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PubMed1993

The interaction of sodium nitroprusside with peripheral white blood cells in vitro: a rationale for cyanide release in vivo.

Isolated monocytes and polymorphonuclear leukocytes release the cyanide anion from the hypotensive agent, sodium nitroprusside. The proposed mechanism involves the production of hydrogen peroxide which oxidizes the substitution inert d6 iron(II) transition metal complex to a labile d5 iron(III) complex. Consequently, the release of cyanide becomes more favoured. This mechanism is supported by the chemical release of the cyanide anion from sodium nitroprusside in vitro by hydrogen peroxide and the demonstrated ability of monocytes and polymorphonuclear leukocytes to generate hydrogen peroxide ex vivo when chemically stimulated by the nitroprusside anion. The results suggest that within a clinical environment white cell counts and cell activation induced as a consequence of disease processes may be important for predicting the toxicity of sodium nitroprusside.

Cells, Cultured↗
PubMed1990

An experimental assessment of cyanide challenge dose-response, time-course and recovery of indicative toxicity parameters.

1. Several sub-lethal doses of cyanide were assayed with the aim of obtaining significant differences in the parameters studied. A dose of 4 mg/kg s.c. was selected. 2. Present studies were carried out to determine the time dependence of the effects produced by s.c. administration of a single dose of potassium cyanide as well as the recovery time of some of the toxicity indicative parameters. 3. It was found that cyanide effects continued for at least 3 days; after the parameters had recovered normal values.

Animals↗
PubMed1992

Comparison of methemoglobin formers in protection against the toxic effects of cyanide.

1. Certain compounds that oxidize hemoglobin to methemoglobin (MHb) also protect against cyanide. 2. Evidence presented here suggests that other mechanisms may be involved. 3. Male Swiss ICR mice were pretreated intraperitoneally (i.p.) with various doses of primaquine phosphate (primaquine), WR6026 (6-methoxy-8-(6-diethylamino-hexylamino) lepidine dihydrochloride), WR238605 (8-[(4-amino-1-methylbutyl) amino]-2,6-dimethoxy-4-methyl-5-(3-trifluoromethylphenoxy) quinoline succinate), p-aminooctoyl-phenone (PAOP), or p-aminopropiophenone (PAPP). 4. The compounds were administered 15 or 60 min before an intramuscular (i.m.) challenge with a 2 x LD50 dose (5.0-5.6 mg/kg) of sodium cyanide (NaCN). 5. Twenty-four hr mortality was assessed and survivors were tested for motor incapacitation. 6. Primaquine, PAPP and PAOP increased survival compared to untreated controls, while the other MHb formers were not effective (P less than 0.05). 7. PAOP is believed to form sufficient MHb only after 3 to 4 hr after administration; however it was found to be effective when administered 15 min before NaCN challenge in this study. 8. This suggests that MHb formation may not be the only factor responsible for PAOP's anti-cyanide efficacy.

Aminoquinolines↗
PubMed1987

Cyanide is a product of the catalase-mediated oxidation of the alcohol deterrent agent, cyanamide.

Cyanide was detected as a product of cyanamide oxidation by bovine liver catalase in vitro under conditions that also produced an active aldehyde dehydrogenase (AlDH) inhibitor. Cyanide formation was directly related to both cyanamide and catalase concentrations and was also dependent on incubation time. The apparent Km for this reaction was 172 microM. Cyanide formation was blocked by ethanol, a known substrate for catalase Compound I. The toxic effects of cyanamide in the dog, a species with limited capacity to conjugate cyanamide by N-acetylation, may be causally related to enhancement of this catalase-mediated pathway for cyanamide metabolism.

Alcohol Deterrents↗
PubMed1990

Protection by exogenous glutathione against hypoxic and cyanide-induced damage to isolated perfused rat livers.

In experiments with isolated perfused livers from fasted rats, addition of 2 mmol/l glutathione (GSH) to the perfusion medium protected against hepatic damage induced by cyanide or hypoxia and reoxygenation as evidenced by leakage of lactate dehydrogenase and hepatic calcium accumulation. In control experiments as well as in experiments with cyanide or hypoxia and reoxygenation, exogenous glutathione resulted in an augmentation of cellular glutathione content, indicating either direct uptake of GSH or stimulation of its intracellular synthesis. The protective effects of glutathione against hypoxic and cyanide-induced hepatotoxicity substantiate the role of oxidative stress in both types of injury.

Animals↗
PubMed1985

Stroma-free methemoglobin solution: an effective antidote for acute cyanide poisoning.

Several aspects of stroma-free methemoglobin solution (SFMS) as a cyanide antidote were investigated using a rat model. Stroma-free methemoglobin solution was more than 90% effective against multiples of the LD90 of cyanide up to and including four times the LD90 and approximately 50% effective against multiples up to and including eight times the LD90. Highly concentrated solutions of SFMS (33 g/dl) did not differ significantly from less concentrated solutions of SFMS (16 g/dl) when compared on the basis of efficacy. Administration of large doses of SFMS alone resulted in no apparent morbidity or mortality. It could be that SFMS is a safe and effective alternative antidote for the treatment of cyanide poisoning.

Acute Disease↗
PubMedDate not supplied

Cyanide overdose: survival with fatal blood concentration without antidotal therapy.

Cyanide poisoning is an uncommon emergency department problem. It has a high mortality, and specific antidotal therapy can be lifesaving. We describe a 23-year-old man who ingested potassium cyanide and survived without antidotal therapy. His blood cyanide concentration was 4.65 mg/L, which is within the lethal range. The arterial venous oxygen saturation gradient was considered in the decision regarding antidote administration. Our experience underscores the importance of supportive care.

Adult↗
PubMed1991

Use of cyanide and diethyldithiocarbamate in the assay of superoxide dismutases.

Eucaryotes have two major forms of superoxide dismutase (SOD), Cu,ZnSOD and MnSOD; in most tissues Cu,ZnSOD is present in higher amounts than MnSOD. To assay MnSOD, Cu,ZnSOD can be inhibited selectively by millimolar concentrations of cyanide ion. However, calculation of MnSOD activity from the differential cyanide inhibition assay is complex and small experimental errors can cause large errors in the calculated MnSOD activity. We have assessed how interaction of cyanide and hydrogen peroxide with cytochrome c can lead to further errors in the xanthine oxidase-cytochrome c assay for SOD. Alternatively, Cu,ZnSOD can be completely inactivated by 50 mM diethyldithiocarbamate (DDC) at 30 degrees C for 1 h without affecting the activity of MnSOD. Since DDC reduces cytochrome c, the treated samples must be thoroughly dialyzed or desalted before assay. In the case of lung homogenates, dialysis is not an extra step since fresh, untreated samples must also be dialyzed or desalted before assaying by the cytochrome c method. Cu,ZnSOD activity is equal to the activity in the untreated sample minus the activity in the DDC-treated portion of the sample. Another copper chelator, triethylenetetramine, did not inactivate Cu,ZnSOD and could not be used instead of DDC. For accurate measurement of both enzymes in samples where MnSOD contributes only a small fraction of the total SOD activity, the DDC method has the advantage that it provides a direct measure of the MnSOD activity without interference by Cu,ZnSOD.

Animals↗
PubMed2006

Degradation of cyanide by Trichoderma mutants constructed by restriction enzyme mediated integration (REMI).

REMI technique was used to construct mutants with improved cyanide-degradation ability from biocontrol fungus Trichoderma koningii strain T30. The plasmid pV2 transformation was confirmed by PCR and Southern blot analysis. Out of 21 transformants, 15 single-copied transformants (71.4%) were found. To compare enzyme activities of rhodanese and cyanide hydratase, T. atroviride T23, T. harzianum T21 and their transformants constructed by REMI previously were also included. Transformants TkB6 (0.173 micromols thiocyanate formed min(-1)mg protein(-1)) from T30 and TaK1 (0.174 micromols thiocyanate formed min(-1)mg protein(-1)) from T23 showed higher rhodanese activity than other transformants and their wild strains. TkA9 (5.53 micromols formamide formed h(-1)mg protein(-1)) from T30 and Th64 (5.35 micromols formamide formed h(-1)mg protein(-1)) from T21 had higher cyanide hydratase activity than other transformants and their wild strains.

Base Sequence↗
PubMed2006

Determination of cyanide in microliter samples by capillary electrophoresis and in-capillary enzymatic reaction with rhodanese.

This paper describes a method for the determination of cyanide using in-capillary enzymatic reaction with rhodanese. Poorly absorbing cyanide is in rhodanese reaction transformed into highly absorbing thiocyanate that is further separated by capillary electrophoresis (CE) and determined spectrophotometrically at 200 nm. Cyanide is thus estimated indirectly from the result of thiocyanate quantification and moreover, it can be easily determined with sufficient sensitivity by means of CE apparatus equipped with common UV detector. The linear detection range for concentration versus peak area for the assay is from 15 to 500 microM (correlation coefficient 0.997) with a detection limit of 3 microM and a limit of quantitation 9 microM. The inter-day reproducibility of the peak area was below 3.2% and the inter-day reproducibility of the migration time below 0.1%. The method is relatively rapid, simple and can be easily automated. Moreover, only limited amount of the sample is required.

Cyanides↗
PubMed2005

In vitro metabolism of a thrombin inhibitor and quantitation of metabolically generated cyanide.

During the metabolic characterization of compound I, 2-{6-cyano-3-[(2,2-difluoro-2-pyridin-2-ylethyl)amino]-2-oxopyrazin-1(2H)-yl]-N-[(3-fluoropyridin-2-yl)methyl]acetamide, evidence was obtained for extensive oxidative bioactivation of the pyrazinone ring system and some of the resulting metabolites were apparently devoid of the cyano moiety. Two assays, a spectrophotometric and a high-pressure liquid chromatography (HPLC) pre-column derivatization method, were evaluated for their ability to detect and quantify cyanide that is metabolically generated from liver microsomal incubations. When I was incubated (45 microM) in the presence of NADPH-fortified human liver microsomes for 2h, 7.5 microM of cyanide was detected using the spectrophotometric assay and 8.9 microM was measured using the HPLC methodology. Overall, the results from the two assays appeared to agree reasonably well with each other. However, the HPLC assay was the preferred method for the evaluation of cyanide formation in vitro due to its sensitivity, reliability, and ease of use.

Biotransformation↗
PubMed1998

The activation of gold complexes by cyanide produced by polymorphonuclear leukocytes. III. The formation of aurocyanide by myeloperoxidase.

There is considerable evidence that the anti-rheumatic gold complexes are activated by their conversion to aurocyanide. In order to understand the mechanism of production of aurocyanide, we investigated the involvement of myeloperoxidase in the reaction. This haem enzyme of neutrophils and monocytes uses hydrogen peroxide to oxidise chloride and thiocyanate to hypochlorous acid and hypothiocyanite, respectively. When aurothiomalate (10 microM) was incubated with thiocyanate (200 microM), hydrogen peroxide (100 microM) and myeloperoxidase (20 nM), it was transformed to a product that was spectrally identical to authentic aurocyanide. Aurothiomalate was quantitatively converted to aurocyanide in about 10 min at pH 6.0 and in 40 min at pH 7.4. Aurocyanide formation occurred after myeloperoxidase had used all the hydrogen peroxide available to produce hypothiocyanite. Thus, the cyanide must have formed from the slow decomposition of hypothiocyanite. The rate of aurocyanide production was increased in the presence of 100 mM chloride, which indicates that hypochlorous acid accelerates the formation of cyanide. Hypochlorous acid (100 to 400 microM) reacted non-enzymatically with thiocyanate (200 microM) and aurothiomalate (10 microM) to produce aurocyanide. Thus, aurocyanide is produced by two processes, involving both the formation of hypothiocyanite and hypochlorous acid. Aurocyanide is an effective inhibitor of the respiratory burst of neutrophils and monocytes and the proliferation of lymphocytes. Therefore, aurothiomalate may attenuate inflammation by acting as a pro-drug which is reliant on neutrophils and monocytes to produce hypothiocyanite. When the hypothiocyanite decays to hydrogen cyanide, the pro-drug is converted to aurocyanide which then suppresses further oxidant production by these inflammatory cells.

Antirheumatic Agents↗
PubMed1981

Effects of pressure and temperature on the reactions of horseradish peroxidase with hydrogen cyanide and hydrogen peroxide.

Reactions of ferric horseradish peroxidase with hydrogen cyanide and hydrogen peroxide were studied as a function of pressure. Activation volumes are small and differ in sign (delta V = 1.7 +/- 0.5 ml/mol for peroxidase + HCN and -1.5 +/- 0.5 ml/mol for peroxidase + H2O2). The temperature dependence of cyanide binding to horseradish peroxidase was also determined. A comparison is made of relevant parameters for cyanide binding and compound I formation.

Enzyme Activation↗
PubMed2000

Enhanced conductometric detection of cyanide in suppressed ion chromatography.

Weak-acid anions such as borate and cyanide, present problems in chemically suppressed ion chromatography, since the acids are weakly ionised, giving low conductivity and therefore decreased sensitivity. For borate this problem was overcome by converting the weak acid to its sodium salt, by the use of a second anion micromembrane suppressor (AMMS) as an ion exchange reactor (IER), flushed by EDTA reagent, to supply sodium ions for the conversion. This paper will discuss the use of this IER system to determine cyanide, which is also a very weak acid, with a similar pKa to borate. The detection limit for cyanide of 50 microM compare favourably with indirect conductivity detection.

Chromatography, Ion Exchange↗
PubMed1980

Determination of cyanide and thiocyanate in biological fluids by gas chromatography-mass spectrometry.

A sensitive, specific and accurate method is described for the determination of cyanide and thiocyanate in biological fluids. Potassium cyanide containing 95% 15N is added to the sample as internal standard and both endogenous cyanide and standard are separated by gas-phase diffusion into sodium hydroxide solution. Cyanogen chloride is prepared by reaction with sodium p-toluenesulphonchloramide and extracted into n-heptane. Quantitative analysis is carried out by gas chromatography-mass spectrometry (GC-MS) with selective ion monitoring of the molecular ions at m/e 61and m/e 62. Thiocyanate levels are determined by a similar procedure in which 15N-labelled sodium thiocyanate is used as internal standard. The method is applicable to a wide range of biological samples and is free from interference by other sample components.

Cyanides↗
PubMed1997

Duration of cyanide-induced conditioned food aversions in possums.

Learned aversions developed following sublethal ingestion of poisons are reported to be long-lived in many pest species. This study aimed to identify the duration of bait aversions following poisoning with a common poison (cyanide) used for possum control in New Zealand. Groups of possums with bait aversions (following cyanide poisoning) were reexposed to the bait (flavoured food) in a 2-choice test, at intervals of 1, 3, 6, 12, or 24 months. The relative intakes of the bait (used as the measure of bait aversion) did not differ between treatments (0.21, 0.21, 0.27, 0.32, and 0.20) for the 5 groups, respectively. The effect of repeated reexposures to the bait was also tested. The proportion of flavoured food eaten was 0.11, 0.19, 0.23, 0.33, and 0.36 for 1 to 5 reexposures, respectively. There was a significant increase in intake with repeated exposure. Thus, cyanide-induced aversions were strong and lasted for at least 24 months. The aversions weakened over several reexposures to the bait, but only for those individuals that had weaker initial aversions.

Animals↗
PubMed1985

Association of high cyanide and low sulphur intake in cassava-induced spastic paraparesis.

Urinary excretion of sulphur compounds was studied in children from a population in Mozambique that had been affected, during a drought, by an epidemic of spastic paraparesis attributed to cyanide exposure from cassava. The children had increased thiocyanate and decreased inorganic sulphate excretion, indicating high cyanide and low sulphur-containing amino-acid intake. Children from a neighbouring cassava-eating area, where no cases of spastic paraparesis had occurred, had lower thiocyanate excretion but higher inorganic sulphate excretion. These results support the hypothesis that the epidemic was due to the combined effects of high dietary cyanide exposure and sulphur deficiency.

Child↗