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PubMed2001

Effect of additives on the flow-analysis determination of weak-acid-dissociable and total cyanide.

The effect of reductants, complexants, and nitrite eliminators on the flow-analysis determination of weak-acid-dissociable and total cyanide has been studied for: 1. cyanide recovery from copper, nickel, and iron complexes; 2. cyanide generation from the reagents in the presence of common interferents; and 3. cyanide consumption by the reagents in the presence of those interferents. In the absence of additives the UV-assisted recovery of (total) cyanide from the iron complexes (using a succinate buffer) was insufficient. Arsenite and hypophosphite had no measurable effect on the recovery, ascorbic acid resulted in total recovery but under these conditions nitrite and sulfite seemed to destroy cyanide. Phenanthroline promoted the recovery of cyanide from iron complexes but led to formation of cyanide from thiocyanate. Citrate resulted in good recovery but in the presence of nitrite cyanide was formed; the recovery with EDTA was also good. It proved necessary to destroy nitrite by use of sulfamic acid. If a combination of EDTA, citrate, and sulfamic acid is used rather high concentrations of thiocyanate, nitrite, thiosulfate, and sulfite can be tolerated in the samples. It is strongly advisable to test modifications of the cyanide determination comprehensively, because some surprising results have been obtained.

Acids↗
PubMed1998

Treatment of cyanide-containing wastewater from the food industry in a laboratory-scale fixed-bed methanogenic reactor.

During the process of producing cassava starch from Manihot esculenta roots, large amounts of cyanoglycosides were released, which rapidly decayed to CN- following enzymatic hydrolysis. Depending on the varying cyanoglycoside content of the cassava varieties, the cyanide concentration in the wastewater was as high as 200 mg/l. To simulate anaerobic stabilization, a wastewater with a chemical oxygen demand (COD) of about 20 g/l was prepared from cassava roots and was fermented in a fixed-bed methanogenic reactor. The start-up phase for a 99% degradation of low concentrations of cyanide (10 mg/l) required about 6 months. After establishment of the biofilm, a cyanide concentration of up to 150 mg CN-/l in the fresh wastewater was degraded during anaerobic treatment at a hydraulic retention time of 3 days. All nitrogen from the degraded cyanide was converted to organic nitrogen by the biomass of the effluent. The cyanide-degrading biocoenosis of the anaerobic reactor could tolerate shock concentrations of cyanide up to 240 mg CN-/l for a short time. Up to 5 mmol/l NH4Cl (i.e. 70 mg N/l = 265 mg NH4Cl/l) in the fresh wastewater did not affect cyanide degradation. The bleaching agent sulphite, however, had a negative effect on COD and cyanide removal. For anaerobic treatment, the maximum COD space loading was 12 g l-1 day-1, equivalent to a hydraulic retention time of 1.8 days. The COD removal efficiency was around 90%. The maximum permanent cyanide space loading was 50 mg CN- l-1 day-1, with tolerable shock loadings up to 75 mg CN- l-1 day-1. Under steady-state conditions, the cyanide concentration of the effluent was lower than 0.5 mg/l.

Ammonia↗
PubMed1983

Effects of thiosulfate on cyanide pharmacokinetics in dogs.

One method to treat cyanide poisoning involves the administration of a combination of sodium thiosulfate and sodium nitrite. Sodium thiosulfate is believed to exert its antidotal effect by serving as a sulfur donor, thereby increasing the rate of rhodanese catalyzed biotransformation of cyanide to thiocyanate. To gain insight into the mechanism of action of thiosulfate on cyanide toxicity, a pharmacokinetic analysis of cyanide distribution and metabolism with and without sodium thiosulfate was conducted in mongrel dogs. A compartmental model for thiocyanate, the major metabolite of cyanide, was developed from plasma concentrations determined at various times after iv administration of thiocyanate; sodium thiosulfate did not alter thiocyanate-model parameters. The model for thiocyanate was coupled to a model for cyanide, and model based equations were fitted to the blood levels of both cyanide and thiocyanate that were measured after iv administration of cyanide. This kinetic analysis showed that thiosulfate increased the rate of conversion of cyanide to thiocyanate over 30-fold. The mechanism of thiosulfate protection appeared to be due to extremely rapid formation of thiocyanate in the central compartment, which thereby limited the amount of cyanide distribution to sites of toxicity.

Animals↗
PubMed1985

Acute cyanide intoxication and central transmitter systems.

In rats treated with sodium cyanide (5-20 mg/kg, ip) dopamine was dose dependently decreased in the striatum within 60 sec. One of the main metabolites of dopamine in the central nervous system, 3-methoxy-4-hydroxyphenylacetic acid (HVA), was decreased in striatum, olfactory tubercle, and hippocampus. However, the oxidatively deaminated metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), was not significantly altered in any of the brain regions studied. Naturally occurring levels of 3,4-dihydroxy-L-phenylalanine (L-dopa), as well as L-dopa accumulated after inhibition of the neuronal L-aromatic amino acid decarboxylase, increased in cyanide-treated rats. The dopamine receptor antagonist spiperone (0.05 mg/kg, ip) slightly increased the survival in acute cyanide intoxication. Sodium cyanide increased the levels of glutamine in frontal cortex and striatum at all doses studied. Glutamic acid was increased in the cerebellum, striatum, and hippocampus after sodium cyanide (5-10 mg/kg, ip). Higher doses decreased glutamic acid in the cerebellum, the frontal cortex, and the striatum. gamma-Aminobutyric acid (GABA) concentrations were diminished at high doses in all regions studied. Cyanide increased the levels of cyclic GMP in the cerebellum. In the striatum cyclic GMP was decreased after sodium cyanide (10 and 20 mg/kg). No significant alterations in the concentrations of acetylcholine or choline were seen in the striatum of cyanide-treated rats. The acetylcholinesterase inhibitor physostigmine and the muscarinic receptor antagonist atropine decreased the survival of mice given sodium cyanide. Acute cyanide intoxication thus produces rapid and fairly specific changes in central dopaminergic and GABA-ergic pathways.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1984

Cerebral cytochrome a,a3 inhibition by cyanide in bloodless rats.

Brain cytochrome a,a3 inhibition is presumed to be the site of lethal histotoxic hypoxia in cyanide poisoning perhaps because of the relative inability of the brain to metabolize cyanide. However, only limited data are available about cyanide toxic effects and possible antagonism in the in vivo brain. In this study, in situ, multiple wavelength, spectrophotometric monitoring of brain cytochrome a,a3 was used to observe oxidation-reduction (redox) responses of cerebral cytochrome a,a3 to intravenous potassium cyanide administration. Bloodless rats prepared by perfluorochemical emulsion (FC-43) exchange transfusion allowed monitoring of cyanide-cytochrome a,a3 interaction without spectral interference by hemoglobin. We found that cyanide-induced transient increases in cytochrome a,a3 reduction level and subsequent redox recovery kinetics were similar in bloodless and normal blood circulated rats. Electroencephalographic activity was maintained until a 50% increase in the reduction level of cytochrome a,a3 was induced with cyanide. Pre-treatment with the cyanide antagonist sodium thiosulfate also protected brain cytochrome a,a3 from cyanide-mediated redox state changes by approximately 4-fold both in normal blood circulated controls and during FC-43 circulation. These latter results indicate that sodium thiosulfate, presumably acting at tissue sites of rhodanese activity, can prevent cerebral cytochrome a,a3 reduction by cyanide even in the virtual absence of blood or circulating proteins.

Animals↗
PubMed1995

The clinical experience of acute cyanide poisoning.

The authors reviewed the clinical manifestations, complications, and the prognosis affected by Lilly Cyanide Antidote in 21 victims of acute cyanide poisoning over a 10-year period. The clinical signs and symptoms in cyanide poisoning are variable. Among 21 cases, loss of consciousness (15), metabolic acidosis (14), and cardiopulmonary failure (9) were the three leading manifestations of cyanide intoxication. Anoxic encephalopathy (6) was not uncommon in the severely intoxicated victims. Diabetes insipidus (1) or clinical signs and symptoms mimicking diabetes insipidus (3) may be an ominous sign to encephalopathy victims. The major cause of fatal cyanide poisoning is the intentional ingestion of cyanide compounds as part of a suicide attempt. Decrease of arteriovenous difference of O2 partial pressure may be a clue for the suspicion of cyanide intoxication. Although the authors cannot show a statistically significant difference (P = .47) for the Lilly cyanide antidote kit in terms of improving the survival rate for victims of cyanide poisoning, the antidote kit was always mandatory in our study in the cases of severely intoxicated victims who survived. Early diagnosis, prompt, intensive therapy with antidote, and supportive care are still the golden rules for the treatment of acute cyanide poisoning, whether in the ED or on the scene.

Acute Disease↗
PubMed2006

Packed cage rotating biological contactor system for treatment of cyanide wastewater.

The aim of this work was to study the efficiency of the packed cage rotating biological contactor (RBC) system with synthetic wastewater (SWW) containing 800 mg/l BOD(5) with various cyanide residue concentrations and hydraulic loading time. The results showed that cyanide had a negative effect to both the system's efficiency and bio-film quality. An increase in cyanide concentration led to a decrease in bio-film growth and the consequent reduction in the removal efficiency of the system. Also, the effluent suspended solids (SS) of the system was increased with increasing cyanide concentrations because the bio-film detached from the media due to the toxicity of the cyanide residue. The system showed the highest COD, BOD(5), TKN and cyanide removal efficiencies of 94.0 +/- 1.6%, 94.8 +/- 0.9%, 59.1 +/- 2.8% and 95.5 +/- 0.6%, respectively, with SWW containing 5 mg/l cyanide under HRT of 8 days, while they were only 88.8 +/- 0.7%, 89.5 +/- 0.5%, 40.3 +/- 1.1% and 93.60 +/- 0.09%, respectively, with SWW containing 40 mg/l cyanide. In addition, the effluent ammonia, nitrite and nitrate were increased with increases in cyanide concentration or loading. However, the system with SWW containing the highest cyanide concentration of 40 mg/l showed almost constant COD and BOD(5) removal efficiencies of 89% and 90%, even when the system was controlled under the lowest HRT of 8 h.

Biofilms↗
PubMed2004

Metabolism of cyanide by Chinese vegetation.

Cyanide is a high-volume production chemical and the most commonly used leaching reagent for gold and silver extraction. Its environmental behavior and fate is of significant concern because it is a highly toxic compound. Vascular plants possess an enzyme system that detoxifies cyanide by converting it to the amino acid asparagine. This paper presents an investigation of the potential of Chinese vegetation to degrade cyanide. Detached leaves (1.5 g fresh weight) from 28 species of 23 families were kept in glass vessel with 100 ml of aqueous solution spiked with potassium cyanide at 23.5 degrees C for 28 h. Cyanide concentrations ranged from 0.83 to 1.0 CN mg l(-1). The disappearance of cyanide from the aqueous solution was analyzed spectrophotometrically. The fastest cyanide removal was by Chinese elder, Sambucus chinensis, with a removal capacity of 8.8 mg CN kg(-1) h(-1), followed by upright hedge-parsley (Torilis japonica) with a value of 7.5 mg CN kg(-1) h(-1). The lowest removal capacity had the snow-pine tree (Credrus deodara (Roxb.) Loud). Results from this investigation indicated that a wide range of plant species is able to efficiently metabolize cyanide. Therefore, cyanide elimination with plants seems to be a feasible option for cleaning soils and water contaminated by cyanide from gold and silver mines or from other sources.

Biodegradation, Environmental↗
PubMed2006

Differences in Michaelis-Menten kinetics for different cultivars of maize during cyanide removal.

Knowledge of the kinetic parameters, the half-saturation constant (K(m)) and the maximum metabolic capacity (v(max)), is very useful for the characterization of enzymes and biochemical processes. Little is known about rates of which vegetation metabolizes environmental chemicals. It is known, however, that vascular plants possess an enzyme system that detoxifies cyanide by converting it into the amino acid asparagine. This study investigated the differences in Michaelis-Menten kinetics of cyanide removal by different cultivars of maize. Detached leaves (1.0 g fresh weight) of seven different cultivars of maize (Zea mays L.) were kept in glass vessels with 100mL of aqueous solution spiked with potassium cyanide at 25+/-0.5 degrees C for 28 h. Four treatment concentrations of cyanide were used, ranging from 0.43 to 7.67 mgCNL(-1). The disappearance of cyanide from the aqueous solution was analyzed spectrophotometrically. Realistic values of K(m) and v(max) were estimated by a computer program using non-linear regression treatment. Lineweaver-Burk plots were also used to estimate the kinetic parameters for comparison. Using non-linear regression treatments, values of v(max) and K(m) were found to be between 10.80 and 22.80 mgCNkg(-1)h(-1), and 2.57 and 7.09 mgCNL(-1), respectively. The highest v(max) was achieved by the cultivars HengFen 1, followed by NongDa 108. The lowest v(max) was demonstrated by JingKe 8. The highest K(m) was found in NongDa 108, followed by HengFen 1. The lowest K(m) was associated with JingKe 8. Results from this study indicated that significant removal of cyanide from an aqueous solution was observed in the presence of plant materials without apparent phytotoxicity, even at the high concentration of cyanide used in this study. All maize cultivars used in this study were able to metabolize cyanide efficiently, although with different metabolic capacities. Results also showed a small variation of metabolic rates between the different cultivars. This leads to the conclusion that plants can be used as a phytoremediation agent in the detoxification of cyanide, presenting a feasible option for cleaning up soils and water contaminated with cyanide.

Biodegradation, Environmental↗
PubMed2006

Photobiomodulation partially rescues visual cortical neurons from cyanide-induced apoptosis.

Near-infrared light via light-emitting diode treatment has documented therapeutic effects on neurons functionally inactivated by tetrodotoxin or methanol intoxication. Light-emitting diode pretreatment also reduced potassium cyanide-induced cell death, but the mode of death via the apoptotic or necrotic pathway was unclear. The current study tested our hypothesis that light-emitting diode rescues neurons from apoptotic cell death. Primary neuronal cultures from postnatal rat visual cortex were pretreated with light-emitting diode for 10 min at a total energy density of 30 J/cm2 before exposing to potassium cyanide for 28 h. With 100 or 300 microM potassium cyanide, neurons died mainly via the apoptotic pathway, as confirmed by electron microscopy, Hoechst 33258, single-stranded DNA, Bax, and active caspase-3. In the presence of caspase inhibitor I, the percentage of apoptotic cells in 300microM potassium cyanide was significantly decreased. Light-emitting diode pretreatment reduced apoptosis from 36% to 17.9% (100 microM potassium cyanide) and from 58.9% to 39.6% (300 microM potassium cyanide), representing a 50.3% and 32.8% reduction, respectively. Light-emitting diode pretreatment significantly decreased the expression of caspase-3 elicited by potassium cyanide. It also reversed the potassium cyanide-induced increased expression of Bax and decreased expression of Bcl-2 to control levels. Moreover, light-emitting diode decreased the intensity of 5-(and -6) chloromethy-2', 7-dichlorodihydrofluorescein diacetate acetyl ester, a marker of reactive oxygen species, in neurons exposed to 300 microM potassium cyanide. These results indicate that light-emitting diode pretreatment partially protects neurons against cyanide-induced caspase-mediated apoptosis, most likely by decreasing reactive oxygen species production, down-regulating pro-apoptotic proteins and activating anti-apoptotic proteins, as well as increasing energy metabolism in neurons as reported previously.

Animals↗
PubMed2002

Anion-exchange chromatography of metal cyanide complexes with gradient separation and direct UV detection.

In the regulatory analysis of water samples, cyanide content is usually expressed in various forms as free cyanide, total cyanide, weak-acid dissociable cyanide, available cyanide, and cyanide amenable to chlorination. Concentration of individual metal cyanide complex, not furnished in any of these methods, is useful in meaningful assessment of toxicity due to cyanide. In the present work, two macroporous anion-exchange columns, having high and intermediate hydrophobicity, were evaluated to achieve separation of cyano complexes of silver, iron, gold, copper, nickel, and cobalt. On the QS-Al SC column, of high hydrophobicity, the monovalent cyano complexes of silver and gold eluted last while the multivalent cyano complexes, e.g. iron and copper, eluted early. It is suggested that the retention order on this column is due to relative hydrophobicity of the metal cyanide complex, and its affect on ion exchange. In contrast, on the QS-A2 SC column of intermediate hydrophobicity, with the exception of cyano complex with Fe, the separation of the cyano complexes of five other metals closely followed an anion-exchange mechanism. Under gradient conditions, the six metal cyanide complexes were well resolved on the QS-A2 SC column and the method with direct UV detection at 215 nm was accurate (spike recovery of 99.8-118.8%) and precise (RSD of 1.0-2.6%).

Anion Exchange Resins↗
PubMedDate not supplied

Focus on smoke inhalation--the most common cause of acute cyanide poisoning.

The contribution of smoke inhalation to cyanide-attributed morbidity and mortality arguably surpasses all other sources of acute cyanide poisoning. Research establishes that cyanide exposure is: (1) to be expected in those exposed to smoke in closed-space fires; (2) cyanide poisoning is an important cause of incapacitation and death in smoke-inhalation victims; and (3) that cyanide can act independently of, and perhaps synergistically with, carbon monoxide to cause morbidity and mortality. Effective prehospital management of smoke inhalation-associated cyanide poisoning is inhibited by: (1) a lack of awareness of fire smoke as an important cause of cyanide toxicity; (2) the absence of a rapidly returnable diagnostic test to facilitate its recognition; and (3) in the United States, the current unavailability of a cyanide antidote that can be used empirically with confidence outside of hospitals. Addressing the challenges of the prehospital management of smoke inhalation-associated cyanide poisoning entails: (1) enhancing the awareness of the problem among prehospital responders; (2) improving the ability to recognize cyanide poisoning on the basis of signs and symptoms; and (3) expanding the treatment options that are useful in the prehospital setting.

Acute Disease↗
PubMed2004

Cyanide binding to truncated hemoglobins: a crystallographic and kinetic study.

Cyanide is one of the few diatomic ligands able to interact with the ferric and ferrous heme-Fe atom. Here, the X-ray crystal structure of the cyanide derivative of ferric Mycobacterium tuberculosis truncated hemoglobin-N (M. tuberculosis trHbN) has been determined at 2.0 A (R-general = 17.8% and R-free = 23.5%), and analyzed in parallel with those of M. tuberculosis truncated hemoglobin-O (M. tuberculosis trHbO), Chlamydomonas eugametos truncated hemoglobin (C. eugametos trHb), and sperm whale myoglobin, generally taken as a molecular model. Cyanide binding to M. tuberculosis trHbN is stabilized directly by residue TyrB10(33), which may assist the deprotonation of the incoming ligand and the protonation of the outcoming cyanide. In M. tuberculosis trHbO and in C. eugametos trHb the ligand is stabilized by the distal pocket residues TyrCD1(36) and TrpG8(88), and by the TyrB10(20) - GlnE7(41) - GlnE11(45) triad, respectively. Moreover, kinetics for cyanide binding to ferric M. tuberculosis trHbN and trHbO and C. eugametos trHb, for ligand dissociation from the ferrous trHbs, and for the reduction of the heme-Fe(III)-cyanide complex have been determined, at pH 7.0 and 20.0 degrees C. Despite the different heme distal site structures and ligand interactions, values of the rate constant for cyanide binding to ferric (non)vertebrate heme proteins are similar, being influenced mainly by the presence in the heme pocket of proton acceptor group(s), whose function is to assist the deprotonation of the incoming ligand (i.e., HCN). On the other hand, values of the rate constant for the reduction of the heme-Fe(III)-cyanide (non)vertebrate globins span over several orders of magnitude, reflecting the different ability of the heme proteins considered to give productive complex(es) with dithionite or its reducing species SO(2)(-). Furthermore, values of the rate constant for ligand dissociation from heme-Fe(II)-cyanide (non)vertebrate heme proteins are very different, reflecting the different nature and geometry of the heme distal residue(s) hydrogen-bonded to the heme-bound cyanide.

Animals↗
PubMed1999

Ferrocyanide ingestion may cause false positives in cyanide determination.

CASE REPORT: The authors present a patient who ingested a cyanide containing solution and arrived at the hospital without any clinical evidence of intoxication but an elevated blood cyanide level. The authors explain this discrepancy with the following hypotheses: 1) the patient ingested cyanide as an iron-chelated complex; and 2) the sulfuric acid used in the standard microdiffusion technique released cyanide from its iron-bound state to result in the observed elevated blood cyanide. Through a series of in vitro analyses, the authors demonstrate the following: 1) the ingested solution tested positive for cyanide with the sulfuric acid technique and negative for cyanide with acetic acid; 2) the presence of a ferrous salt in the ingested product by a colorimetric redox titration technique; and 3) release of a small fraction of the total cyanide from ferrocyanide by the sulfuric acid technique. The authors conclude: 1) the patient ingested potassium ferrocyanide; and 2) the strong acid used in the cyanide microdiffusion assay will liberate cyanide that is chelated to iron to yield false positive results.

Adult↗
PubMed2004

Carbon monoxide and cyanide poisoning in fire related deaths in Victoria, Australia.

OBJECTIVE: This study was undertaken to examine the association of hydrogen cyanide and carboxyhaemoglobin in victims of fire related deaths in Australia. The secondary aim was to document demographic data about Australian fire related deaths. METHODS: An observational retrospective study was undertaken of autopsy reports from the Victorian Institute of Forensic Medicine. Reports of fire related deaths were electronically searched using the terms burns, "smoke" or "fire" as a cause of death in the calender years 1992 to 1998. Data on the circumstances of the fire and results of toxicological screening were obtained on 178 persons. Additional whole blood cyanide levels were determined if blood samples were available in storage. Demographics of the victims were analysed, as well as the relationship between carboxyhaemoglobin and whole blood cyanide levels. RESULTS: Most (82%) of the victims died at the scene, whilst 32 victims died after a period of hospitalisation (hours to weeks). Suicide as a result of self-immolation was the reported cause of death in 32 cases. Most of the fires were in houses (114) and cars (29). The blood ethanol level was zero in 112 cases; the remaining cases (53) had a mean level of 0.17%. Other central nervous system (CNS) depressants were recorded in 49 of the 134 cases that received a complete toxicological screen. Carboxyhaemoglobin levels were measured in only 154 of 178 cases. The carboxyhaemoglobin level was zero in 43 cases. The remaining cases (111) had a mean level of 40%; with 44 cases having a level greater than 50%, a level considered to be potentially lethal. Whole blood hydrogen cyanide levels were measured in only 138 of 178 cases. The hydrogen cyanide level was zero in 52 cases. The remaining cases (86) had a mean level of 1.65 mg/L; with 11 cases having a level greater than 3.0 mg/L (potentially fatal). Blood ethanol levels were significantly correlated with both carboxyhaemoglobin (R = 0.22, P < 0.01) and cyanide (R = 0.36, P < 0.001). In addition, a significant correlation (r = 0.34) between carboxyhaemoglobin and hydrogen cyanide levels was noted. CONCLUSIONS: This study showed a correlation between elevated blood ethanol and whole blood cyanide levels (r = 0.36, p < 0.001) and between elevated carboxyhaemoglobin and hydrogen cyanide levels (r = 0.34). Although the mean cyanide level was 1.3 mg/L (above the level some consider potentially toxic) in those cases with a carboxyhaemoglobin level of greater than 10%, there is insufficient data to permit recommendations for clinical care. Further studies are required on those victims that reach hospital alive.

Adolescent↗
PubMed1997

A new biological assay for measuring cyanide in blood.

UNLABELLED: Clinical diagnosis of cyanide poisoning is complicated by the lack of an easy, convenient assay for cyanide concentration in blood. Therapy may be delayed with unconfirmed diagnosis because the conventional antidote to cyanide poisoning exposes patients to substantial risks. We developed a new spectrophotometric assay to measure cyanide by extraction into a sodium hydroxide trap, followed by the addition of exogenous methemoglobin as a colormetric indicator. Samples of blood from 15 healthy subjects and 5 patients who had received prolonged nitroprusside infusions were assayed. To optimize assay characteristics, methemoglobin concentrations, pH, temperature, incubation time, and buffer strengths were varied. Duplicate samples were assayed by using the polarographic method for assay validation. Over a range from 300 ng/mL to 7 microg/mL, the correlation between methods was r = 0.983. Interassay and intraassay variability were 5% and 2%, respectively. Samples drawn from the five patients and tested by using both methods yielded a correlation of r = 0.978. This new assay for cyanide in blood may greatly facilitate the diagnosis and treatment of cyanide ingestion. The use of methemoglobin as the colorimetric indicator in the assay contributes to its low cost and ease of use. IMPLICATIONS: Cyanide, an important factor in death from burn-related inhalation injury, is difficult and time-consuming to measure. We developed a new, rapid blood test for cyanide using methemoglobin as a colormetric indicator. A rapid, accessible test for cyanide may speed the diagnosis and treatment of cyanide poisoning.

Adult↗
PubMed1984

Photodegradation of sodium nitroprusside: biologic activity and cyanide release.

Because the belief that cyanide is released from nitroprusside in vivo recently was challenged, the authors performed a series of experiments that examined the conditions under which nitroprusside is degraded. These experiments include an examination of the release of cyanide and nitric oxide from nitroprusside in vitro, the release of cyanide in vivo, and a comparison of the biologic activity of intact and degraded nitroprusside. Nitroprusside in aqueous solution degraded when exposed to white or blue light but not to red light. While light at 20 microW X cm-2 produced 40% apparent photodegradation after 6 h exposure, while white light at 220 microW X cm-2 produced 100% apparent photodegradation after 2 h exposure. At 10% apparent photodegradation, 10% of the nitrosyl ligand was recovered as free nitric oxide, and 0.4% of the cyanide ligand was recovered as free cyanide. Following a 2-h infusion of light-protected nitroprusside in seven patients, cyanide concentrations ranged from 1.4 to 45.5 microM and 0.09 to 3.2 microM in blood and plasma, respectively. These values were not changed by exposing the samples to white light (220 microW X cm-2) for 4 h. Intact and photodegraded nitroprusside produced identical hypotensive responses in rats as would be expected, since the nitrosyl ligand was detected in solution following degradation, and it mediates this action. Cyanide was released from nitroprusside, both on its exposure to light in vitro and also in vivo. The latter was not an artifact of the assay for cyanide. Nitroprusside releases cyanide in vivo, and cyanide toxicity is a true complication of its use.

Animals↗
PubMed1987

In vitro cyanide release from sodium nitroprusside.

In vitro release of cyanide from sodium nitroprusside in 5% dextrose in water solution following exposure or non-exposure to fluorescent light (500 ft candles or 791 microwatt per square cm [muWcm-2]), was measured by a cyanide-specific ion electrode at 4, 8, 24, 48, and 72 h. The cyanide concentrations were significantly increased at 24 h in the light-exposed solution. In this group, 100% of the cyanide was released from sodium nitroprusside at 72 h exposure to light. However, cyanide concentrations showed no significant changes for 72 h in the light-protected solutions, which were either exposed to 500 foot candles fluorescent light or stored in a dark room. Less than 2.5% of the cyanide was released from sodium nitroprusside at 72 h in both of the light-protected groups. No significant differences in cyanide concentrations were observed at 8 h among the exposed or non-exposed solutions. After 24 h of exposure, the cyanide concentrations in the exposed group were significantly higher than those of the two light-protected solutions. However, there were no significant differences between the cyanide concentration in the light-protected solutions. These results substantiate the safety of sodium nitroprusside solution for 24 h if the sodium nitroprusside containing solutions are properly protected from light. An additional study performed showed that a significant amount of cyanide released from sodium nitroprusside was adsorbed to the surface of polyvinylchloride.

Cyanides↗