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PubMed1994

Dopaminergic neurotoxicity of cyanide: neurochemical, histological, and behavioral characterization.

Previous reports have shown that dopamine (DA) is depleted in the brains of animals treated with cyanide. To develop a model for studying the mechanisms of cyanide-induced changes in dopaminergic systems, mice were treated with cyanide (KCN, 6 mg/kg, sc) twice a day for 7 days and 16 hr after the last dose neurochemical, histological, or behavioral parameters were evaluated. DA levels in KCN-treated animals decreased in the striatum (41%), hippocampus (30%), and cerebral cortex (13%) as compared to saline-treated controls. In striatal and hippocampal tissues, but not in cerebral cortex, malondialdehyde levels increased 43 and 57%, respectively, as compared to controls, indicating that peroxidation of lipids occurred in these brain areas. Over 30% of the treated mice exhibited decreased locomotor activity and akinesia, which were suppressed by l-DOPA (100 mg/kg, ip). Tyrosine hydroxylase (TH) immunohistochemical examination of brains from cyanide-treated animals showed a reduced number of TH-positive cells in substantia nigra, indicating a loss of dopaminergic neurons. In contrast, acute cyanide (KCN, 6 mg/kg, sc) did not produce significant neurochemical or behavioral changes. Under these treatment conditions, cyanide produces a central dopaminergic toxicity which is characterized by decreased DA levels in select brain areas, impaired locomotor activity, and neuronal damage.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

A study of experimental cyanide encephalopathy in the acute phase--physiological and neuropathological correlation.

A study was performed to elucidate the significance of various physiological factors contributing to the pathogenesis of experimental cyanide encephalopathy, such as the systemic arterial blood pressure, venous pressure, common carotid blood flow and local blood flow of the cerebral grey and white matters, and blood gas including pH. The histology and topography of the brain damage was also analysed. Twenty-one cats were divided into four groups. The animals in groups 1, 2 and 3 were subjected to continuous infusion of 0.2% sodium cyanide solution and to the ensuing hypotension below 100 mm Hg by administering a ganglion-blocking drug and by respiratory arrest. Severe damage developed in the deep cerebral white matter, corpus callosum, pallidum and substantia nigra, but the damage of the cerebral cortex and hippocampus was not remarkable. The animals in group 4 that were subjected to cyanide infusion without significant hypotension (above 100 mm Hg), but to the same degree of acidosis as that of the other groups, had similar morphological changes, but to a lesser degree. On the basis of our physiological and morphological findings, we speculated that the pathophysiological factors of tissue hypoxia and subsequent hypotension operated in cyanide leucoencephalopathy. The topographic selectivity seemed to be related to the characteristic cerebral vascular system, and the severity of the white matter lesions was related to the intensity of both hypoxia and hypotension during cyanide infusion, but not to the extent of acidosis, total dose of cyanide or duration of its infusion per se.

Acute Disease↗
PubMedDate not supplied

The origin of proteins: Heteropolypeptides from hydrogen cyanide and water.

Evidence from laboratory and extraterrestrial chemistry is presented consistent with the hypothesis that the original heteropolypeptides on Earth were synthesized spontaneously from hydrogen cyanide and water without the intervening formation of chi-amino acids, a key step being the direct polymerization of atmospheric hydrogen cyanide to polyaminomalononitrile (IV) via dimeric HCN. Molecular orbital calculations (INDO) show that the most probable structure for (HCN)2 is azacyclopropenylidenimine. Successive reactions of hydrogen cyanide with the reactive nitrile side chains of IV then yield heteropolyamidines which are converted by water to heteropolypeptides. To study this postulated modification of a homopolymer to a heteropolymer, poly-chi-cyanoglycine (IX) was prepared from the N-carboxyanhydride of chi-cyanoglycine. Hydrolysis of IX, a polyamide analog of the polyamidine IV, yielded glycine. However, when IX was hydrolysed after being treated with hydrogen cyanide, other chi-amino acids were also obtained including alanine, serine, aspartic acid and glutamic acid, suggesting that the nitrile groups of IX (and therfore of IV) are indeed readily attacked by hydrogen cyanide as predicted. Further theoretical and experimental studies support the view that hydrogen cyanide polymerization along these lines is a universal process that accounts not only for the past formation of primitive proteins on Earth, but also for the yellow-brown-orange colors of Jupiter today and for the presence of water-soluble compounds hydrolyzable to chi-amino acids in materials obtained from environments as diverse as the moon, carbonaceous chondrites and the reaction chambers used to simulate organic synthesis in planetary atmospheres.

Amino Acids↗
PubMed2002

Low prevalence of ataxic polyneuropathy in a community with high exposure to cyanide from cassava foods.

INTRODUCTION: Ataxic polyneuropathy, which occurs in endemic form in an area in southwest Nigeria, is attributed to exposure to cyanide from cassava foods. Exposure to cyanide from cassava is, however, not exclusive to this endemic area. In this study, the occurrence of ataxic polyneuropathy was compared in two communities in Nigeria, one located in the endemic area and the other located outside the endemic area. Both communities have been shown to have high exposure to cyanide from cassava foods. METHOD: The prevalence of ataxic polyneuropathy in Jobele, Nigeria, a community located outside the endemic area, was compared with the prevalence of ataxic polyneuropathy in Ososa, Nigeria, a reference community located in the endemic area. Subjects aged 10 years and above in both communities were screened for ataxic polyneuropathy. Ataxic polyneuropathy was diagnosed if sensory gait ataxia and sensory polyneuropathy were present. The intake of cassava foods, biomarkers of exposure to cyanide, and intake of protein and sulphur were measured. RESULTS: Prevalence of ataxic polyneuropathy were 490 per 10,000 in Ososa, and 17 per 10,000 in Jobele. The age-adjusted prevalence ratio is 4 (95% CI 0-9). The mean intake of all cassava foods in Jobele was 7 meals/person/week (95% CI 6-8), while the mean intake of all cassava foods in Ososa was 10 meals/person/week (95 % CI 9-11). The concentration of thiocyanate in the plasma was above the reference limit in 65% (95% CI 57-73) in Jobele, and 40 % (95% CI 27-52) in Ososa. The intake of protein was significantly lower in Ososa than in Jobele, but the concentrations of glutathione, cysteine and gamma-glutamylcysteine in the plasma were within the same range in Jobele and Ososa. CONCLUSION: This study shows that the occurrence of ataxic polyneuropathy is low in a community where exposure to cyanide is high. This suggests that exposure to cyanide is not a direct cause of ataxic polyneuropathy.

Adolescent↗
PubMed2003

Arabidopsis sulfurtransferases: investigation of their function during senescence and in cyanide detoxification.

Sulfurtransferases (STs) and beta-cyano- l-alanine synthase (CAS) are suggested to be involved in cyanide detoxification. Therefore, the accumulation of ST1 and CAS RNAs, and the ST and CAS protein levels and enzyme activities were determined in Arabidopsis thaliana Heynh. plants grown under different conditions. Senescence-associated processes were successfully induced by natural aging, by jasmonate methyl ester and by darkness in whole plants and detached leaves, as demonstrated by the expression of the senescence marker genes SAG12 and SAG13. However, the changes in RNA accumulation and protein levels of ST and CAS did not correlate with the expression of these senescence marker genes; the specific ST and CAS activities either decreased (ST) or increased (CAS). In another experiment, Arabidopsis plants were sprayed with cyanide to investigate the role of ST and CAS in cyanide detoxification. The expression of ST and CAS at the RNA and protein levels, and also the enzyme activities, remained equal in cyanide-treated and control plants. Incubation with 1-aminocyclopropane-1-carboxylic acid, the precursor of ethylene, increased while fumigation with ethylene decreased expression and activity of ST and CAS. In summary, cyanide does not induce the expression or enhance the activity of ST and CAS in Arabidopsis. For both proteins the evidence for a role in cyanide detoxification or induced senescence is low.

Acetates↗
PubMed2005

Natural cyanide degradation and impact on Ili River drainage areas from a Goldmine in Xinjiang autonomous region, China.

The Ili River is a very important river to the northwest of China and Kazakhstan. The Axi Goldmine is located in the upstream of a branch of the Ili River. The cyanide from the goldmine effluent is a threat to the downstream areas. According to our study, the natural degradation of cyanide conforms to a negative exponential equation in the tailings impoundment, second wastewater pond and even in the receiving streams if the dilution action from other streams were deducted. In the combined action of dilution and natural decomposing, the cyanide from the goldmine effluent does not pose a hazard to the trunk of the Ili River in the normal producing states. The equations of cyanide degradation in the streams and the hydrology parameters could be used to assess the environmental impact on the downstream areas if accidental discharges of cyanide occurred. The available way of decreasing the cyanide impact on the streams is to increase the rate of recycled water so that the lower the wastewater level in the tailing impoundment and the second wastewater pond, the lower is the amount of leakage of wastewater to the streams.

Biodegradation, Environmental↗
PubMed1990

Potentiometric measurements of hydrogen and cyanide ions in buffered media.

Potentiometric measurements of hydrogen and cyanide levels were studied in different buffered media that are used in biological experiments. The addition of 1-10mM NaCN increased the pH (from 7.2-7.5 up to 9.5) of either bicarbonate/phosphate-buffered (artificial cerebrospinal fluid (ACSF), sera, and whole blood) or Hepes-buffered solutions in a concentration-dependent manner. While in aerated ACSF this increase was transient (half-relaxation time less than 4 min), the increase in pH was sustained in Hepes buffer. A mathematical model that predicts the maximum cyanide-induced increases in pH was derived. When NaCN was added to either ACSF or Hepes-buffered solutions, a Nernst relation was obtained, but deviations from Nernstian responses resulted when NaCN was added to sera or whole blood. These responses, however, differed substantially from the theoretical results that were based on the relative amounts of ionized cyanide present in the various pH environments. In addition, attempts were made to indirectly examine the formation and escape of HCN by calculating the time constants of decay (tau d) of the cyanide-induced potentiometric responses. With progressively higher NaCN concentrations in ACSF, the values of tau d did not decrease, but were constant. As predicted, however, the values of tau d were larger when solutions were covered or had higher initial pH values. These results suggest that in the solutions tested, the cyanide electrode used in the present study measured the total amount rather than the ionized portion of dissolved cyanide and that the values of tau d do not correspond to formation/escape rates of HCN.

Buffers↗
PubMed1988

A mitochondrial chemiluminescence evoked by a novel mixed copper(II)-cyanide complex/acetaldehyde cyanohydrin chelate: a kinetic analysis suggesting a role for membrane-bound vicinal sulfhydryls.

Cyanide added to mitochondria in the presence of copper and acetaldehyde evokes a chemiluminescence which follows series pseudo-first-order kinetics: (formula; see text) An evaluation of the effects of protein (mitochondria), copper, cyanide, acetaldehyde, and oxygen on the kinetic parameters shows that k1 is influenced by protein, cyanide (at low concentrations), and oxygen while k2 is influenced by cyanide, acetaldehyde (at low, less than 11.9 mM, and high, greater than 35.6 mM, concentrations), and oxygen. The integral light increases linearly with the square root of total copper(II) and with the square of the total acetaldehyde. The sustained emissions appear to reflect an initial oxidative event mediated by a novel mixed copper(II)-cyanide complex/acetaldehyde cyanohydrin chelate. Cu(I) formed by the reduction of Cu(II), probably by mitochondrial vicinal sulfhydryls, reacts with dioxygen to form an O2-copper complex which reacts with acetaldehyde to form the acetyl-1-hydroxyhydroperoxyl radical. This radical disproportionates by the Russell mechanism to generate electronically excited singlet and triplet carbonyl functions and singlet oxygen species whose emissive relaxations to the ground state display as the observed chemiluminescence. The kinetic evidence indicates that there are two Cu(I)-oxygen cyanide complexes transferring O2- to acetaldehyde. This evidence addresses the mechanisms of autoxidation of low-molecular-weight Cu(I) complexes with dioxygen. A suggested role for the involvement of vicinal sulfhydryl groups in the reactions is shown, kinetically, by the influence of copper and acetaldehyde on the integral light.

Acetaldehyde↗
PubMed1988

Microsomal metabolism of acetonitrile to cyanide. Effects of acetone and other compounds.

Oral acetone exposure delays and potentiates acetonitrile toxicity in rats. Results of previous pharmacokinetic studies suggested that acetone exerted a biphasic effect on the metabolism of acetonitrile to cyanide; the presence of acetone in vivo appeared to inhibit the metabolism of acetonitrile to cyanide, whereas the disappearance of acetone from serum was followed by stimulation of acetonitrile metabolism. The current experiments were designed to characterize further the metabolism of acetonitrile to cyanide and the effects of acetone and other compounds upon this metabolism. Liver microsomes were isolated and pooled 24 hr after oral pretreatment of female Sprague-Dawley rats (180-250 g) with acetone (1960 mg/kg) or water. Microsomal metabolism of acetonitrile to cyanide was found to be oxygen and NADPH dependent, and heat-inactivated tissue was unable to catalyze the reaction. NADH antagonized the NADPH-dependent metabolism of acetonitrile. The metabolism of acetonitrile to cyanide was linear with protein concentrations of 0-8 mg per incubation. Following a characteristic lag period of 10 min, the reaction was linear from 15 to 30 min. This metabolism was inhibited by carbon monoxide, metyrapone and SKF 525-A. Acetone pretreatment (-24 hr) in vivo increased the apparent Vmax for acetonitrile metabolism without affecting the apparent Km. When added in vitro, acetone competitively inhibited the metabolism of acetonitrile, with a KI of 0.41 mM. Dimethyl sulfoxide (KI = 0.51 mM) and ethanol (KI = 0.11 mM) were also competitive inhibitors of acetonitrile metabolism, and aniline HCl (KI = 4.77 microM) appeared to be a mixed inhibitor. These data are consistent with the hypothesis that the metabolism of acetonitrile to cyanide is mediated by a specific acetone-inducible isozyme of cytochrome P-450.

Acetone↗
PubMed1992

Corticosterone accelerates hypoxia- and cyanide-induced ATP loss in cultured hippocampal astrocytes.

Glucocorticoids potentiate injury to the rodent hippocampus following a variety of metabolic insults, including hypoxia/ischemia, both in vitro and in vivo. We have examined whether corticosterone (CORT), the principal glucocorticoid in the rat, could exacerbate hypoxic energy failure in cultured hippocampal astrocytes. Exposure to 6 h of atmospheric hypoxia (100% N2) or to 30 min of cyanide did not cause any detectable cell injury, although moderate astrocyte damage did occur alter 6 h of hypoxia in the absence of glucose. Both cyanide and hypoxia significantly reduced astrocyte ATP content, a decline that was further reduced when glucose was omitted. A 30 min exposure to 100 microM glutamate elevated ATP content under normoxic conditions but enhanced the cyanide-induced loss of ATP. A 24 h pre-treatment with CORT did not influence normoxic ATP levels but potentiated the loss of ATP following both cyanide and hypoxia. CORT also exacerbated the loss of ATP seen after combined exposure to cyanide and glutamate, as well as that following cyanide + 0 mM glucose. These results indicate that both CORT and glutamate can potentiate hypoxia-induced energy failure in hippocampal astrocytes, albeit by different mechanisms.

Adenosine Triphosphate↗
PubMed1988

Cyanide-related changes in cerebral O2 delivery and metabolism in fluorocarbon-circulated rats.

Cyanide-induced cytotoxicity is primarily a result of inhibition of O2 uptake by the terminal enzyme of the mitochondrial respiratory chain, cytochrome-c oxidase (cytochrome aa3). The oxidase in the brain is highly vulnerable to cyanide cytotoxicity, but few studies have evaluated the effects of cyanide on cerebral oxygen metabolism. In the present study, we measured oxidation-reduction responses of cerebrocortical cytochrome aa3 to cyanide and related changes in cerebral blood flow (CBF) and O2 metabolism (CMRO2). Accurate measurement of cytochrome aa3 redox state in vivo by reflectance spectrophotometry was accomplished by using fluorocarbon-circulated rats to eliminate spectral interference from hemoglobin. The data indicate that constant intravenous infusions of cyanide caused rapid, progressive reduction responses by cerebrocortical cytochrome aa3 concomitant with increases in CBF of up to 200%. However, CMRO2 was maintained near normal until cerebral O2 delivery began to fall. These cerebral oxidative responses to cyanide may be explained either by redistribution of intracellular O2 supply to mitochondria respiring in an O2-dependent manner or by branching effects within brain mitochondria in vivo.

Animals↗
PubMed1989

Cyanide release from nitroprusside in the isolated, perfused, bloodless liver and hindlimbs of the rat.

When sodium nitroprusside in artificial medium was perfused through the isolated liver and hindlimbs of a rat at the near physiological flow rate of 8.5 ml min-1, free cyanide was found in the perfusate. The liver reached a steady-state ratio of cyanide released/nitroprusside perfused of about 1.5 (or approximately 30% of the total nitroprusside cyanide) within 15 min, and maintained that rate for about 1.5 hr. In the hindlimbs cyanide was released at a much slower rate (7.5 to 18.8% of the total), and the release did not achieve a steady state even after 1.5 hr. Even after small corrections for cyanide extraction by both tissues, the rate of cyanide release by either tissue was probably more rapid than that resulting from static incubations in blood.

Animals↗
PubMed1987

The metabolism of acetonitrile to cyanide by isolated rat hepatocytes.

The metabolism of saturated nitriles, including acetonitrile, has been assumed to occur by a cytochrome P-450-dependent oxidation at the alpha-carbon, yielding a cyanohydrin intermediate which may spontaneously degrade to hydrogen cyanide and an aldehyde. However, results of studies in our laboratory suggest that formaldehyde is not a metabolite of acetonitrile. Since acetonitrile is structurally similar to iodomethane, a substrate for glutathione (GSH) S-transferases, we hypothesized that the metabolism of acetonitrile to cyanide might also occur by a nucleophilic substitution reaction involving GSH. The present studies were conducted to investigate these hypotheses and to further our study of the effects of acetone on acetonitrile metabolism. Female Sprague-Dawley rats were pretreated with buthionine sulfoximine BSO (4 mmol/kg ip, at -4 and -2 hr), cobalt heme (90 mumol/kg sc, at -48 hr), acetone (1960 mg/kg po, at -24 hr), or vehicle, and hepatocytes were isolated after collagenase perfusion of the liver. BSO reduced the cellular GSH content by greater than 80%, but did not appear to affect the metabolism of acetonitrile: the liberation of cyanide correlated with cytochrome P-450, and not GSH, concentrations. Cobalt heme depleted hepatocellular cytochrome P-450 (-45%) content, decreased cell yield and viability, and resulted in a marked reduction in the metabolism of acetonitrile to cyanide. Cobalt heme did not affect the recovery of sodium cyanide from hepatocyte suspensions. Pretreatment of rats with acetone resulted in a twofold increase in the metabolism of acetonitrile to cyanide. Addition of acetone in vitro inhibited acetonitrile metabolism, with an IC50 of 319 microM.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetone↗
PubMed1988

Potentiation of evoked adrenal catecholamine release by cyanide: possible role of calcium.

The effect of cyanide on release of catecholamines was evaluated in isolated bovine adrenal glands stimulated with 4 different agonists. Cyanide (0.1-1 mM) increased catecholamine release induced by barium or cadmium 2-3-fold. Acetylcholine or potassium induced secretion of adrenal catecholamines was also enhanced by cyanide, but only to the extent of 30-50%. These data suggest that cyanide acts by multiple mechanisms to enhance evoked catecholamine release. The above results may be partly explained by the fact that cyanide inhibited 45Ca efflux from stimulated bovine adrenals. Changes in plasma membrane permeability may be crucial in the alterations of ion flux and evoked catecholamine release caused by cyanide.

Acetylcholine↗
PubMed1992

The in vivo effects of cyanide and its antidotes on rat brain cytochrome oxidase activity.

The in vivo effects of sodium cyanide and its antidotes, sodium nitrite, sodium thiosulfate and 4-dimethylaminophenol (DMAP), as well as the alpha-adrenergic blocking agent phentolamine, on rat brain cytochrome oxidase were studied. The course of inhibition was time-dependent and a peak of 40% was attained between 15 and 20 min after the s.c. injection of 1.3 LD50 (12 mg/kg) of cyanide. Pronounced dose-dependence was observed in the inhibition of the enzyme, at this relatively low, but lethal dose. Further observation was impossible because of rapidly lethal effects of cyanide. In animals artificially ventilated with room air, observation was possible up to 60 min. However, maximum inhibition was also 40%. When antidotes were applied 30 min after 20 mg/kg of cyanide, marked reactivation of cytochrome oxidase activity was observed with all antidotes (particularly with thiosulfate) except for phentolamine which had no effect. Prevention of methemoglobin forming with toluidine blue did not affect the reactivating ability of nitrite or DMAP, thus suggesting more complex protective mechanisms then simple methemoglobin formation. The high efficacy of thiosulfate may be attributed to its rhodanese catalyzed, direct binding to free blood cyanide, leading thus to its dissociation from cytochrome oxidase. The theory that cytochrome oxidase inhibition is a basic mechanism of cyanide toxicity could not be disproved.

Aminophenols↗
PubMed1987

Detoxication of cyanide in the chicken by conversion to thiocyanate, as influenced by the availability of transferable sulphur.

The urinary excretion of thiocyanate by hens after dosage with cyanide (30 mumol) has been studied in a series of acute experiments involving 6 hr urine collection periods. More than half of the dose could be recovered as thiocyanate when cyanide was given by intravenous infusion and the rate of excretion closely paralleled plasma thiocyanate concentration. Little cyanide was excreted directly. The excretion of thiosulphate fell by an amount that suggested that availability of sulphane sulphur might limit the extent of conversion. However, neither thiosulphate nor sulphur amino acids enhanced thiocyanate excretion when they were infused together with cyanide; indeed, thiocyanate excretion decreased as the level of sulphur compound given was increased. Both nitrite and sulphite depressed thiocyanate excretion also but they differed in their effects on plasma thiocyanate levels and the pattern of urinary excretion. Comparison of excretion from both sides of the kidneys separately emphasised the importance of the first pass of cyanide in its conversion to thiocyanate. The results suggest that although sulphur availability may be limited the in vivo production of sulphite also restricts cyanide detoxication.

Animals↗
PubMed1989

Cyanide intoxication--I. An oral chronic animal model.

The effects of oral chronic cyanide administration to mice were studied. Cyanide intoxication was confirmed by the increased levels of this poison and the concomitant inhibition of cytochrome oxidase activity in liver, brain, heart and blood. The detoxifying enzyme rhodanese was measured. The state of the sulfane sulfur pool was investigated by determination of the cyanide labile-sulfur levels. A clear correlation between rhodanese activity and sulfur content was obtained as a consequence of cyanide action. These results support the belief that rhodanese plays a fundamental role in the detoxification process of cyanide, in preventing cyanide reaching the target tissues.

Administration, Oral↗
PubMed1991

The effect of cyanide on vitamin C uptake by human polymorphonuclear leukocytes.

1. Cyanide inhibited the uptake of vitamin C by human polymorphonuclear leukocytes (PMNs). 2. Preincubation of PMNs with cyanide had no effect on cytochalasin B-inhibitable uptake of dehydroascorbic acid (DHA) (the reversibly oxidized and transportable form of vitamin C). 3. Preincubation of DHA with cyanide resulted in inhibition of DHA uptake. 4. Vitamin C uptake was decreased by cyanide to the same degree as it was by glutathione (GSH), which effectively reduces DHA to ascorbic acid. The effects of cyanide and GSH were not additive. 5. The data are consistent with the hypothesis that cyanide inhibition of vitamin C uptake represents the chemical elimination of extracellular DHA rather than the inhibition of active transport in these cells.

Animals↗