Neurotoxicity cyanides

Osuntokun BO. 1972. Chronic cyanide neurotoxicity and neuropathy in Nigerians. Plant Foods for Human Nutrition 2 215-266. 

See also Cyanide Neurotoxicity Occupational Exposure Limits Respiratory Tract Sensory Organs. 

Patel, M. N., Yim, G. K., Isom, G. E. (1992). Potentiation of cyanide neurotoxicity by blockade of ATP-sensitive potassium channels. Brain Research, 593, 114-116. 

Neurotoxicity. Clinical signs indicative of disturbances of the nervous system in exposed humans have been well documented in short-term studies at high doses and appear to be reversible. These effects are characteristic of cyanide toxicity. Animal studies confirm findings in humans. In longer-term studies, effects on the nervous system have also been reported, but it is not certain if these effects are permanent or reversible following termination of acrylonitrile exposure. 

Johnson JD, Meisenheimer TL, Isom GE. 1986. Cyanide-induced neurotoxicity Role of neuronal calcium. Toxicol Appl Pharmacol 84 464-469. 

Kanthasamy AG, Borowitz JL, Pavlakovic G, et al. 1994. Dopaminergic neurotoxicity of cyanide neurochemical, histological, and behavioral characterization. Toxicol Appl Pharmacol 126 (1) 156-163. 

Kanthasamy AG, Maduh EU, Peoples RW, et al. 1991a. Calcium mediation of cyanide-induced catecholamine release Implications for neurotoxicity. Toxicol Appl Pharmacol 110 275-282. 

Maduh EU, Johnson JD, ArdeltBK, etal. 1988. Cyanide-induced neurotoxicity Mechanisms of attenuation by chlorpromazine. Toxicol Appl Pharmacol 96 60-67. 

Maduh EU, Turek JJ, Borowitz JL, etal. 1990b. Cyanide-induced neurotoxicity Calcium mediation of morphological changes in neuronal cells. Toxicol Appl Pharmacol 103 214-221. 

In animal studies acetone has been found to potentiate the toxicity of other solvents by altering their metabolism through induction of microsomal enzymes, particularly cytochrome P-450. Reported effects include enhancement of the ethanol-induced loss of righting reflex in mice by reduction of the elimination rate of ethanol increased hepatotoxicity of compounds such as carbon tetrachloride and trichloroethylene in the rat potentiation of acrylonitrile toxicity by altering the rate at which it is metabolized to cyanide and potentiation of the neurotoxicity of -hexane by altering the toxicokinetics of its 2,4-hexane-dione metabolite.Because occupationally exposed workers are most often exposed to a mixmre of solvents, use of the rule of additivity may underestimate the effect of combined exposures. ... 

Johnson, J.D., Meisenheimer, T.L., Isom, G.E. (1986). Cyanide-induced neurotoxicity role of neuronal calcium. Toxicol. Appl. Pharmacol. 84 464-9. 

Yamamoto, H., Tang, H. (1998). Effects of 2-amino-7-phospho-nohepatanoic acid, melatonin or NG-nitro-L-arginine on cyanide or N-methyl-D-aspartate-induced neurotoxicity in rat cortical cells. Toxicol. Lett. 94 13-18. 

Yamamoto, H.-a. and Tang, H.-W., Effect of carbetapentane or melatonin on cyanide-induced neurotoxicity in mice, Jpn. J. Toxicol. Environ. Health, 6, 488-491, 1996a. 

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