Cyanide drugs

Certain xenobiotics are very toxic even at low levels (eg, cyanide). On the other hand, there are few xenobiotics, including drugs, that do not exert some toxic effects if sufficient amounts are administered. The toxic effects of xenobiotics cover a wide spectrum, but the major effects can be considered under three general headings (Figure 53-1). 

Some drugs produce effects at relatively small doses, following which it does not matter how much more you administer. A small dose of cyanide, for example, will leave you just as dead as a large dose. But most drug effects are dose-dependent. A small glass of wine at dinner has much less of an effect than four pints of lager afterwards. Even placebos have dose-related therapeutic... 

Cyanides, including metal-cyanide complexes Drug residues Chromium, cadmium, lead, mercury, nickel. dissolve material used in sealing a site... 

Despite intense study of the chemical reactivity of the inorganic NO donor SNP with a number of electrophiles and nucleophiles (in particular thiols), the mechanism of NO release from this drug also remains incompletely understood. In biological systems, both enzymatic and non-enzymatic pathways appear to be involved [28]. Nitric oxide release is thought to be preceded by a one-electron reduction step followed by release of cyanide, and an inner-sphere charge transfer reaction between the ni-trosonium ion (NO+) and the ferrous iron (Fe2+). Upon addition of SNP to tissues, formation of iron nitrosyl complexes, which are in equilibrium with S-nitrosothiols, has been observed. A membrane-bound enzyme may be involved in the generation of NO from SNP in vascular tissue [35], but the exact nature of this reducing activity is unknown. 

Such dideoxynucleosides as CNT (306) and the potent anti-HIV drug ddC (307) have been obtained (280), respectively, from the butenolide 248 and from its saturated analogue. Thus, conjugate addition of cyanide to 248, followed by reduction of the lactone group, acetylation of HO-1, and coupling with silylated thymine, afforded, after deprotection, compound 306. 

Vesey et al. 1976) and a series of commercially important, simple, aliphatic nitriles (e.g., acetonitrile, propionitrile, acrylonitrile, n-butyronitrile, maleonitrile, succinonitrile) (Willhite and Smith 1981) release cyanide upon metabolism. These drugs and industrial chemicals have been associated with human exposure to cyanide and have caused serious poisoning and, in some cases, death. 

Methods for Determining Biomarkers of Exposure and Effect. Besides environmental exposure, exposure to cyanide can also occur from consumption of cyanide-containing food, metabolism of certain drugs, and smoking cigarettes. Since so many factors can influence cyanide exposure, the exact correlation between cyanide concentrations in the body and its level in the environment has not been made. Therefore, measuring cyanide and/or thiocyanate levels in blood and urine cannot be used as a biomarker for exposure to low cyanide concentrations. Analytical methods of required sensitivity and reliability to detect cyanide and thiocyanate in blood, plasma, and urine of both unexposed and exposed persons are available (see Table 6-1 and Table 6-3). Further studies determining biomarkers for exposure to low cyanide concentrations would be useful. 

Uses Organic synthesis (vitamins and drugs) analytical chemistry (cyanide analysis) solvent for anhydrous mineral salts denaturant for alcohol antifreeze mixtures textile dyeing waterproofing fungicides rubber chemicals. 

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