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PubMed1991

A study on house fire victims: age, carboxyhemoglobin, hydrogen cyanide and hemolysis.

Correlation among age, concentrations of carboxyhemoglobin and hydrogen cyanide, oxygen density and hemolysis were studied in 120 house fire victims. Victims aged over 60 years comprised approximately 50% of the pooled subjects. Blood samples were mainly collected from the left ventricle, but sometimes from both the right and left ventricles. The concentration of carboxyhemoglobin ranged from 1-95%, of which 71 persons (59.7%) died with carboxyhemoglobin concentrations below 60%. Carboxyhemoglobin concentrations below 10% were found in 9 persons (7.5%). Most of these cases involved the elderly persons. In this paper, we report on the death of elderly victims as a result of low carboxyhemoglobin concentrations. A significant correlation of blood carboxyhemoglobin concentrations existed between the right and left ventricles. The concentration of carboxyhemoglobin in the left ventricle was significantly higher than that in the right. Two out of 31 victims whose hydrogen cyanide concentrations were determined, succumbed to hydrogen cyanide poisoning, having a high concentration of hydrogen cyanide and a low concentration of carboxyhemoglobin. On analysis, oxygen density was found to be low in 13 persons. A negative correlation was shown between carboxyhemoglobin concentration and hemolysis. Inasmuch as hemolysis may indicate the extent of heat dissociation, hemolysis should provide an index of carbon monoxide dissociation from carboxyhemoglobin. In the present study of victims, possible causes of death i.e., carbon monoxide gas poisoning, hydrogen cyanide poisoning, oxygen deprivation, burning, shock due to burns and others were estimated. The survival time for elderly victims was considered to be short.

Adolescent↗
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↗
PubMed1991

Alternative sulphur donors for detoxification of cyanide in the chicken.

1. Urinary excretion of thiocyanate by hens after dosage with cyanide was studied over 3 hr periods during which various sulphur sources were infused. 2. With 20 mumoles cyanide, endogenous sulphur supplies appeared to be almost sufficient. 3. With 45 mumoles cyanide, thiocyanate excretion was doubled with 90 mumoles of sulphur donor. Higher doses of mercaptopyruvate were also effective but not rhodanese substrates (thiosulphate or methanethiosulphonate): they interfered with thiocyanate excretion and may also have suppressed its formation. 4. Mercaptopyruvate and rhodanese substrates also differed in their effects on blood cyanide concentration and on the excretion of isotope from radiolabelled cyanide.

Animals↗
PubMed2004

Excitation and emission wavelength ratiometric cyanide-sensitive probes for physiological sensing.

We characterize three new fluorescent probes that show both spectral shifts and intensity changes in the presence of aqueous cyanide, allowing for both excitation and fluorescence emission wavelength ratiometric and colorimetric sensing. The relatively high binding constants of the probes for cyanide enables a distinct colorimetric change to be visually observed with as little as 10 microM cyanide. The response of the new probes is based on the ability of the boronic acid group to interact with the CN(-) anion, changing from the neutral form of the boronic acid group R-B(OH)(2) to the anionic R-B(-)(OH)3 form, which is an electron-donating group. The presence of an electron-deficient quaternary heterocyclic nitrogen center and a strong electron-donating amino group in the 6 position on the quinolinium backbone provides for the spectral changes observed upon CN(-) complexation. We have determined the binding constants for the ortho-, meta-, and para-boronic acid probes to be 0.12, 0.17, and 0.14 microM(-3). In addition we have synthesized a control compound that does not contain the boronic acid moiety, allowing for structural comparisons and a rationale for the sensing mechanism to be made. Finally we show that the affinity for monosaccharides, such as glucose or fructose, is relatively low as compared to that for cyanide, enabling the potential detection of cyanide in physiologies up to lethal levels.

Biosensing Techniques↗
PubMed2005

Carbonic anhydrase inhibitors. Inhibition of isozymes I, II, IV, V and IX with complex fluorides, chlorides and cyanides.

The inhibition of five human carbonic anhydrase (hCA, EC 4.2.1.1) isozymes, the cytosolic hCA I and II, the membrane-bound hCA IV, the mitochondrial hCA V and the tumour associated, transmembrane hCA IX, with complex anions incorporating fluoride, chloride and cyanide, as well as B(III), Si(IV), P(V), As(V), Al(III), Fe(II), Fe(III), Pd(II), Pt(II), Pt(IV), Cu(I), Ag(I), Au(I) and Nb(V) species has been investigated. Apparently, the most important factors influencing activity of these complexes are the nature of the central metal ion/element, and its charge. Geometry of these compounds appears to be less important, since both linear, tetrahedral, octahedral as well as pentagonal bipyramidal derivatives led to effective inhibitors. However, the five isozymes showed very different affinities for these anion inhibitors. The best hCA I inhibitors were cyanide, dicyanocuprate and dicyanoaurate (K(I)s in the range of 0.5-7.7 microM), whereas the least effective were fluoride and hexafluoroarsenate. The best hCA II inhibitors were cyanide, hexafluoroferrate and tetrachloroplatinate (K(I)s in the range of 0.02-0.51 mM), whereas the most ineffective ones were fluoride, hexafluoroaluminate and chloride. The best hCA IV inhibitors were dicyanocuprate (K(I) of 9.8 microM) and hexacyanoferrate(II) (K(I) of 10.0 microM), whereas the worst ones were tetrafluoroborate and hexafluoroaluminate (K(I)s in the range of 124-126 mM). The most effective hCA V inhibitors were cyanide, heptafluoroniobate and dicyanocuprate (K(I)s in the range of 0.015-0.79 mM), whereas the most ineffective ones were fluoride, chloride and tetrafluoroborate (K(I)s in the range of 143-241 mM). The best hCA IX inhibitors were on the other hand cyanide, heptafluoroniobate and dicyanoargentate (K(I)s in the range of 4 microM-0.33 mM), whereas the worst ones were hexacyanoferrate(III) and hexacyanoferrate(II).

Anions↗
PubMed2004

Biological degradation of cyanide compounds.

Cyanide compounds are produced as waste products of a number of industrial processes and several routes for their removal from the environment are under investigation, including the use of biodegradation. The most recent developments in this area have come from studies of the hydrolytic and oxidative pathways for biodegradation and the conditions that affect their activity. The biodegradation of cyanide under anaerobic conditions has also recently demonstrated the feasibility for concomitant biogas generation, a possible economic benefit of the process. Significant advances have been reported in the use of plants for the phytoremediation of cyanide compounds and evidence for the biodegradation of thiocyanate and metal-cyanide complexes has become available. Despite these advances, however, physical and economic factors still limit the application of cyanide biodegradation, as do competing technologies.

Bacteria↗
PubMed2004

Calcium ions: its role in cyanide neurotoxicity.

Cyanide is a well-established poison known for its rapid lethal action and toxicity. The central nervous system is one of the main target sites for cyanide toxicity. Cyanide also alters the brain biogenic amine levels. In the present study the role of calcium ions in cyanide toxicity was evaluated using the calcium channel blocker diltaizem (DIL) in Wistar strain albino rats. This study showed that DIL pretreatment prevented cyanide induced changes in the dopaminergic and serotonergic system in the corpus striatum.

Animals↗
PubMed2004

Inhibition of aerobic respiration and dissimilatory perchlorate reduction using cyanide.

The effect of low concentrations of cyanide on dissimilatory perchlorate and chlorate reduction and aerobic respiration was examined using pure cultures of Azospira sp. KJ. Cyanide at a concentration of 38 microM inhibited cell growth on perchlorate, chlorate and molecular oxygen, but it did not inhibit the activity of chlorite dismutase. When oxygen accumulation was prevented by adding an oxygen scavenger (Oxyrase or L-cysteine), however, cells completely reduced perchlorate in the presence of cyanide. It was concluded that the inhibition of dissimilative perchlorate reduction by cyanide at this concentration was a consequence of oxygen accumulation, not inhibition of the enzymes used for perchlorate reduction. This finding on the effect of cyanide on respiratory enzymes provides a new method to control and study respiratory enzymes used for perchlorate reduction.

Bacteria, Aerobic↗
PubMed2005

[Sodium thiosulfate for acute cyanide poisoning: study in a rat model].

Unlike practices in the United States where it is associated with other antidotes, sodium thiosulfate is not used for emergency therapy for cyanide poisoning in France. The purpose of this study was to develop a rat model using intraperitoneal injections of sodium thiosulfate at a dose of 225 mg/kg to test its therapeutic efficacy for acute cyanide poisoning. Efficacy was assessed directly by quantifying arterial blood cyanide and indirectly using markers of hypoxia: serum lactate and arteriolization of venous blood gases. Cyanide poisoning induced intense biological anomalies which were persistent (serum lactate) or transient (blood gases). Sodium thiosulfate was found to be an effective antidote in the rat enabling rapid normalization of hypoxia markers and clearing of cyanide from arterial blood.

Animals↗
PubMed2003

Crystal structures of cyanide complexes of P450cam and the oxygenase domain of inducible nitric oxide synthase-structural models of the short-lived oxygen complexes.

The crystal structure of the ternary cyanide complex of P450cam and camphor was determined to 1.8A resolution and found to be identical with the structure of the active oxygen complex [I. Schlichting et al., 2000, Science 287, 1615]. Notably, cyanide binds in a bent mode and induces the active conformation that is characterized by the presence of two water molecules and a flip of the carbonyl of the conserved Asp251. The structure of the ternary complex of cyanide, L-arginine, and the oxygenase domain of inducible nitric oxide synthase was determined to 2.4A resolution. Cyanide binds essentially linearly, interacts with L-Arg, and induces the binding of a water molecule at the active site. This water is positioned by backbone interactions, located 2.8A from the nitrogen atom of cyanide, and could provide a proton required for O-O bond scission in the hydroxylation reaction of nitric oxide synthase.

Animals↗
PubMed2002

Unusual cyanide bindings to a heme-regulated phosphodiesterase from Escherichia coli: effect of Met95 mutations.

In order to understand heme environment of a heme-regulated phosphodiesterase (Ec DOS), the binding behavior of cyanide to the Fe (III) complex was examined. Interestingly, the rate of cyanide binding to full-length Ec DOS was unusually slow with k(on)=0.0022mM(-1)s(-1), while the rate for the isolated heme domain of Ec DOS (0.045mM(-1)s(-1)) was 20-fold higher. Ala and Leu mutations at Met95, which has been suggested to be a heme axial ligand, increased the k(on) rate 11- and 8-fold, respectively, and dramatically decreased the cyanide dissociation rate from the isolated heme domain. His mutation at Met95, on the other hand, caused a 17-fold decrease in the k(on) value. We discuss the unusual cyanide binding behavior and the role of Met95 in controlling cyanide binding.

Azides↗
PubMed1999

Cyanide binding to Lucina pectinata hemoglobin I and to sperm whale myoglobin: an x-ray crystallographic study.

The x-ray crystal structures of the cyanide derivative of Lucina pectinata monomeric hemoglobin I (L. pectinata HbI) and sperm whale (Physeter catodon) myoglobin (Mb), generally taken as reference models for monomeric hemoproteins carrying hydrogen sulfide and oxygen, respectively, have been determined at 1.9 A (R-factor = 0. 184), and 1.8 A (R-factor = 0.181) resolution, respectively, at room temperature (lambda = 1.542 A). Moreover, the x-ray crystal structure of the L. pectinata HbI:cyanide derivative has been studied at 1.4-A resolution (R-factor = 0.118) and 100 K (on a synchrotron source lambda = 0.998 A). At room temperature, the cyanide ligand is roughly parallel to the heme plane of L. pectinata HbI, being located approximately 2.5 A from the iron atom. On the other hand, the crystal structure of the L. pectinata HbI:cyanide derivative at 100 K shows that the diatomic ligand is coordinated to the iron atom in an orientation almost perpendicular to the heme (the Fe-C distance being 1.95 A), adopting a coordination geometry strictly reminescent of that observed in sperm whale Mb, at room temperature. The unusual cyanide distal site orientation observed in L. pectinata HbI, at room temperature, may reflect reduction of the heme Fe(III) atom induced by free radical species during x-ray data collection using Cu Kalpha radiation.

Animals↗
PubMed1981

Blood carboxyhaemoglobin and cyanide levels in fire survivors.

Blood carboxyhaemoglobin and cyanide concentrations were measured in 53 fire survivors, 36 of whom had clinical evidence of smoke inhalation. Carboxyhaemoglobin and cyanide levels were raised only in patients with smoke inhalation. Blood carboxyhaemoglobin measurement can be used to confirm the diagnosis of severe smoke inhalation in cases in which the clinical data are inconclusive, provided that the time of sampling after exposure is taken into account. A nomogram has been constructed for this purpose. There is no quick method of measuring blood cyanide levels, but the close relation between cyanide and carboxyhaemoglobin levels suggests that carboxyhaemoglobin concentrations, which can be rapidly and easily measured, could be used to identify those who might benefit from treatment with cyanide antidotes.

Apnea↗
PubMed1979

Reactions of molybdenum-sulphur compounds with cyanide: chemical evolution and deactivation of molybdoenzymes.

Reactions of molybdenum-sulphur compounds with cyanide are reported which may be relevant to (1) the chemical evolution of molybdoenzymes and (2) deactivation of molybdoenzymes by cyanide. (1) With aqueous cyanide MoS2 gave thio-bridged complex anions [(Mo(CN)6)2(mu-S)]6- and [(Mo(CN)4(mu-S))2]6-. Under prebiotic conditions such complexes could have been formed similarly from molybdenite and may have been precursors of molybdoenzymes. (2) Only those compounds which contained terminal sulphur bound to molybdenum (i.e., Mo = S groups), viz. oxothiomolybdates and the complex [(Mo(mu-S)(S)(Et2NCS2))2], reacted with cyanide; thiocyanate was formed and the molybdenum underwent two-electron reduction. That the cyanolysable sulphur of xanthine oxidase reacts in the same way with cyanide suggests the presence of a Mo = S group which could be a structural feature of the enzyme or could have been formed by initial cyanolysis of a bound persulphide or cysteine residue.

Biological Evolution↗
PubMed1991

Lack of evidence for a percent saturation gap in cyanide poisoning.

STUDY OBJECTIVES: To determine if toxic concentrations of cyanide in blood result in a difference between calculated and measured percent hemoglobin oxygen saturation (percent saturation gap). DESIGN: An in vitro laboratory study. SETTING: Hospital laboratory. TYPE OF PARTICIPANTS: Arterial blood from five stable patients residing in a tertiary hospital ICU. Venous blood samples obtained from five healthy volunteers. INTERVENTIONS: Two-mL aliquots from each blood sample were placed into four test tubes and mixed with phosphate buffer. Cyanide was added to three of the tubes so that the four tubes contained 0, 6, 12, and 25 mg/L cyanide. MEASUREMENTS AND MAIN RESULTS: The percent saturation gap was calculated by subtracting the percent oxyhemoglobin measured on an oximeter from the percent saturation calculated by a blood gas analyzer. Using two-tailed, paired t tests, we could not demonstrate a difference in mean percent saturation gaps between arterial samples or venous samples with and without cyanide. All blood samples had a normal percent saturation gap (P greater than .99 by Fisher's exact test). We had greater than a 95% chance of demonstrating a difference in mean percent saturation gaps of only 0.46% in arterial blood and of 3.3% in venous blood if such a difference existed. CONCLUSIONS: Our results, as well as a review of the literature, indicate that there are no data supporting the suggestion that a percent saturation gap should imply the diagnosis of poisoning by inorganic cyanide.

Adult↗
PubMed2003

Some histologic and biochemical evidence for mitigation of cyanide-induced tissue lesions by antioxidant vitamin administration in rabbits.

The effect of antioxidant vitamins on cyanide-induced tissue damage was investigated in New Zealand White rabbits using a combination of colorimetric, spectrophotometric, enzymatic, gravimetric and histological methods. Three groups of rabbits (six per group) were used in a 4-week feeding experiment. One group received pure grower's mash, while a second group was fed mash containing 400 ppm inorganic cyanide. The third group received daily oral doses of vitamins A, C and E, in addition to mash and 400 ppm cyanide. There were significant decreases (P < 0.05) in activities of superoxide dismutase (SOD), catalase and alkaline phosphatase (AP) in the liver, lung and kidney of the two groups given cyanide, but the decreases were significantly lower (P < 0.05) in the group fed antioxidant vitamins. In addition, the antioxidant vitamin supplementation led to marked reductions in the severity of histopathological degeneration in these tissues. These results strongly suggest that cyanide-induced tissue lesions may be relieved by adequate intake of antioxidant vitamin supplements.

Animals↗
PubMed1999

Caffeine and carbonyl cyanide m-chlorophenylhydrazone increased evoked and spontaneous release of luteinizing hormone-releasing hormone from intact presynaptic terminals.

In bullfrog sympathetic ganglia, the ryanodine-sensitive Ca2+ store and mitochondria modulate [Ca2+] within nerve terminals. We used caffeine (10 mM) and carbonyl cyanide m-chlorophenylhydrazone (10 microM) to assess how these Ca2+ stores affect release of a neuropeptide, luteinizing hormone-releasing hormone, from these nerve terminals. Release of luteinizing hormone-releasing hormone was evoked by electrical stimulation to presynaptic nerves and was monitored as a late slow excitatory postsynaptic potential in ganglionic neurons. Caffeine increased release of luteinizing hormone-releasing hormone similarly whether the release was evoked by 4 or 20 Hz stimulations (by 2.7 +/- 1.1- and 3.2 +/- 0.9-fold, mean +/- S.E.M., n = 27, respectively). Carbonyl cyanide m-chlorophenylhydrazone augmented release of luteinizing hormone-releasing hormone evoked by 4 Hz stimulation much more strongly (by 11.8 +/- 1.8-fold) than it increased the release evoked by 20 Hz stimulation (by 3.6 +/- 1.3-fold, n = 25). We detected spontaneous release of luteinizing hormone-releasing hormone as a slow hyperpolarization in response to a brief application of an antagonist to the receptors for luteinizing hormone-releasing hormone in 65% (34 of 52) and 39% (11 of 28) of the ganglionic B and C neurons, respectively. Caffeine increased spontaneous release of luteinizing hormone-releasing hormone by 2.3 +/- 0.7-fold (n = 6) whereas carbonyl cyanide m-chlorophenylhydrazone increased this release by 4.27- and 1.76-fold (n = 2). Facilitation of Ca2+ release from the intracellular store by caffeine and inhibition of mitochondrial Ca2+ removal by carbonyl cyanide m-chlorophenylhydrazone increased spontaneous as well as evoked release of luteinizing hormone-releasing hormone. Moreover, caffeine increments of evoked release did not depend on the firing frequency of the nerve whereas carbonyl cyanide m-chlorophenylhydrazone augmentations of evoked release strongly depended on the firing frequency.

Acetylcholine↗
PubMed2002

In vitro and in vivo attenuation of experimental cyanide poisoning by alpha-ketoglutarate.

Treatment of cyanide poisoning generally includes methemoglobin forming agents, like amyl nitrite and/or sodium nitrite (SN), in combination with sodium thiosulphate (STS). However, in many instances of cyanide poisoning, use of nitrites are contraindicated due to their strong vasoactive properties. alpha-Ketoglutarate (alpha-KG) antagonises cyanide by cyanohydrin formation and is considered a promising antidote for cyanide poisoning. In the present study, pre-treatment (30 min) and simultaneous treatment (0 min) of alpha-KG (5 mM) was found to confer significant protection against 5 mM potassium cyanide (KCN) induced cytotoxicity in rat thymocytes as measured by eosin Y exclusion and leakage of intracellular lactate dehydrogenase (LDH), but could not prevent the mitochondrial dysfunction (MTT assay), depletion of cellular GSH (reduced glutathione) and DNA damage. The post-treatment (5 or 30 min) of alpha-KG did not offer any protection on any of the above parameters. Results of in vitro studies were also supported by in vivo data. Pre-treatment of peroral (p.o.) alpha-KG (0.125-2.0 g/kg) exhibited dose and time dependent effects and was found to be effective even when given upto 60 min prior to KCN (p.o.). Addition of STS significantly enhanced the protective efficacy of alpha-KG at all the doses and time intervals. A 10 min pre-treatment of alpha-KG increased the LD(50) of KCN 7.6-fold, which was further increased to 25.6-fold by the addition of both SN and STS. Simultaneous treatment of alpha-KG (2.0 g/kg) increased the LD50 of KCN 5.4-fold which was increased to 18.1-fold by the addition of STS. However, addition of SN did not confer any additional protection. In the presence of SN+STS, a decrease in the dose of alpha-KG exhibited a dose-dependent decrease in protection, but still a >10-fold protection could be observed at 1.0 g/kg dose of alpha-KG. Considering the efficacy and safety of peroral alpha-KG, a promising treatment regimen consisting of alpha-KG+STS or alpha-KG+SN+STS is proposed, depending upon the individual situation.

Animals↗