Cyanide metabolism

Knowles, C.J. and Bunch, A.W. (1986) Microbial cyanide metabolism. Advances in Microbial Physiology, 27, 73-111. 

Beminger, T.A., L.V. Meyer, E. Siess, O. Schon, and F.D. Goebel. 1989. Leber s hereditary optic atrophy further evidence for a defect of cyanide metabolism Brit. Jour. Ophthalmol. 73 314-316. 

Tewe, 0.0. 1982a. Protein supplementation of cassava diets for growing pigs effects on performance, nutrient utilization and cyanide metabolism. Nutr. Rep. Inter. 25 451-462. 

Tewe, 0.0. 1988. Performance, nutrient utilization and cyanide metabolism in African giant rats (Cricetomys gambianus Waterhouse) fed varying dietary levels of cassava peels. Anim. Technol. 39 77-82. 

Dahl, A.R. 1989. The cyanide-metabolizing enzyme rhodanese in rat nasal respiratory and olfactory mucosa. Toxicol. Lett. 45 199-205. 

Cyanide metabolizes in the human body to thiocyanate, and its biodegradation products include ammonia, carbon dioxide, nitrate, or nitrogen (Richards and Shieh 1989). The detection of thiocyanate in body fluids may indicate cyanide exposure. Similarly, the amounts of cyanide degradation products formed in an environmental medium could be used to measure cyanide s biodegradation rate. A summary of methods for determining environmental degradation products is shown in Table 6-4. Suitable analytical methods are available to detect all of these compounds (Pettigrew and Fell 1973 Richards and Shieh 1989). 

Ansell M, Lewis FAS. 1970. A review of cyanide concentrations found in human organs A survey of literature concerning cyanide metabolism, normal, non-fatal, and fatal body cyanide levels. J Forensic Med 17 148-155. 

Devlin DJ, Smith RP, Thron CD. 1989b. Cyanide metabolism in the isolated, perfused, bloodless hindlimbs or liver of the rat. Toxicol Appl Pharmacol 98 338-349. 

Kato T, KameyamaM, Nakamura S, et al. 1985. Cyanide metabolism in motor neuron disease. Acta Neurol Scand 72 151-156. 

WilsonJ. 1965. Leber s hereditary optic atrophy A possible defect of cyanide metabolism. Clin Sci 29 505-515. 

Lewis JL, Rhoades CE, Bice DE, et al. 1992. Interspecies comparison of cellular localization of the cyanide metabolizing enzyme rhodanese within olfactory mucosa. Anat Rec 232(4) 620-627. 

Approximately 13% of a single oral dose to rats of 116 mg/kg bw of bromochloroacetonitrile was excreted in urine within 24 h as thiocyanate, the product of released cyanide metabolized by rhodanese (lARC, 1991). 

Knowles, C. J., Bunch, A.W. Microbial cyanide metabolism. Adv Microbiol Physiol 1986 27 73-111. 

Baumeister, R.G., H.Schievelbein, and G.Zickgraf-Rudel. 1975. Toxicological and clinical aspects of cyanide metabolism. Arzneimittelforschung. 25(7) 1056-1064. 

Gastric, P.A., Farnden, K.R and Conn, E.E. (1972) Cyanide metabolism in higher plants. 5. The formation of asparagine from fj-cyanoalanine. Arch. Biochem. Biophys., 152, 62-9. 

Aminlari, M., Vaseghi, T., and Kargar, M. A., The cyanide-metabolizing enzyme rhodanese in different parts of the respiratory system in sheep and dogs, Toxicol. Appl. Pharmacol., 124, 64—71, 1994. 

Cyanide metabolism in the body is very rapid and can occur at 0.017 mg/min/kg (Agency... 

Comprehensive reviews on biological cyanide transformations may be found in the literature i36, 37l Reviews on microbial cyanide metabolism have been published by Knowles 38, 391 and Knowles and Bunch [40l... 

The lethal effect of acrylonitrile increased in rats when coadministered with organic solvents (Gut et al. 1981), although the latter decreased the formation of cyanide. Metabolic cyanide formation was found to play only a minor role in the inhalation toxicity of acrylonitrile (Peter and Bolt 1985). This was in contrast to the toxicity of methylacrylonitrile, where the observed clinical symptoms suggest a metabolically formed cyanide. 

A minor route of metabolism is the oxidation of cyanide to cyanate (CNO-), which occurs via enzymatic and nonenzymatic pathways. The interaction of cystine and cyanide to form 2-amino thiazoline 4-carboxylic acid and its tautomer accounts for approximately 20% of cyanide metabolism. This increases with toxic doses of cyanide. However, the protection conferred by forming cyanate derivatives is limited because of the cell s inability to utilize oxygen during cyanide intoxication. 

Vennesland B, Castric PA, Conn EE, Solomonson LP, Volini M, Westley J. Cyanide metabolism. Fed Proc. 1982 41 2639-2648. 

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