (1984) J. Biol. Chem. 259, 1593-1600). This paper reports studies conducted to determine the stability of inactivated dopamine beta-hydroxylase. Inactivation of the enzyme by m-hydroxybenzyl cyanide at pH 6.4 is halted by lowering the pH to approximately 5.0 with acetate, fumarate, pyridine, or phosphate buffer in the presence of tyramine. However, if tyramine is omitted, reactivation occurs. The extent of reactivation is dependent upon the final pH value and buffer used to adjust the pH. Reactivation is observed as the pH is lowered from 6.4 to below 5.7 with acetate, fumarate, or HCl. With phosphate, reactivation occurs at any pH value from 6.9 to 4.5 but is greater at lower pH values. Thus, inactivation and reactivation have opposite pH dependencies. Also, reactivation is dependent upon the elapsed time of inactivation. At early times, no reactivation is observed when phosphate is used to adjust the pH, but reactivation is observed later in the inactivation reaction. Reactivation to 100% of the original activity does not occur under these conditions. These data suggest at least two inactivation mechanisms by benzyl cyanides: 1) formation of a tightly bound or covalent adduct between dopamine beta-hydroxylase and enzyme-bound mandelonitrile (or a rearranged form of this molecule), and 2) reversible inhibition resulting from cyanide binding to enzyme-Cu2+. Studies with radiolabeled p-hydroxybenzyl cyanide as well as EPR studies of dopamine beta-hydroxylase-Cu2+ are reported in the following paper.

Adrenal Medulla↗
PubMedDate not supplied

[Relation between cyanide-resistant respiration, effectiveness and rate of growth of Candida valida on ethanol].

The object of this work was to study the correlation between the growth rate of Candida valida and its cyanide-resistant respiration, as well as to investigate the effect of cyanide-resistant oxidase on biomass yield in the course of continuous cultivation of the yeast. The inhibition of cellular respiration by cyanide was shown to be directly correlated with the biomass yield. The intensity of cyanide-resistant respiration depended on the growth rate of the culture, and was lowest at the highest growth rates. It has been concluded that, when cyanide-resistant oxidase appears in the yeast cells, it functions simultaneously with the main respiratory chain. Cyanide-resistant respiration can be inhibited under the optimal conditions of the culture growth.

Candida↗
PubMedDate not supplied

[The effect of sodium cyanide and its antidotes on the isolated perfused rat heart].

The experiments were performed to investigate the effects of cyanide and several antidotes (sodium nitrite, DMAP, sodium thiosulfate and phentolamine) on isolated perfused rat heart to further elucidate the mechanism of action of cyanide and its antidotes. Sodium cyanide (40, 50 and 60 mg/ml) produced maximum effects on amplitude, heart rate and coronary flow, after 3 min, regardless of the event recorded. Some dose-dependence was noted, especially on the heart rate, somewhat less on amplitude and almost none on the coronary flow up to 15 min, but notable afterwards. Some spontaneous recovery occurred in each event, the most significant being that of the heart rate. Antidotes per se did not differ significantly in their action on isolated rat heart. All values, with some variations, were maintained within 10-20% of control. Antidotes, injected 1 min after sodium cyanide produced the most evident effects on amplitude and heart rate -- all antidotes practically and almost instantly neutralized the depressant effect of cyanide. Nitrite and particularly DMAP, were the most effective on coronary flow while other antidotes, although effective up to 3 min, did not much differ from cyanide alone throughout the rest of observation.

Aminophenols↗
PubMed1996

Determination of cyanide using a microbial sensor.

A microbial cyanide sensor was prepared, consisting of immobilized Saccharomyces cerevisiae and an oxygen electrode. When the electrode was inserted into a solution containing glucose, the respiration activity of the microorganisms increased. The change in the respiration activity is monitored with the oxygen electrode. When cyanide is added to the sample solution, the electron transport chain reaction of the respiration system in the mitochondria is inhibited, resulting in a decrease in respiration. The inhibition is caused by cyanide binding with respiration enzymes such as the cytochrome oxidase complex in the mitochondrial inner membrane. Therefore, the cyanide concentration can be measured from the change in the respiration rate. When the sensor was applied to a batch system at pH 8.0 and 30 degrees C, the cyanide calibration curve showed linearity in the concentration range between 0.3 microM and 150 microM CN-.

Cyanides↗
PubMed1994

Microbial degradation of metal complexed cyanides and thiocyanate from mining wastewaters.

A microbiological examination of the soil from a cyanide wastewater storage basin was carried out. The storage basin contained water from the cyanidation process of gold extraction, and it was composed principally of simple cyanide, metal complexed cyanide, mainly cuprocyanide, ferro-ferricyanides and thiocyanate. Pseudomonas species were the principal bacteria identified in the soil. Using the storage basin soil as a seed sludge, its potential for the biodegradation of all the cyanide complexes in the mining wastewater was studied in the laboratory, using batch, fed-batch and continuous processes. The ammonia and sulphate produced were quantified. The presence of intermediate products was suspected. In the continuous process, total degradation of all cyanide was observed at a dilution rate of 0.066 day(-1).

Journal Article↗
PubMed1997

Biological treatment of gold ore cyanidation wastewater in fixed bed reactors.

The treatment of a cyanidation effluent containing thiocyanate, free cyanide, and complexed cyanide was continuously performed for a period of 6 months. Activated carbon, pozzolana, and a mixture of pumice stone and zeolite were tested as supports in fixed bed reactors. Activated carbon adsorbed the different forms of cyanide. In contrast, the other supports did not remove any pollutants from the effluent during an adsorption experiment. All supports successfully allowed fixation of bacteria. More than 90% of the thiocyanate was biologically decomposed into NH4+, CO2 and SO4(2-), even when increasing the feed flow-rate and the pollutant concentrations. Free and complexed cyanides were eliminated, probably through a combination of precipitation and biological degradation. The oxidation of ammonium into nitrate was only performed by the activated carbon-containing column and with the more diluted feeding. The nitrification process was inhibited in all reactors when the cyanide concentrations and feed flow-rates were increased.

Journal Article↗