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At least 19 recordsLinked to original sources
PubMed1993

Changes in the parameters of oxygen metabolism in a clinical course recovering from potassium cyanide.

Poisoning with potassium cyanide is usually fatal because of the inhibition of cytochrome oxidase. The parameters of oxygen metabolism in a patient with cyanide poisoning who was admitted in a coma with seizures was monitored. The administration of amyl nitrite and sodium thiosulfate led to a rapid improvement: the parameters reflecting oxygen metabolism improved and the plasma level of cyanide decreased. The patient revived 1 1/2 hours after treatment. The arterial ketone body ratio (AKBR), which is the ratio of acetoacetate to beta-hydroxybutyrate in arterial blood and which reflects the redox state in liver mitochondria, improved dramatically following treatment. Because the AKBR changes in relation to electron transport in liver mitochondria, it seems to be a logical parameter for evaluating the effect of potassium cyanide poisoning on electron transport. The AKBR also reflects the efficacy of treatment for cyanide poisoning.

3-Hydroxybutyric Acid↗
PubMed2001

Cholestatic hepatitis caused by acute gold potassium cyanide poisoning.

INTRODUCTION: Poisoning after oral ingestion of gold potassium cyanide is rarely reported. A case of suicidal ingestion of gold potassium cyanide (potassium dicyanoaurate; CAS# 13967-50-5) is described. CASE REPORT: A 27-year-old man attempted suicide by ingesting 5 mL gold potassium cyanide solution. He developed vomiting, hyperamylasemia, and hepatic dysfunction. Cyanide poisoning was not detected but acute gold toxicity was noted. Pathologic findings of the liver showed centrilobular cholestasis with eosinophilic degeneration. The whole blood and serum gold were 4361 and 6011 microg/L, respectively, and the 24-hour urine gold was 429 microg/d in samples obtained on day 4. CONCLUSION: Gold-induced hepatotoxicity has been seen infrequently in patients receiving gold therapy. Reported agents include sodium aurothiomalate, sodium aurothiopropranol sulfonate, aurothioglucose, aurothiopolypeptide (Auro-detoxin), auric sulfide, and gold thiosulfate, our report adds gold potassium cyanide.

Acute Disease↗
PubMed1983

Inhibition of p-nitroanisole O-demethylation in perfused rat liver by potassium cyanide.

The effect of potassium cyanide on p-nitroanisole O-demethylation in perfused rat livers has been examined. Cyanide (2 mM), an inhibitor of cytochrome oxidase, diminished p-nitroanisole O-demethylation by 50-75% in perfused livers from normal and phenobarbital-treated rats, but had much less effect on hepatic microsomal p-nitroanisole O-demethylation. The inhibition was also observed in livers where the activity of the pentose phosphate shunt was abolished by pretreatment with 6-aminonicotinamide. Cyanide infusion decreased hepatic ATP/ADP ratios and cellular concentrations of glutamate, alpha-ketoglutarate, and isocitrate, but caused an increase in the NADP+/NADPH ratio. Rates of NADPH generation via the pentose phosphate shunt were unchanged by cyanide, and hepatic concentrations of glucose 6-phosphate were markedly increased by cyanide. Thus, inhibition of p-nitroanisole metabolism could not be explained solely by a direct interaction of cyanide with mixed-function oxidases or diminished NADPH generation via the pentose cycle. These data indicate that cyanide inhibits mixed-function oxidation in intact cells by diminishing the generation of NADPH from sources other than the pentose cycle. Further, these data are consistent with the hypothesis that some NADPH for mixed-function oxidation arises from cyanide-sensitive mitochondrial sources.

Animals↗
PubMed1988

Pharmacokinetics of intravenous potassium cyanide.

The pharmacokinetics of intravenously injected potassium cyanide have been studied in Beagle bitches. In the period up to about 80 min after dosing, blood levels fell in a manner consistent with first-order elimination kinetics. Thereafter blood cyanide concentrations fell at a slower rate, indicating that a second phase of slower elimination had been entered.

Animals↗
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↗
PubMed1983

Excretion of 14C-labeled cyanide in rats exposed to chronic intake of potassium cyanide.

The excretion of an acute dose of 14C-labeled cyanide in urine, feces, and expired air was studied in rats exposed to daily intake of unlabeled KCN in the diet for 6 weeks. Urinary excretion was the main route of elimination of cyanide carbon in these rats, accounting for 83% of the total excreted radioactivity in 12 hr and 89% of the total excreted radioactivity in 24 hr. The major excretion metabolite of cyanide in urine was thiocyanate, and this metabolite accounted for 71 and 79% of the total urinary activity in 12 hr and 24 hr, respectively. The mean total activity excreted in expired air after 12 hr was only 4%, and this value did not change after 24 hr. Of the total activity in expired air in 24 hr, 90% was present as carbon dioxide and 9% as cyanide. When these results were compared with those observed for control rats, it was clear that the mode of elimination of cyanide carbon in both urine and breath was not altered by the chronic intake of cyanide.

Animals↗
PubMed1991

Increase in the expression of muscarinic cholinergic receptors in isolated, neonatal rat cardiac myocytes treated with potassium cyanide.

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.

Adenosine Triphosphate↗
PubMed1988

The efficacy of superactivated charcoal in treating rats exposed to a lethal oral dose of potassium cyanide.

Due to the apparent low binding capacity of activated charcoal for potassium cyanide (KCN) in vitro, the use of oral activated charcoal therapy for oral exposure to cyanide compounds is controversial. In our study, rats were given a lethal oral dose of ground granular KCN (35 or 40 mg/kg) in a gelatin capsule followed immediately by either 4 g/kg of superactivated charcoal in a 20% suspension or a similar volume of deionized water. Signs of cyanide toxicosis occurred rapidly, with a mean time to signs of 3.3 and 2.7 minutes in control animals receiving 35 or 40 mg/kg KCN, respectively. All 26 of the control rats showed signs, and all but one in the 35 mg/kg group died within 19 minutes. Only 12 of 26 rats treated with superactivated charcoal showed signs of KCN toxicosis and eight of those animals died. Oral exposure of rats to lethal doses of KCN can be treated effectively by immediate administration of superactivated charcoal.

Administration, Oral↗
PubMed1993

Potassium cyanide protects Escherichia coli from complement killing by the inhibition of C3 convertase activity.

The exact mechanism by which deposited C5b-9 complexes kill Gram-negative bacteria is unclear. It has been proposed that during complement activation the membrane attack complex triggers an energy dependent process in Gram-negative bacteria that mediates destruction of the inner membrane. This observation in part resulted from the survival of Gram-negative bacteria that were incubated with an uncoupler (DNP) or an inhibitor (KCN) of oxidative phosphorylation during complement activation. In a reexamination of this issue we employed potassium cyanide (KCN) to block energy dependent pathways and observed a dose dependent inhibition of C9 uptake on E. coli J5 during serum incubation, suggesting that cyanide was interfering with complement activation. To verify the effect on complement activation we chose specifically to study the effects of KCN on the C3 convertase of the classical pathway. Sensitized sheep erythrocytes were employed as our model system. This system allowed us to construct a series of stable intermediates that were used to test the effect of cyanide on the formation and activity of precursors of the classical pathway C3 convertase. The data illustrate that the concentrations of potassium cyanide that inhibit complement killing of J5 also inhibit C3 convertase activity on sensitized sheep erythrocytes. The results of this study refute the principal observation made by other investigators, that potassium cyanide protects bacteria from complement killing by inhibiting bacterial energy dependent pathways that spark inner membrane destruction. A better scenario is that the organisms survive because cyanide inhibits complement activation.

Animals↗
PubMedDate not supplied

[Dynamics of the activity of cytochrome oxidase and glutathione level in tissues of rats, poisoned with potassium cyanides and nitriles].

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.

Animals↗
PubMedDate not supplied

Simple, rapid, and portable chromatographic tetrazolium reduction method for detection of potassium cyanide in medicinal drugs and confectionery.

A simple, rapid, and portable paper chromatographic method for detection of potassium cyanide in medicinal drugs and a few confectionery samples is described. Potassium cyanide is extracted in methanol and concentrated. Acetone-water-1.5% EDTA (4 + 5.5 + 0.5) mixture is used as the solvent system for paper chromatography. The KCN chromatograms appear as pink spots on paper due to reduction of the chromogenic salt 2-(4-iodophenyl)-3-(4-nitrophenyl)-5-phenyl tetrazolium chloride; phenazonium methosulfate is a catalyst. Microgram amounts of KCN can be separated and detected in the laboratory or the marketplace because of the simplicity of the method.

Chromatography, Paper↗
PubMedDate not supplied

Quantification of expired metabolites following potassium cyanide administration: a new method.

A sensitive and specific radiolabel method for measuring expired hydrogen cyanide (HCN) or carbon dioxide (CO2) derived from cyanide was developed. An ethanol collecting solution containing a 10(-2) M of cobalt chloride trapped 88% of the H14CN passed through the solution following acid volatilization of a known amount of K14CN. The range of linearity, r = 0.998, exceeded the 0.01 to 0.1 mumoles tested for measuring the pulmonary metabolites. The cobalt chloride collecting solution trapped less than 0.02% of the 10 to 100 mumoles of 14CO2 generated by acid hydrolysis of 14C-sodium bicarbonate (NaH14CO3). Introduction of a second collecting solution specific for CO2, composed of ethanol: ethanolamine (2:1, v/v), was used to collect the CO2 derived from cyanide. Following the subcutaneous (sc) administration of 4.6 mg/kg of potassium cyanide (KCN) and 4.5 microcuries (microCi) K14CN, 1 to 2% and 2 to 3% of the dose was expired as H14CN and 14CO2, respectively.

Animals↗
PubMed1985

The oxidative disposition of potassium cyanide in mice.

The role of oxidative metabolism in the disposition of potassium cyanide (KCN), was investigated in mice administered KCN, (4.6 mg/kg, s.c.) containing 4.5 microCi [14C]KCN. The expired pulmonary metabolites, [14C]hydrocyanic acid (HCN) and 14CO2, were collected and analyzed. Approximately 1% and 2% of the KCN dose was expired as [14C]HCN and 14CO2, respectively. Expiration of the pulmonary metabolites was decreased following pretreatment with sodium nitrite, sodium thiosulfate, oxygen, or a combination of cyanide antidotes. Treatment with hydrogen peroxide lowered the amount of [14C]HCN expired and did not alter the expiration of 14CO2. Treatment with 3-amino-1,2,4-triazole (catalase inhibitor), superoxide dismutase, or diethyldithiocarbamic acid (superoxide dismutase inhibitor) did not change the amount of [14C]HCN expired. However, superoxide dismutase significantly increased the amount of 14CO2 expired, whereas diethyldithiocarbamic acid decreased 14CO2 expiration. The results from these studies suggest that in vivo cyanide can be oxidized to CO2 and treatment with agents that alter the availability of endogenous superoxide and/or hydrogen peroxide can alter the rate of cyanide oxidation.

Amitrole↗
PubMed1978

A circadian susceptibility/resistance rhythm for potassium cyanide in male BALB/cCr mice.

Circadian rhythms in mortality and/or survival time following a single intraperitoneal injection of a LD50 of potassium cyanide were studied. In two investigations, different but comparable subgroups of inbred male BALB/cCr mice were treated at 4-h intervals (under conditions standardized for chronobiologic study) during 24-h spans. Mice were observed for exact time-to-death during the first hour after treatment as well as overall mortality during the entire 24-h post-injection span following each KCN treatment timepoint. In both studies, mortality from KCN exhibited a 24-h rhythm. Highest mortality occurred in mice injected at 1600 (80% mortality) in Experiment 1 and 2000 (100% mortality) in Experiment II. Lowest mortality occurred at 0400 (40% mortality) in Experiment I and 0800 (30% mortality) in Experiment II. The need to consider the circadian organization of physiologic function when bioassaying toxicity is discussed.

Animals↗
PubMed1990

[Potassium cyanide poisoning treated with hydroxocobalamin].

A fifteen-year-old girl, with a clean medical history, was admitted to the intensive care unit 90 minutes after ingestion of 2.5 g potassium cyanide. She had typical signs of severe cyanide poisoning including deep coma, circulatory failure, and major metabolic acidosis. Gastric lavage and antidotal treatment with 4 g hydroxocobalamin and 8 g sodium hyposulfite was administered without delay together with supportive treatment consisting of mechanical ventilation with FIO2, blood alkalinisation and administration of beta-stimulants. These measures led to a rapid clinical improvement. The ventilatory support was discontinued after 24 hours and the patient left the intensive care unit on the fourth day with only slightly impaired mental status. She survived despite a very high blood cyanide concentration (494 mumol.l-1 on admission) probably because of the rapid symptomatic and antidotal treatment.

Acidosis↗
PubMed1984

Analysis of brain metabolism changes induced by acute potassium cyanide intoxication by 31P NMR in vivo using chronically implanted surface coils.

Chronic implantation of surface coils on the skull has been developed to record 31P NMR spectra of the brain in unanesthetized rats. Intraperitoneal sublethal potassium cyanide doses induce strong and reversible changes in high-energy phosphate compounds in the brain, similar in part to those induced by ischemia. These effects are dose-dependent as far as phosphocreatine, inorganic orthophosphates and pH are concerned; ATP does not seem to be altered by KCN doses ranging from 3 to 5 mg/kg but starts decreasing at a dose of 6 mg/kg. The fraction of Mg2+ complexed ATP which could be estimated as about 90% was not affected by KCN intoxication. For high doses (6 mg/kg) a new peak, appearing on the upfield side of the inorganic phosphate peak, may correspond to an acidic compartment, the significance of which is discussed.

Adenosine Triphosphate↗
PubMed1982

Molecular interaction of acrylonitrile and potassium cyanide with rat blood.

The interaction of acrylonitrile (VCN) with rat blood has been investigated at the molecular level in an attempt to understand the possible mechanism of its toxicity. The results obtained were compared to those with potassium cyanide (KCN), a compound known to liberate cyanide (CN-) in biologic conditions. The radioactivity derived from K14CN was eliminated faster than that from [1-14C]VCN. Up to a maximum of 94% of 14C from VCN in erythrocytes was detected covalently bound to cytoplasmic and membrane proteins, whereas 90% of the radioactivity from KCN in erythrocytes was found in the heme fraction of hemoglobin. Determination of specific activity showed that binding occurred more in vivo than in vitro which indicated that the VCN molecule was bioactivated inside erythrocytes. These results indicate that KCN interacts mainly through CN- liberation and binding to heme, whereas VCN, which binds to cytoplasmic and membrane proteins, may cause damage to red cells by mechanisms other than release of CN-.

Acrylonitrile↗