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PubMed1999

A simple, rapid and sensitive semimicro method for the measurement of cyanide in blood.

Conventional methods do not meet the clinical need for rapid cyanide measurements. We report a procedure which can provide a result in 10 min. It should be of particular interest to laboratories serving cardiac or renal units which use the hypotensive agent sodium nitroprusside, and burns units to which fire victims may be admitted suffering the effects of HCN from inhaled smoke. A sample of blood (100 microL) is mixed with H3PO4, containing a surfactant, and the HCN is trapped in an alkaline mixture of 1,2-dinitrobenzene and 4-nitrobenzaldehyde in 2-methoxyethanol. The catalytic action of cyanide, which produces purple 2-nitrophenylhydroxylamine, is stopped with acetone after 6 min. The absorbance measured at 560 nm shows a linear relationship with the cyanide concentration, but the slope varies with the ambient temperature. Since KCN added to both 50 mmol/L NaOH and blood gives similar assay results, any inaccuracy arising from changes in temperature can be avoided by running standards at the same time as the blood sample.

Clinical Laboratory Techniques↗
PubMed1990

The effect of storage upon cyanide in blood samples.

CDPA blood of human origin was 'spiked' with a solution of potassium cyanide at four different concentrations. When such blood was left in contact with the atmosphere for up to 10 min an appreciable amount of the cyanide was lost. Stoppered tubes containing the 'spiked' blood were stored at -20 degrees C and 4 degrees C for up to 6 months. Most samples, especially those 'spiked' at the highest concentrations, showed a loss of cyanide.

Blood Preservation↗
PubMed1992

Fatal cyanide poisoning from cassava-based meal.

Three patients admitted to the Accident and Emergency Unit of Lagos University Teaching Hospital (LUTH) after eating a cassava based meal 'Gari' died shortly after admission. The patients vomited and complained of abdominal pain immediately after the meal. They were unconscious with renal failure and died of cardiopulmonary arrest. The cyanide levels in the blood and urine averaged 1.12 and 0.54 mg l-1, respectively. Cassava contains cyanogenic glycosides which slowly release cyanide and this may have been responsible for the death of these patients. There is an urgent need to establish maximum tolerable levels of cyanide in 'Gari' and other cassava food products.

Adolescent↗
PubMed1995

Therapeutic efficacy of sodium nitrite and 4-dimethylaminophenol or hydroxylamine co-administration against cyanide poisoning in rats.

1. The therapeutic efficacy of combined treatment of sodium nitrite (NaNO2) and 4-dimethylaminophenol (DMAP) or hydroxylamine (H2NOH) was investigated in potassium cyanide (KCN) intoxication in male rats. 2. Therapy with NaNO2 (0.27 mmol kg-1) + DMAP (0.09 mmol kg-1) or NaNO2 + H2NOH (0.09 mmol kg-1, produced a protection index (ratio of LD50 of KCN in rats receiving therapy to an LD50 of KCN in rats given only 0.9% saline) of 2.5 and 2.0 respectively. 3. Both the regimens exhibited a beneficial effect in terms of improving the survival time and postural defects in rats exposed to 2 LD50 KCN. 4. NaNO2 + DMAP showed a significant protective effect in the disposition of the plasma cyanide level at different time intervals. 5. The NaNO2 + DMAP regimen was superior to NaNO2 + N2NOH in terms of reactivating the inhibited brain cytochrome oxidase enzyme. 6. The addition of sodium thiosulphate (Na2S2O3) in both the regimens increased the degree of protection. 7. The results suggest that combined therapy with NaNO2 + DMAP could significantly reduce the toxic effects of cyanide, compared with NaNO2+H2NOH treatment.

Aminophenols↗
PubMed1996

Cyanide toxicity in mice pretreated with diethylamine nitric oxide complex.

1. Since the literature suggested a portion of the overall toxicity of cyanide (CN) may be affected by nitric oxide, we investigated a long acting NO releasing complex (diethylamine/nitric oxide (DEA/NO)) which may exhibit vasodilatory as well as other nitric oxide effects to determine its ability to modify CN toxicity. Sodium nitrite, a vasodilator commonly used to treat cyanide toxicity thought to act by methemoglobin (MHb) formation, can be rapidly transformed to nitric oxide (NO). 2. Mice (n = 10 per dose) were administered one of five doses of sodium cyanide (NaCN) intraperitoneally (4.28, 5.08, 6.03, 7.17 and 8.52 mg kg-1). DEA/NO was given intravenously (20 mg kg-1) 2 min prior to NaCN. As a control, NG-monomethyl-L-arginine (L-NMMA), which inhibits NO synthesis, was administered intravenously (70 mg kg-1) to mice, 3 min prior to DEA/NO. 3. Before CN toxicity studies, we determined whether DEA/NO was producing MHb by collecting tail vein blood from mice and measuring MHb levels. For example, 4 min after DEA/NO administration (5, 10, and 20 mg kg-1), MHb levels were 1.27 +/- 0.28%, 2.60 +/- 0.26% and 6.53 +/- 0.54% respectively. O2 capacity was also decreased in a dose related manner. Carboxyhemoglobin or percent O2 saturation, on the other hand, was not significantly inhibited. The LD50 increased from 5.75 +/- 0.026 (CN alone) to 7.66 +/- 0.021 mg kg-1 (CN+DEA/NO) resulting in a protective ratio of 1.73. 4. Results suggest the following: (1) L-NMMA, which inhibits the synthesis of endogenous NO, appears to exacerbate the DEA/NO (or exogenous NO) response; (2) DEA/NO appears to reduce the toxicity of CN which suggests that a portion of CN toxicity may be affected by a NO component; and (3) low DEA/NO doses may act via a direct effect while higher doses (40 mg kg-1) may allow for formation of a concentration of MHb which can bind CN to form cyanomethemoglobin and reduce the toxicity of CN.

Animals↗
PubMed2003

Cyanide toxicosis in goats after ingestion of California Holly (Heteromeles arbutifolia).

Cyanogenic glycosides are found in many native and naturalized plants throughout North America. The glycosides themselves are not toxic, but they yield hydrogen cyanide (hydrocyanic or prussic acid) when they are hydrolyzed by beta-glycosidases, either as a result of injury to the plant cells or by microbial action in the rumen. Hydrogen cyanide is readily absorbed from the gastrointestinal tract. Cyanide ion binds with iron in cytochrome oxidase, interfering with cellular respiration. The clinical effects are peracute, often resulting in death less than 1 hour after ingestion. This study describes a case that resulted in significant morbidity and mortality in a herd of goats after exposure to California holly (Heteromeles arbutifolia).

Animals↗
PubMed1997

Effects of nucleotides on cyanide-resistant respiratory activity in mitochondria isolated from antimycin A-treated yeast Hansenula anomala.

Mitochondria were isolated from Hansenula anomala induced for cyanide-resistant respiration by antimycin A-treatment. Cyanide-resistant respiratory activity in isolated mitochondria was stimulated by AMP, ADP, dAMP, and GMP, but not by ATP, adenosine, cAMP, 2'(3')-AMP, CMP, and UMP. Effects of nucleotides were also observed on cyanide-resistant and salicylhydroxamate-sensitive decylubiquinol oxidase activity. Carbonylcyanide m-chlorophenylhydrazone, oligomycin, and carboxyatractyloside did not affect activation of decylubiquinol oxidase activity by AMP. It is suggested that purine nucleoside 5'-monophosphate or diphosphate stimulates alternative oxidase activity from the outer surface of the mitochondrial inner membrane with a mechanism different from respiratory control. Alternative oxidase activity might be controlled by adenine nucleotides posttranscriptionally in fungi.

Adenine Nucleotides↗
PubMed2005

Life-threatening interaction between complementary medicines: cyanide toxicity following ingestion of amygdalin and vitamin C.

OBJECTIVE: To describe a case of severe accidental cyanide poisoning following a single ingestion of amygdalin with therapeutic intent. CASE SUMMARY: A 68-year-old patient with cancer presented to the emergency department shortly after her first dose (3 g) of amygdalin with a reduced Glasgow Coma Score, seizures, and severe lactic acidosis requiring intubation and ventilation. The patient also ingested 4800 mg of vitamin C per day. She responded rapidly to hydroxocobalamin treatment. The adverse drug reaction was rated probable on the Naranjo probability scale. DISCUSSION: Amygdalin and laetrile (a synthetic form of amygdalin) are commonly used as complementary or alternative medicine (CAM) for the treatment of cancer. Vitamin C is known to increase the in vitro conversion of amygdalin to cyanide and reduce body stores of cysteine, which is used to detoxify cyanide. Amygdalin has been used for decades by patients with cancer who are seeking alternative therapies, and severe reactions have not been reported with this dose. An interaction with vitamin C is a plausible explanation for this life-threatening response. CONCLUSIONS: This case highlights the fact that CAMs can produce life-threatening toxicity. This case also adds a further note of caution, namely, the potential for serious interactions between CAMs, particularly where there is no tradition of concomitant use.

Acidosis↗
PubMedDate not supplied

Cyanide insensitive iron superoxide dismutase in Euglena gracilis. Comparison of the reliabilities of different test systems for superoxide dismutases.

Two proteins (P1 and P2, with weights of 57,500 and 27,500 respectively) were isolated from Euglena gracilis. Both proteins show cyanide-insensitive superoxide dismutase activity in the "classical" superoxide dismutase assay, using xanthine-xanthine oxidase as O2.- generator. If O2.- is generated chemically (autoxidation of reduced anthraquinone), photochemically (illuminated riboflavine) or pulse radiolytically, only protein P1 but not P2 shows SOD activity. Protein P1 contains 1 g atom (determined: 0.82) iron (no Mn or Cu) per mole protein and may thus be defined as iron-superoxide dismutase. Protein P2, showing the spectral properties of a flavoprotein, exhibits the activities of ferredoxin-NADP-oxidoreductase and "diaphorase". The cyanide-insensitive SOD-activity of this Diaphorase" in the xanthine oxidase-assay for superoxide dismutase makes this classical and commonly used test unreliable for assay cyanide insensitive SOD activities. The existence of the "prokaryote-type" of superoxide dismutase (Fe-SOD) in Euglena gracilis is exceptional for an eukaryotic, autotrophically grown organisms.

2,6-Dichloroindophenol↗
PubMed1980

Haemoglobin determination without cyanide on Hemalog-8.

The most common method for determination of haemoglobin is the cyanmet-haemoglobin method which is recommended by the International Committee for Standardization in Haematology (ICSH). Determination of haemoglobin is one of the most used methods in hospital laboratories. One disadvantage with the method is the use of cyanide in the reagent, which demands cautious preparation and use. The intention of our investigation was to replace the cyanide reagent for Hemalog-8 with a reagent not containing cyanide. It is shown that the change of reagent did not influence the results of the analysis.

Cyanides↗
PubMed1981

Cyanide poisoning.

In recent years, the increasing use of laetrile has been added to the traditional sources of exposure to cyanide in industry, chemistry labs, and fumigation. The events in Jonestown in 1978 were a grim reminder of the lethality of cyanide. Nonetheless, advancement in new modes of treatment has been slow. The traditional method of treatment used in the United States is effective, but not without its own morbidity and mortality. Using two case reports as models, we review here the topic of cyanide poisoning including sources of exposure, pathophysiology, clinical manifestations of both acute and chronic exposure, and modes of treatment. Although there is currently no accepted alternate treatment in this country, review of the literature shows promise in other modalities being investigated in Europe, including hydroxocobalamin, cobalt salts, and particularly aminophenols.

Adult↗
PubMed1993

Hydroxocobalamin as a cyanide antidote: safety, efficacy and pharmacokinetics in heavily smoking normal volunteers.

The safety, efficacy and pharmacokinetic parameters of 5 g of hydroxocobalamin given intravenously, alone or in combination with 12.5 g of sodium thiosulfate, were evaluated in healthy adult men who were heavy smokers. Sodium thiosulfate caused nausea, vomiting, and localized burning, muscle cramping, or twitching at the infusion site. Hydroxocobalamin was associated with a transient reddish discoloration of the skin, mucous membranes, and urine, and when administered alone produced mean elevations of 13.6% in systolic and 25.9% in diastolic blood pressure, with a concomitant 16.3% decrease in heart rate. No other clinically significant adverse effects were noted. Hydroxocobalamin alone decreased whole blood cyanide levels by 59% and increased urinary cyanide excretion. Pharmacokinetic parameters of hydroxocobalamin were best defined in the group who received both antidotes: t1/2 (alpha), 0.52 h; t1/2 (beta), 2.83 h; Vd (beta), 0.24 L/kg; and mean peak serum concentration 753 mcg/mL (560 mumol/L) at 0-50 minutes after completion of infusion. Hydroxocobalamin is safe when administered in a 5 gram intravenous dose, and effectively decreases the low whole blood cyanide levels found in heavy smokers.

Adult↗
PubMed1994

Chronic cyanide poisoning in relation to blindness and tropical neuropathy.

Within a group of 20 patients showing optic atrophy and macula degeneration, 14 patients could be examined for neurological and audiometric defects. In 6 patients neurological signs and symptoms were observed. Nine patients reported loss of hearing and in 3 of them a severe perceptive deafness was seen in the audiogram. In 3 of the 14 patients a combination of severe neurologic and audiologic symptoms developed and in two of them a high thiocyanate concentration in serum was observed. The occurrence of perceptive deafness and posterior column sensory loss in the lower extremities in four of the patients made the diagnosis of polyneuropathy the most plausible. Although a similarity to chronic myelopathies caused by nutritional cyanide poisoning cannot be denied, the mean thiocyanate concentration in plasma 24 mumol/L (1.39 mg/L), and the cyanide levels in the blood 0.09 mumol/L (2.3 micrograms/L) were substantially lower than those found in other individuals during periods of extreme drought in which food only consisted of the bitter variety of cassava. The role of cyanide in the etiopathology of this polyneuropathy is unknown.

Adolescent↗
PubMed1976

The occurrence of cyanide in certain smoked meat products.

Fifteen samples of smoked reindeer meat, two samples of smoked mutton from Iceland and five samples of smoked salamitype fermented sausage were analysed for their cyanide (CN) content by a steam distillation method. The mean cyanide content of the smoked reindeer meat was found to be 1.38 +/- 1.01 mg CH/kg, range 0.27--4.27 mg/kg. The two smoked mutton samples, contained 1.93 and 1.78 mg CN/kg and the mean cyanide content of the five Salami samples was found to be 0.19 +/- 0.13 mg CH/kg, range 0.06--0.40 mg/kg. The toxicological aspects of the findings are discussed, with special reference to the possible effects of nitrate and nitrite in the products.

Animals↗
PubMed1975

Inhibition of DNA replication in Escherichia coli by cyanide and carbon monoxide.

The inhibition of DNA replication in aerobically growing Escherichia coli by cyanide or carbon monoxide occurs within about 20 s at 15 degrees, as previously reported by Cairns and Denhardt (Cairns, J., and Denhardt, D.T. (1968) J. Mol. Biol. 36, 335-342). This rapid inhibition can be explained by the nearly complete depletion of both intracellular ATP and deoxynucleoside triphosphates which occurs during the time that replication stops. There is probably no direct effect of carbon monoxide on any of the enzymes involved in replication because this reagent has no effect on replication rate or ATP level in anaerobic cells. These cells produce ATP by glycolysis. The inhibition of replication by cyanide, a highly reactive compound, appears to be more complex since anaerobically growing cells can still be completely inhibited, although higher concentrations are required than for aerobically growing cells. The sensitivity of anaerobic cells to cyanide is probably due to the ability of this highly reactive compound to react nonspecifically with many proteins and other molecules.

Adenosine Triphosphate↗
PubMed2001

Does prolonged cyanide exposure have a diabetogenic effect?

Cyanide exposure through cassava consumption has been associated with the development of malnutrition-related diabetes mellitus (MRDM). However, there are few experimental reproductions of this disease. In the present study 42 rats received 0, 9.0 or 12.0 mg KCN/kg bw/d for 15 d, 26 pigs were dosed with 0, 2.0, 4.0 or 6.0 mg KCN/kg for 74 d, and 34 goats received 0, 0.3, 0.6, 1.2 or 3.0 mg KCN/kg for 5 mo. At the end of each experimental period, plasma samples were obtained for glucose and thiocyanate measurement, and the pancreas was collected for histopathologic study. No significant differences in plasma glucose concentrations occurred between groups. The pancreas had no pathology. Chronic cyanide exposure did not promote diabetogenic effects in rats, swine or goats, suggesting that cyanide is not responsible for MRDM in humans.

Animals↗
PubMed2001

Cyanide toxicity in the surgical intensive care unit: a case report.

Hypertension is a widespread entity in the surgical intensive care unit. Not only is the clinical spectrum varied, but the armamentarium available to the clinician is also wide-ranging. Sodium nitroprusside, a potent vasodilator with a short half-life, is often used for hypertensive crisis and to deliberately maintain a low blood in certain clinical conditions. Cyanide toxicity is a known complication of sodium nitroprusside use. Herein is reported a case of probable cyanide toxicity in an elderly trauma patient. The pharmacology of sodium nitroprusside and the pitfalls of making the diagnosis of cyanide toxicity are discussed.

Aged↗
PubMed2002

MR changes after acute cyanide intoxication.

We describe MR changes that occurred 3 and 6 weeks after a suicide attempt with cyanide. The toxicity of cyanide causes damage, primarily to the basal ganglia, and those changes were visible as altered signal intensity on the first MR images. Extensive areas of hemorrhagic necrosis were seen 6 weeks later. Our case shows pseudolaminar necrosis along the central cerebral cortex 3 weeks after cyanide poisoning, showing that the sensorimotor cortex is also a site for toxic necrosis because of its high oxygen dependency.

Adult↗