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Hydrogen cyanide metabolites

Enander, Sundwall, and Sorbo - -- 7 found that either oral or Intramuscular administration of 11 to rats at 500 or 100 mg/kg, respectively, increased by many times the urinary excretion of thiocyanate. From the amount of thlocynanate excreted above the base line, the quantity of hydrogen cyanide produced in metabolism of the oxime was calculated to be 0.1 mg/kg—a little more than one-third the LD50 for rats by lntraperitoneal injection. Urine from rats given 120 ymol of II intramuscularly or 400 pmol by mouth contained 3.9-7.8% N-methylpyridinlum-2-nltrlle methanesulfonate. When this compound was injected Intramuscularly into rats at 90 mg/kg, thiocyanate was excreted in the urine in Increased amounts. Also present in the urine was a metabolic product that yielded cyanide on acidification of the urine, similar to a cyanide-yielding metabolite of II found earlier. [Pg.300]

Acetonitrile can be acutely lethal when absorbed in high doses. Acetonitrile is metabolized to a hydroxyl metabolite by cytochrome P450 in the liver. Subsequent metabolism through catalase enzymes produces hydrogen cyanide. Once metabolized, the mechanism of action is the same as expected for... [Pg.28]

Animal susceptibility to acetonitrile varies by animal species and route of administration. Overall, animal susceptibility is mediated by the animal s ability to absorb and metabolize acetonitrile into its toxic metabolite, hydrogen cyanide. [Pg.29]

As described below, urinary metabolites have been identified for vesicants, nerve agents, 3-quinuclidinyl benzilate (BZ), hydrogen cyanide and the RCAs, CS, CR and capsaicin. Protein adducts have been identified for vesicants, nerve agents and phosgene, and DNA adducts for sulphur and nitrogen mustards. With the rapid advances being made in proteomics and metabo-nomics, new biological markers of exposure will undoubtedly be identified in the near future. [Pg.128]

Cyanides of alkali metals are extremely toxic and the poisoning effects of sodium and potassium cyanides are well documented. Hydrogen cyanide, which is the toxic metabolite of nitriles, is more toxic than sodium or potassium cyanide. The order of toxicity in rabbits is as follows HCN > NaCN > KCN with LD50 values of... [Pg.317]

As a class of compounds, the two main toxicity concerns for nitriles are acute lethality and osteolathyrsm. A comprehensive review of the toxicity of nitriles, including detailed discussion of biochemical mechanisms of toxicity and structure-activity relationships, is available (12). Nitriles vary broadly in their ability to cause acute lethality and subtle differences in structure can greatly affect toxic potency. The biochemical basis of their acute toxicity is related to their metabolism in the body. Following exposure and absorption, nitriles are metabolized by cytochrome p450 enzymes in the liver. The metabolism involves initial hydrogen abstraction resulting in the formation of a carbon radical, followed by hydroxylation of the carbon radical. Metabolism at the carbon atom adjacent (alpha) to the cyano group would yield a cyanohydrin metabolite, which decomposes readily in the body to produce cyanide. Hydroxylation at other carbon positions in the nitrile does not result in cyanide release. [Pg.218]


See other pages where Hydrogen cyanide metabolites is mentioned: [Pg.7]    [Pg.71]    [Pg.920]    [Pg.179]    [Pg.37]    [Pg.92]    [Pg.128]    [Pg.127]    [Pg.920]    [Pg.148]    [Pg.153]    [Pg.343]    [Pg.353]    [Pg.113]    [Pg.74]    [Pg.3961]    [Pg.24]    [Pg.363]    [Pg.524]    [Pg.213]    [Pg.217]    [Pg.273]    [Pg.274]    [Pg.287]    [Pg.287]    [Pg.310]    [Pg.222]    [Pg.908]    [Pg.908]    [Pg.218]    [Pg.48]    [Pg.71]    [Pg.517]    [Pg.202]   


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