1690
T3D1686
Mandelonitrile
Mandelonitrile is a chemical compound of the cyanohydrin class. Small amounts of mandelonitrile occur in the pits of some fruits. Mandelonitrile is broken down into cyanide and benzaldehyde by the enzyme mandelonitrile lyase. Partitioning studies showed that blood cyanide was about 98.5% associated with the red cell fraction.
532-28-5
9548674
C8H7NO
133.052760
-10°C
Oral (L96) ; inhalation (L96) ; dermal (L96)
Organic nitriles decompose into cyanide ions both in vivo and in vitro. Consequently the primary mechanism of toxicity for organic nitriles is their production of toxic cyanide ions or hydrogen cyanide. Cyanide is an inhibitor of cytochrome c oxidase in the fourth complex of the electron transport chain (found in the membrane of the mitochondria of eukaryotic cells). It complexes with the ferric iron atom in this enzyme. The binding of cyanide to this cytochrome prevents transport of electrons from cytochrome c oxidase to oxygen. As a result, the electron transport chain is disrupted and the cell can no longer aerobically produce ATP for energy. Tissues that mainly depend on aerobic respiration, such as the central nervous system and the heart, are particularly affected. Cyanide is also known produce some of its toxic effects by binding to catalase, glutathione peroxidase, methemoglobin, hydroxocobalamin, phosphatase, tyrosinase, ascorbic acid oxidase, xanthine oxidase, succinic dehydrogenase, and Cu/Zn superoxide dismutase. Cyanide binds to the ferric ion of methemoglobin to form inactive cyanmethemoglobin. (L97)
Organic nitriles are converted into cyanide ions through the action of cytochrome P450 enzymes in the liver. Cyanide is rapidly absorbed and distributed throughout the body. Cyanide is mainly metabolized into thiocyanate by either rhodanese or 3-mercaptopyruvate sulfur transferase. Cyanide metabolites are excreted in the urine. (L96)
202 to 300 milligrams for an adult human (cyanide salts). (T86)
No indication of carcinogenicity to humans (not listed by IARC).
Exposure to high levels of cyanide for a short time harms the brain and heart and can even cause coma, seizures, apnea, cardiac arrest and death. Chronic inhalation of cyanide causes breathing difficulties, chest pain, vomiting, blood changes, headaches, and enlargement of the thyroid gland. Skin contact with cyanide salts can irritate and produce sores. (L96, L97)
Cyanide poisoning is identified by rapid, deep breathing and shortness of breath, general weakness, giddiness, headaches, vertigo, confusion, convulsions/seizures and eventually loss of consciousness. (L96, L97)
Antidotes to cyanide poisoning include hydroxocobalamin and sodium nitrite, which release the cyanide from the cytochrome system, and rhodanase, which is an enzyme occurring naturally in mammals that combines serum cyanide with thiosulfate, producing comparatively harmless thiocyanate. Oxygen therapy can also be administered. (L97)
2009-06-22T16:08:27Z
2014-12-24T20:24:26Z
Thiosulfate sulfurtransferase (Q16762)
3-mercaptopyruvate sulfurtransferase (P25325)
(L96)
C00561
18450
CPD-1125
C045516
Mandelonitrile
true
Thiosulfate sulfurtransferase (Q16762)
3-mercaptopyruvate sulfurtransferase (P25325)
(L96)
OC(C#N)C1=CC=CC=C1
C8H7NO
InChI=1/C8H7NO/c9-6-8(10)7-4-2-1-3-5-7/h1-5,8,10H
InChIKey=NNICRUQPODTGRU-UHFFFAOYNA-N
133.1473
133.052763851
Exogenous
Liquid
HMDB60486
7827597