Cyanide, biochemical effects

Smith L, Kruszyna H, Smith RP. 1977. The effect of methemoglobin on the inhibition of cytochrome c oxidase by cyanide, sulfide or azide. Biochem Pharmacol 26 2247-2250. 

Munoz, M.J., M. Carballo, and J.V. Tarazona. 1991. The effect of sublethal levels of copper and cyanide on some biochemical parameters of rainbow trout along subacute exposition. Comp. Biochem. Physiol. 100C 577-582. 

Cyanide poisoning is associated with changes in various physiological and biochemical parameters. The earliest effect of cyanide intoxication in mice seems to be inhibition of hepatic rhodanese... 

Davis, R.H., E.A. Elzubeir, and J.S. Craston. 1988. Nutritional and biochemical factors influencing the biological effects of cyanide. Pages 219-231 in D. Evered and S. Harnett (eds.). Cyanide Compounds in Biology. Ciba Foundation Symposium 140. John Wiley, Chichester. 

Richards and Shieh 1989 Shivaraman et al. 1985). In a study to evaluate the effect of cyanide on biochemical oxidation conducted in sealed vessels, a 50% loss of cyanide at concentrations <6 mg/L in 2 natural river waters occurred at times estimated to range from <10 to 24 days (Ludzack et al. 1951). The rate of loss appeared to be linear with time. These data may represent a biodegradation half-life however, the possibility of loss by chemical reaction was not addressed in this study. 

Cassel GE, Persson S-A, Stenstrom A. 1994. Effects of cyanide in vitro and the activity of monoamine oxidase in striatal tissue from rat and pig. Biochem Pharmacol 47(3) 499-504. 

Isom GE, Liu DHW, Way JL. 1975. Effect of sublethal doses of cyanide on glucose catabolism. Biochem Pharmacol 24 871-875. 

Johnson JD, Conroy WG, Isom GE. 1987. Effect of pentobarbital on cyanide-induced tremors in mice and calcium accumulation in PC12 cells. Biochem Pharmacol 36 1747-1749. 

Ludzack FJ, Moore WA, Krieger HL, et al. 1951. Effect of cyanide on biochemical oxidation in sewage and polluted water. Sewage Ind Wastes 23 1298-1307. 

Dixon M. 1927. The effect of cyanide on the Schardinger enzyme. Biochem J 21 840. 

Freeman JJ, Hayes EP Microsomal metabolism of acetonitrile to cyanide Effects of acetone and other compounds. Biochem Phar-... 

Prickaerts, J., Blokland, A., Bothmer, J., Honig, W., Markerink-Van Ittersum, M., Jolles, J. (1998). Acute effects of acetyl-L-carnitine on sodium cyanide-induced behavioral and biochemical deficits. 

Acute cyanide poisoning requires prompt and rapid treatment. The biochemical basis for an effective mode of treatment consists of creating a relatively nontoxic porphyrin-ferric complex that can compete effectively... 

Borders CL Jr and Fredivich I (1985). A comparison of the effects of cyanide, hydrogen peroxide, and phenylglyoxal on eukaryotic and prokaryotic Cu, Zn superoxide dismutases. Arch Biochem Biophys, 241, 472-476. 

Camu F (1969). Effect of imidazole and cyanide upon rat tissue lipolysis. Arch Int Physiol Biochem, 77, 663-666. 

Reversal of the effects of isoniazid on hepatic cytochrome P-450 hy potassium ferri-cyanide. Biochem. Pharmacol. 31, 249-251. 

Liesivuori and Savolainen (1991) studied the biochemical mechanisms of toxicity of methanol and formic acid. Formic acid is an inhibitor of the enzyme mitochondrial cytochrome oxidase causing histotoxic hypoxia. It is, however, a weaker inhibitor than cyanide and hydrosulfide anions. The effects of its acidosis are dilation of cerebral vessels, facilitation of the entry of calcium ions into cells, loss of lysosomal latency, and deranged production of ATP, the latter affecting calcium reabsorption in the kidney tubules. Also, urinary acidification from formic acid and its excretion may cause continuous recycling of the acid by the tubular cell Cl-/formate exchanger. Such sequence of events probably causes an accumulation of formate in urine. Other than methanol, methyl ethers, esters, and amides also metabolize forming formic acid. 

The LD50 value in mice from intravenous administration of tabun has been reported as 0.287 mg/kg (Tripathi and Dewey 1989). Gupta and coworkers (1987) investigated acute toxicity of tabun and its biochemical consequences in the brain of rats. An acute nonlethal dose of 200 pg/kg was injected subcutaneously. Within 0.5-1 hour, the toxicity was maximal it persisted for 6 hours, accompanied by a sharp decline in acetylcholinesterase activity. The prolonged inhibition of this enzyme in muscle and brain may be due to storage aud delayed release of tabun from nonenzymic sites. In addition, cyanide released from a tabun molecule could cause further delay in recovery from its toxic effects. Atropine and its combination with various compounds may offer protection against tabun (see Sections 39.2 and 39.3). 

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