Elevated Concentrations Of Cyanide Research Articles

Chemical and Clinical Aspects of Metal-Containing Antidotes for Poisoning by Cyanide.

Physiological metabolism of cyanide takes place by a single major pathway that forms non-toxic thiocyanate that is subsequently excreted. Rhodanese is the primary enzyme to execute metabolism of cyanide with minor pathways from other sulfurtransferases in vivo. The rhodanese enzyme depends on sulfur donor availability to metabolize cyanide and poisoning occurs at elevated cyanide concentrations in vivo. Cyanide interacts with over 40 metalloenzymes, but its lethal action is non-competitive inhibition of cytochrome c oxidase, halting cellular respiration and causing hypoxic anoxia. Only a handful of antidotes for treatment of cyanide poisoning are known; they are primarily inorganic compounds and metal complexes which are intended to intercept cyanide before it inhibits cellular respiration. The inorganic compounds manipulate hemoglobin, forming methemoglobin, or supply sulfur for the rhodanese enzyme. The metal complexes intercept the cyanide and bind it before reaching its target. Cobalt complexes of corrins and vitamin B12 derivatives are the state-of-the-art agents, while the longest employed complex, Co2EDTA, is designed to deliver "free" cobalt for binding of cyanide. Compounds that are in development are discussed from the point of how they are designed to intercept cyanide. The challenge of reversing the cyanide inhibition of cytochrome c oxidase is based on the catalytic active site structure and reactivity. General information about history and occurrence of poisoning and clinical symptoms is discussed and the challenges related to analytical methods available to analyze blood cyanide levels and to confirm the presence of cyanide poisoning.

Effect of thiocyanate on BIOX® organisms: Inhibition and adaptation

Stringent environmental legislation and the desire to become zero discharge have motivated mining operations to treat and recycle process water. Cyanidation tailings effluent contains elevated concentrations of cyanide and thiocyanate (SCN−), precluding recycling to the BIOX® process without prior treatment to reduce SCN− to below 1mg/l. The current study investigated the effect of SCN− on individual microbial species. Iron oxidation by Leptospirillum ferriphilum was not affected by SCN− concentrations below 0.5mg/l, with concentration dependent inhibition observed between 0.75 and 1.25mg/l and complete inhibition of iron oxidation above 1.25mg/l. Sulphur oxidation by Acidithiobacillus caldus showed a similar trend, with limited inhibition below 1.25mg/l and almost complete inhibition above 1.25mg/l. Repeated sub-culturing at low concentrations induced adaptation, with adapted cultures currently growing at SCN− concentrations of 7mg/l. The phenomenon of inhibition at low concentration, with subsequent adaptation was repeated in stirred tank reactors, leaching a pyrite/arsenopyrite concentrate.

Transport of Ferrocyanide by Two Eucalypt Species and Sorghum

The wastes from some industrial processes and the tailings from gold mining contain elevated concentrations of cyanide, which reacts with iron in the media to form iron cyanide complexes. This research examined the transport and possible metabolism of ferrocyanide by two native Australian trees, blue mallee and sugar gum, and by sorghum. Hydroponic studies using 15N-labeled ferrocyanide showed that both tree species transported ferrocyanide into roots and displayed significant increases in 15N enrichment and concentration with no evidence of phytotoxicity. A subsequent experiment with blue mallee and membrane-transport inhibitors showed that 15N enrichment was significantly inhibited in the presence of the protonophore carbonyl cyanide m-chlorophenylhydrazone, suggesting that ferrocyanide uptake is mediated partly by H+-symporters. A study of the time dependence of 15N translocation showed a rapid equilibration of 15N from ferrocyanide in the root of blue mallee, accompanied by a slow increase in shoot 15N, suggestive of the metabolism of ferrocyanide in plant roots. A similar experiment with sorghum showed a more rapid translocation of 15N, suggesting that the transport and/or metabolism of ferrocyanide by roots of this species may differ. The results offer additional incentive for the use of these species as vegetative cover over cyanidation wastes and for cyanide phytoremediation.

The protection of wildlife from mortality: Hypothesis and results for risk assessment

Wildlife deaths associated with cyanide-bearing tailings dams are a significant environmental issue that has affected the gold mining industries for many years and still characterized by little knowledge about how to measure, monitoring, reduce or eliminate those deaths. The purpose of this paper is statistically to determine: the potential for establishing causal relations between exposure to cyanide (in its most common species relevant to tailings) and response (measured by death counts), to develop a protocol of data analysis, the understanding of the significance of data gaps, and the effect of likely risk management interventions to achieve the goals of the International Cyanide Management Code (ICMC); [ICMC The International Cyanide Management Institute. International cyanide management code, the international cyanide management institute 2005, www.cyanidecode.org.]. However, operator's certification under the ICMC is difficult because of the limited data and potentially serious under-estimation of the death counts. This is due to observational skill and monitoring frequency, the small size of the carcasses, large extent of tailings facilities, carcasses loss by; entombment in tailings, sink, or taken by scavenging wildlife. This (1st order or bounding) assessment results focus on bird-deaths, which appear to be most frequent at sites where elevated cyanide concentrations are found. Those results indicate that the empirical causal associations we generate support the hypotheses that: • Cyanide intake and bird-deaths is not linear, and that relationship is characterized by a threshold at approximately 50 mg weak-acid-dissociable cyanide (WADCN) per litre of tailings waste (50 mg/L); and • The counts of either wildlife deaths or visitations on tailings dams decrease as the surface area of the supernatant decreases. This paper also develops the basis for a complete risk assessment study to be based on additional data gathering activities and detailed statistical analyses. These two activities, combined with a risk management plan also being developed, will provide a tool for compliance with the ICMC.

Acute oral toxicity of sodium cyanide in birds.

Sensitivities of six avian species, black vulture (Coragyps atratus), American kestrel (Falco sparverius), Japanese quail (Coturnix japonica), domestic chicken (Gallus domesticus), eastern screech-owl (Otus asio), and European starling (Sturnus vulgaris), to acute poisoning by sodium cyanide (NaCN) were compared by single dose LD50's. Three species, domestic chickens, black vultures, and turkey vultures (Cathartes aura), were dosed with NaCN to determine cyanide residues in those that died and also in survivors, in addition to postmortem fate. Three flesh-eating species (black vulture, American kestrel, and eastern screech-owl; LD50's 4.0-8.6 mg/kg) were more sensitive to NaCN than three species (Japanese quail, domestic chicken, and European starling; LD50's 9.4-21 mg/kg) that fed predominantly on plant material. Elevated concentrations of cyanide were found in the blood of birds that died of cyanide poisoning; however, concentrations in birds that died overlapped those in survivors. Blood was superior to liver as the tissue of choice for detecting cyanide exposure. No gross pathological changes related to dosing were observed at necropsy.

The role of cyanide liberation in the acute toxicity of aliphatic nitriles

The acute ip LD50 values for a series of six aliphatic nitriles were determined in mice and compared with acetone cyanohydrin and sodium cyanide. When sodium thiosulfate was given in multiple injections, it protected mice against death by acetonitrile, propionitrile, n-butyronitrile, malononitrile, or succinonitrile. In contrast, multiple injections of sodium nitrite protected mice against death by acrylonitrile, n-butyronitrile, and malononitrile, but not against acetonitrile, propionitrile, or succinonitrile. Single prophylactic doses of either thiosulfate or nitrite protected mice against death by either acetone cyanohydrin or sodium cyanide. Only sodium cyanide and acetone cyanohydrin predictably produced death within 5 min. All other nitriles produced death at widely varying intervals from a few minutes to many hours. Only acetone cyanohydrin and cyanide inhibited the activity of purified preparations of cytochrome c oxidase in vitro and in equimolar concentrations. Pretreatment of mice with carbon tetrachloride protected them against death from all nitriles except acetone cyanohydrin. Elevated concentrations of cyanide were found in the livers and brains of mice given lethal doses of all of the nitriles, acetone cyanohydrin, or sodium cyanide. The tissue concentrations of cyanide were substantially reduced in all cases when thiosulfate was also given or when nitriles were given to carbon tetrachloride-pretreated mice. Cyanide was liberated when n-butyronitrile or succinonitrile were incubated with mouse liver slices or NADPH-fortified mouse hepatic microsomal preparations. This reaction was inhibited when the livers were taken from mice pretreated with carbon tetrachloride or when SKF-525A was added in vitro to normal liver slices. Acetone cyanohydrin in all systems tested behaved qualitatively and quantitatively like its molar equivalent in cyanide. The results suggested that the other nitriles examined here possess little, if any, acute toxicity in the absence of normal hepatic function and that these nitriles were activated by hepatic mechanisms to release cyanide which can account for their major acute toxic effects.