134 Hydrogen cyanide Hydrogen cyanide (with the historical common name of Prussic acid) is a chemical compound with chemical formula HCN. It is a colorless, extremely poisonous liquid that boils slightly above room temperature at 26 C (79ЎF). A hydrogen cyanide concentration of 300 mg/m3 in air will kill a human within 10Р60 minutes.[38] A hydrogen cyanide concentration of 3500 ppm (about 3200 mg/m3) will kill a human in about 1 minute.[38] The toxicity is caused by the cyanide ion, which halts cellular respiration by acting as a non-competitive inhibitor for an enzyme in mitochondria called cytochrome c oxidase. 74-90-8 768 CHN 27.010900 Colorless gas or liquid. -13.4°C 1000 mg/mL at 25 °C [METCALF,RL (1978)] Oral (L96) ; inhalation (L96) ; dermal (L96) Cytochrome c oxidase subunit 1 (P00395) Cytochrome c oxidase subunit 2 (P00403) Cytochrome c oxidase subunit 3 (P00414) Cytochrome c oxidase subunit 4 isoform 1, mitochondrial (P13073) Cytochrome c oxidase subunit 4 isoform 2, mitochondrial (Q96KJ9) Cytochrome c oxidase subunit 5A, mitochondrial (P20674) Cytochrome c oxidase subunit 5B, mitochondrial (P10606) Cytochrome c oxidase polypeptide 6A1, mitochondrial (P12074) Cytochrome c oxidase polypeptide 6A2, mitochondrial (Q02221) Cytochrome c oxidase subunit VIb isoform 1 (P14854) Cytochrome c oxidase subunit VIb isoform 2 (Q6YFQ2) Cytochrome c oxidase polypeptide VIc (P09669) Cytochrome c oxidase polypeptide 7A1, mitochondrial (P24310) Cytochrome c oxidase polypeptide 7A2, mitochondrial (P14406) Cytochrome c oxidase polypeptide 7B, mitochondrial (P24311) Cytochrome c oxidase polypeptide 7B2, mitochondrial (Q8TF08) Cytochrome c oxidase subunit 7C, mitochondrial (P15954) Cytochrome c oxidase polypeptide 8A, mitochondrial (P10176) Cytochrome c oxidase polypeptide 8C, mitochondrial (Q7Z4L0) Catalase (P04040) Thyroid peroxidase (P07202) Eosinophil peroxidase (P11678) Glutathione peroxidase 1 (P07203) Glutathione peroxidase 2 (P18283) Glutathione peroxidase 3 (P22352) Phospholipid hydroperoxide glutathione peroxidase, mitochondrial (P36969) Epididymal secretory glutathione peroxidase (O75715) Glutathione peroxidase 6 (P59796) Glutathione peroxidase 7 (Q96SL4) Tyrosinase (P14679) (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) LD50: 3700 ug/kg (Subcutaneous, Rat) (N010) LD50: 810 ug/kg (Intravenous, Rat) LD50: 3700 ug/kg (Oral, Mouse) LD50: 2990 ug/kg (Intraperitoneal, Mouse) LC50: 142 ppm over 30 minutes (Inhalation, Rat) (T32) 50 to 60 mg (oral) or 270 ppm (inhaled for an adult human. (T37, T50) No indication of carcinogenicity to humans (not listed by IARC). Hydrogen cyanide is a precursor to many chemical compounds, ranging from polymers to pharmaceuticals. (L101) 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) 2009-03-06T18:58:08Z 2026-04-05T16:43:58Z Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L96) http://en.wikipedia.org/wiki/Hydrogen cyanide C01326 18407 HCN D006856 Hydrogen cyanide 6076 true Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L96) C#N CHN InChI=1S/CHN/c1-2/h1H LELOWRISYMNNSU-UHFFFAOYSA-N 27.0253 27.010899037 Exogenous Liquid HMDB60292 CHEMBL183419 748 CHEM000123 DTXSID9024148 NS00077168 formonitrile