friendly cyanide source, potassium hydroxide ..
In a 13-week study, male Sprague-Dawley rats were administered potassium cyanide in drinking-water at a dose level of 40, 80, or 160/140 mg/kg body weight per day. These doses correspond to 16, 32, and 64/56 mg cyanide/kg body weight per day (Leuschner et al., 1989). Histopathological investigation of the brain, heart, liver, testes, thyroid, and kidneys did not reveal adverse effects. Urinary protein excretion was increased in dosed animals, and dose-dependent increases were observed in organ weights; these were interpreted to have arisen from decreased food and water consumption caused by decreased palatability.
scope and is expected to be of great utility in organic synthesis
Hydrogen cyanide has a pa of 9.22; thus, at physiological pH (about pH 7), hydrocyanic acid is distributed in the body as hydrogen cyanide and is not present as the free cyanide ion. Hence, the form of cyanide to which exposure occurs, the salt or the free acid, does not influence distribution, metabolism, or excretion from the body (ECETOC, 2004). Inhaled or percutaneously absorbed hydrogen cyanide passes immediately into the systemic circulation. The distribution of cyanide to the various tissues is rapid and fairly uniform. Somewhat higher levels are generally found in the liver, lungs, blood, and brain. The tissue levels of hydrogen cyanide were 0.75, 0.42, 0.41, 0.33, and 0.32 mg/100 g of tissue in lung, heart, blood, kidney, and brain, respectively, in a man who died following inhalation exposure to hydrogen cyanide gas (Gettler & Baine, 1938; Ballantyne, 1983a; ATSDR, 1997; ECETOC, 2004). In contrast, high proportions of ingested sodium and potassium cyanide will pass through the liver and are detoxified by the first-pass effect.
In a 13-week repeated-dose toxicity study (NTP, 1993) in which sodium cyanide was administered in drinking-water, there were no mortalities or clinical signs (associated with central nervous system effects) or histopathological effects in the brain, thyroid, or other organs of rats or mice exposed to doses up to 12.5 and 26 mg/kg body weight per day, respectively. The reproductive tract in the males was the most sensitive organ to cyanide exposure in this study: lowered weight of testis and epididymis, together with a decrease in the number of spermatid heads in the testis and decreased motility of epididymal sperm, were observed at the highest dose level. The NOAEL in this study, 4.5 mg/kg body weight per day, is consistent with the only available long-term study, in that no adverse effects were observed in rats after 2 years of exposure to cyanide in the diet at 10.8 mg cyanide/kg body weight per day (Howard & Hanzal, 1955). It is also roughly consistent with the NOAEL in the 14-week inhalation study (Monsanto Co., 1984a) in which the airborne systemic no-effect level of 204 mg ACH/m3 can be estimated to correspond to a daily dose of approximately 15 mg cyanide/kg body weight per day.
nucleophilic substitution - halogenoalkanes and cyanide ions
In studies with rats orally administered potassium cyanide and maintained for up to 4 weeks on either a balanced diet or a diet lacking the sulfur amino acids L-cystine and L-methionine, a strongly positive linear relationship was found between blood cyanide and plasma cyanate (OCN–) concentration (Tor-Agbidye et al., 1999). It was suggested that in Africa, where there are protein-deficient populations whose levels of sulfur-containing amino acids are low, cyanide (from prolonged use of cassava) may conceivably be converted to cyanate, which is known to cause neurodegenerative disease in humans and animals.
For the salts such as sodium cyanide and potassium cyanide, ..
DNA repair tests in WP67, CM871, and WP2 with potassium cyanide were negative (De Flora et al., 1984). Potassium cyanide induced both time- and dose-dependent DNA fragmentation accompanied by cytotoxicity in rat thymocytes . Cyanide also induced DNA damage in baby hamster kidney cells (BHK-21) , where, unlike thymocytes, internucleosome DNA fragmentation was not observed (Bhattacharya & Rao, 1997). The cytotoxic mode of double strand breaks in the pathogenesis of DNA fragmentation was studied by Vock et al. (1998), employing an A549 human epithelial-like lung carcinoma cell line treated with potassium cyanide. Induction of double strand breaks by potassium cyanide was observed only after cell viability was reduced to less than 60%, indicating that double strand breaks were the consequence of extragenomic damage, as a secondary effect of high cytotoxicity in combination with cell lethality.
It is obtained by acidification of cyanide salts
No testicular DNA synthesis inhibition was detected in mice after a single oral potassium cyanide dose of 1 mg/kg body weight (Friedman & Staub, 1976).