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PubMed1975

Toxicological and clinical aspects of cyanide metabolism.

This contribution deals with the occurrence of cyanide and its biological pathways in the body. Especially possibilities of detoxification are pointed out. Intoxications are caused by acute and chronical cyanide uptake. Tobacco amblyopia, retrobulbar neuritis in pernicious anaemia, Leber's optic atrophy, Nigerian nutritional neuropathy, and sterility in female heavy smokers are attributed to cyanide intoxication. Various methods for treating acute and chronic cyanide intoxication are discussed.

Acute Disease↗
PubMedDate not supplied

[The experimental treatment of cyanide poisoning with a methemoglobin solution].

The stroma-free methemoglobin solution proved to be an effective antidote against acute cyanide poisoning in experiment. The poisoning was induced by intraperitoneal administration to rats of cyanide solutions in doses of 5, 10 and 15 mg/kg. Methemoglobin solutions were injected intravenously in doses of 2 and 4 g/kg. All the rats given methemoglobin solution after the administration of cyanide survived. Spectrophotometry of rat urine demonstrated rapid excretion of methemoglobin cyanide.

Animals↗
PubMedDate not supplied

Removal of cyanides by electrooxidation.

The paper describes a study on electro-oxidation of cyanides complexed with copper, present in metal plating wastewater. A detailed voltammetric study has indicated that formation in situ of the electrocatalytic film of copper oxide and electro-oxidation of cyanides probably occurs at the same anode potential. By contrary to other materials at which electro-oxidation of cyanide also occurs, at copper oxide elimination of cyanide occurs at a potential lower then the potential of hydroxide ion discharge.

Copper↗
PubMedDate not supplied

Allyl disulfide as donor and cyanide as acceptor of sulfane sulfur in the mouse tissues.

Cytoplasm of mammalian glial cells was reported to contain Gomori-positive cytoplasmic granulation (GPCG), whose biological role is unknown. The present study attempted to discover conditions facilitating GPCG formation and to elucidate their relationship with sulfane sulfur metabolism. To address these problems, we investigated in vivo the effect of both allyl disulfide (DADS), occurring in garlic (sulfane sulfur donor) and cyanide (sulfane sulfur acceptor) on number of GPCG-containing glial cells in the mouse brain. In parallel, sulfane sulfur level and activity of rhodanese and 3-mercaptopyruvate sulfurtransferase (MpST) were determined in the mouse brain and liver. Cyanide caused a drop in GPCG number in the brain, while activity of sulfurtransferases and sulfane sulfur level remained unchanged. Slight but significant cyanide-induced rise in MpST activity was observed only in the liver, which indicates a possibility of enhancement of its detoxification in reaction with mercapropyruvate in this organ. DADS, a sulfur donor, increased GPCG number in the brain, whereas activity of sulfurtransferases and sulfane sulfur level did not change. However, in the liver, DADS elevated both sulfurtransferase activity and sulfane sulfur level. These observations suggest that DADS can constitute a source of sulfane sulfur for the liver, thereby activating anaerobic sulfur metabolism and sulfane sulfur transfer. Consequently, this leads to the increase in sulfane sulfur level in plasma, in which it is transported in the form of albumin hydropersulfides and can be used for cyanide detoxification or stored in glial cells as GPCG. Therefore, it is not excluded that GPCG observed in the brain of mice and other mammals can be a source and a store of sulfane sulfur in mammals.

Allyl Compounds↗
PubMed1991

Cyanide ingestion. Case studies of four suicides.

Deliberate ingestion of cyanides is relatively rare, as reflected in the Registrar General's figures. There are no pathognomonic specific autopsy findings and even the distinctive smell may be missed by some individuals. We present four cases of cyanide ingestion, one of which appears to be the first reported case of magnesium cyanide poisoning in humans. The problems involved in investigating deaths from cyanide ingestion are discussed.

Adult↗
PubMed1991

Cyanide-induced increases in plasma catecholamines: relationship to acute toxicity.

Cyanide is known to initiate release of catecholamines from chromaffin cells and isolated adrenals but the effect of cyanide on plasma catecholamine levels has not been reported. The present study demonstrates that cyanide produces marked elevation of plasma catecholamines in mice. A sublethal dose of KCN (5 mg/kg, sc) significantly increased plasma norepinephrine (NE) and epinephrine (EPI) at 5 min after administration, and the elevated levels returned to normal at 15 min. At a dose of 10 mg/kg, NE and EPI plasma levels remained elevated over a 15 min period. Multiple exposures to sublethal doses of KCN (5 mg/kg, sc, 4 doses at 15 min intervals) produced a steep, sustained rise in plasma NE and EPI. Administration of KCN (15.6 micrograms) directly into the lateral ventricles of the brain caused convulsions and respiratory depression, but did not affect plasma catecholamine levels. Pretreatment with pargyline did not alter the magnitude of the response to KCN. Adrenalectomy prevented the increase in plasma EPI and had no influence on plasma NE levels, indicating cyanide acts directly on the adrenals to stimulate EPI release. It is proposed that KCN directly stimulates the sympathoadrenal axis to increase plasma catecholamine levels.

Adrenal Glands↗
PubMed1990

Studies of cobalamin as a vehicle for the renal excretion of cyanide anion.

To examine the ability of hydroxocobalamin (vitamin B12a, HO-Cbl) to counteract the toxicity of cyanide by promoting the renal excretion of cyanide anion, we studied the pharmacokinetics of HO-Cbl and cyanocobalamin (vitamin B12, CN-Cbl) given in high doses to dogs. After administration of intravenous bolus doses of HO-Cbl and CN-Cbl (5, 10, 25 mg/kg) to female foxhounds, peak plasma concentrations were attained within 1 minute, after which the cobalamins disappeared from plasma in a manner consistent with two-phase distribution and elimination kinetics. While mean t1/2 measurements for the initial distribution phase were similar for HO-Cbl and CN-Cbl, the secondary excretion phase was more prolonged for HO-Cbl than for CN-Cbl (t1/2, 94.75 minutes vs 62.64 minutes, respectively). Pharmacokinetic data permitted the design of a HO-Cbl infusion schedule that resulted in stable plasma concentrations in test animals. When NaCN was then given intravenously to animals preloaded with HO-Cbl (20 micrograms/ml plasma), conversion of HO-Cbl to CN-Cbl in vivo, was documented by both thin-layer and high-performance liquid chromatographic analysis of successive urine samples. Moreover, in dogs preloaded with HO-Cbl (20 micrograms/ml plasma), up to 10% of the cyanide administered as NaCN infusions was recovered in urine as CN-Cbl by 60 minutes, compared with less than 0.3% in dogs not treated with HO-Cbl. In addition, under these conditions of HO-Cbl loading, the minimum doses of NaCN required to produce sublethal signs of cyanide toxicity (hypotension, tachypnea, tachycardia) were found to be increased to levels that in some cases exceeded normally lethal doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Suspected cyanide poisoning in smoke inhalation: complications of sodium nitrite therapy.

A 78 year old man was found comatose, apneic, and asystolic after closed-space smoke inhalation. He was successfully resuscitated to pulse and blood pressure at the scene. A cyanide component to the poisoning was suspected and two 300 mg doses of sodium nitrite were administered, resulting in significant hypotension. Although high methemoglobin levels were not induced, when added to simultaneously obtained carboxyhemoglobin levels, the total amount of non-oxygen transporting hemoglobin remained nearly constant for about 4-1/2 hours before hyperbaric oxygen (HBO) therapy could be administered. The patient later died in multi-organ system failure. Admission whole blood cyanide level was only 0.34 mcg/mL. These sodium nitrite adverse effects can be avoided by slow intravenous infusion and by administering only recommended doses. In smoke inhalation victims with suspected cyanide poisoning, sodium thiosulfate should be administered first, and sodium nitrite withheld until after the patient is receiving HBO therapy. When available, hydroxocobalamin (which neither induces methemoglobinemia nor causes hypotension) may be the specific cyanide antidote of choice for victims of smoke inhalation.

Aged↗
PubMed1986

Cyanide poisoning from laetrile ingestion: role of nitrite therapy.

A 4-year-old child ingested laetrile and almost died of cyanide poisoning. Treatment with the Lilly cyanide antidote kit resulted in rapid, complete recovery. Extremely high whole blood cyanide levels were documented. The necessity for use of the antidote kit in serious cyanide poisoning has recently been questioned. This case demonstrates benefit from antidotal treatment.

Acute Disease↗
PubMed1988

Chronic cyanide poisoning: unifying concept for alcoholic and tropical pancreatitis.

We hypothesize that chronic cyanide toxicity may explain the occurrence of calcific pancreatitis in chronic alcoholic individuals in affluent Western nations and malnourished children and young adults in developing tropical regions. In alcoholic persons the source of cyanide is cigarette smoke, and in tropical countries the source could be cassava or other plants. The cyanide hypothesis is consistent with the known epidemiologic and metabolic characteristics of these two contrasting forms of pancreatitis. We believe that continued chronic cyanide poisoning could reinforce any independent effect of alcohol or malnutrition on the pancreas, resulting in an exaggerated and perhaps irreversible form of the disease.

Alcoholism↗
PubMed1985

Cyanide intoxication among silver-reclaiming workers.

Thirty-six former workers in a silver-reclaiming facility who had been exposed over a long-term to excessive levels of cyanide were studied to determine acute and residual toxic reactions. The study involved physical examinations, laboratory studies, and a questionnaire to determine levels of exposure, symptoms during employment, and current symptoms. Questionnaire data showed that during the time of active employment there was a high prevalence of symptoms that are consistent with acute cyanide toxic reactions. A significant positive trend for prevalence of cyanide-related symptoms measured against levels of exposure was demonstrated, supporting a dose-response effect. Some symptoms occurring seven or more months after exposure had ceased also exhibited a dose-response trend. Mild abnormalities of vitamin B12, folate, and thyroid function were detected and suggest long-term cyanide effects.

Adult↗
PubMed1985

Influence of dietary cyanide on immunoglobulin and thiocyanate levels in the serum of Liberian adults.

Serum thiocyanate, antibody titers to thiocyanates, and serum immunoglobulins (IgM, IgG, IgA) were measured in 73 Liberian adults normally consuming diets of low, moderate, high, or no (control) cassava-derived cyanide (CN(-)). When control and low groups (n = 40; daily intake less than 0.60 mg CN(-) per kg body weight) were contrasted with moderate and high groups (n = 33; daily intake greater than or equal to 0.60 mg CN(-) per kg body weight), the authors observed that (1) one-time serum thiocyanate measurements were not sensitive to long-term cyanide intake; however, (2) antibody titers to thiocyanates were positively correlated with cassava-based cyanide intakes (r = .22, P = 0.05); and (3) serum IgM, IgG, and IgA levels were elevated in individuals regularly consuming moderate and high levels of dietary cyanide. Possible responsible mechanisms and health implications are discussed.

Adolescent↗
PubMed1980

Mechanisms of inactivation of molybdoenzymes by cyanide.

The reduced forms of xanthine oxidase, xanthine dehydrogenase, aldehyde oxidase, and sulfite oxidase are inactivated by cyanide. Following gel filtration to remove excess of reductant and cyanide, the isolated enzymes remain inactive. Thiocyanate, a product of inactivation of the oxidized forms of the xanthine- and aldehyde-oxidizing enzymes by cyanide, is not released during inactivation of the reduced enzymes. Studies with [14C]cyanide show that, while stoichiometric binding is required for the onset of inactivation, its continued binding is not essential to maintenance of the inactivated state. Electron paramagnetic resonance and absorption spectroscopic studies on the isolated inactivated enzymes show that prosthetic groups other than molybdenum are fully oxidized but that the molybdenum centers are modified. Reactivation is accomplished by incubation with suitable oxidants. Aerobic reactivation of inactive sulfite oxidase required only 1 eq of ferricyanide/active site. However, under rigorously anaerobic conditions, 3 to 4 mol of ferricyanide/active site were reduced, indicating that the molybdenum centers in the inactive enzyme had been reduced below the levels attained by the native enzyme during catalysis.

Aldehyde Oxidoreductases↗
PubMedDate not supplied

[Absence of a correlation between the respiratory resistance of bacteria to cyanide and their cytochrome d content].

The object of this work was to study whether a correlation existed between the content of cytochrome d in different bacterial cells and the inhibition of their respiration by cyanide. No correlation was found between the concentration of cytochrome d and the degree of resistance to cyanide of the bacterial respiration. Just as the cyanide-resistant respiration of eukaryotic microorganisms, the cyanide-resistant respiration of bacteria was concluded to involve the operation of oxidase whose nature was not cytochromic .

Aerobiosis↗
PubMed1983

[Structural changes in L-cell mitochondria exposed to cyanide].

Using light and electron microscopy, as well as stereological analysis, a study was made of structural changes in mitochondria of cultured L-cells acted upon with 1 mM cyanide. After 23 hours of incubation, in cells cultured in the presence of cyanide the volume density of mitochondria, the volume of the average mitochondrion and the surface area of its membranes increased nearly twice as much. Concurrently, the number of mitochondria decrease also practically two-fold without any reliable changes in the surface area of membranes per unit of mitochondrion volume. A shorter (7 hours) incubation of L-cells in the presence of cyanide results in a decreased volume density of mitochondria in the cytoplasm, decreased volume of the average mitochondrion, without any significant changes in other above mentioned parameters. It is supposed that the changes in mitochondria under a prolonged cyanide treatment of cells are conditioned by the fusion of mitochondria as well as by a compensatory increase in the total surface of mitochondrial membranes.

Animals↗
PubMed1984

The influence of pralidoxime mesylate on the measurement of cyanide concentrations in solutions.

Pralidoxime mesylate (P2S) can interfere with the colorimetric analysis for cyanide in solutions. Apparent increases in cyanide concentrations, related to the presence of P2S, are most marked at extreme pH values. At acid pH there is a direct interference by P2S, and at alkaline pH the P2S molecule is cyanogenic. Prompt analysis and the use of a cyanide separation technique minimizes the artifactual increase in measured cyanide concentrations. This effect is insignificant at pH 7.4.

Colorimetry↗
PubMed1981

Amygdalin toxicity studies in rats predict chronic cyanide poisoning in humans.

Significant amounts of cyanide are released when amygdalin (Laetrile), a cyanogenic glycoside, is given orally or intravenously to rats. The amount of cyanide liberated following oral administration is dependent in part on the bacterial flora of the gut and can be suppressed by antibiotic pretreatment of the animals. Bacteria from human feces likewise hydrolyze amygdalin with release of cyanide. Humans taking amygdalin orally in the hope of preventing cancer are likely to be exposed to levels of cyanide in excess of that associated with the development of tropical ataxic neuropathy in people of underdeveloped countries where food containing cyanogenic glycosides is a staple part of the diet.

Amygdalin↗
PubMed1995

Effects of cyanide on the neural mechanisms controlling breathing in the neonatal rat in vitro.

The effects of hydrogen cyanide (HCN) on the neural mechanisms controlling breathing were studied. Two in vitro experimental models were utilized; the brain stem-spinal cord and the medullary slice preparations isolated from neonatal rats. Cyanide, at concentrations deemed lethal in vivo (50 microM), caused a modest (< 15%) depression of the frequency and amplitude of inspiratory rhythmic discharge when added to the bathing media. Moreover, the neuronal network underlying respiratory rhythmogenesis continued to function for hours in the presence of very high concentrations of cyanide (600 microM). We hypothesize that the rapid suppression of breathing caused by cyanide in vivo is due to changes in neuronal excitability in respiratory modulating populations in the CNS rather than due to perturbations of cellular oxidative metabolism or neurons within respiratory rhythm generating centres.

Animals↗