1399 Cobalt(II) cyanide Cobalt(II) cyanide is a chemical compound of cobalt and cyanide. It is used as a catalyst and in the preparation of cyanide complexes. Cobalt is a metallic element with the atomic number 27. It is found naturally in rocks, soil, water, plants, and animals. In small amounts cobalt is an essential element for life, as it is part of vitamin B12. However, excess exposure is known to exhibit toxic effects. (L29, L30, L483) 542-84-7 68336 C2CoN2 110.939350 Blue powder. Insoluble in water. Dihydrate degraded with dissolution by NaCN, KCN, NH4OH, HCl. Inhalation (L96) ; oral (L96) ; dermal (L96) Cobalt is believed to exhibit its toxicity through a oxidant-based and free radical-based processes. It produces oxygen radicals and may be oxidized to ionic cobalt, causing increased lipid peroxidation, DNA damage, and inducing certain enzymes that lead to cell apoptosis. Cobalt has also been shown to block inorganic calcium channels, possibly impairing neurotransmission. Cobalt can also chelate lipoic acids, impairing oxidation of pyruvate or fatty acids. In addition, cobalt may inhibit DNA repair by interacting with zinc finger DNA repair proteins, and has also been shown to inhibit heme synthesis and glucose metabolism. Cobalt may activate specific helper T-lymphocyte cells and interact directly with immunologic proteins, such as antibodies (IgA and IgE) or Fc receptors, resulting in immunosensitization. (L29) 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) Cobalt and cyanide are absorbed though the lungs, gastrointestinal tract, and skin. Since cobalt is a component of the vitamin B12 (cyanocobalamin), it is distributed to most tissues of the body. Cobalt is transported in the blood, often bound to albumin, with the highest levels being found in the liver and kidney. It is excreted mainly in the urine and faeces. 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. (L29, L96) 200 to 300 milligrams for an adult human (cyanide salts). (T86) 2B, possibly carcinogenic to humans. (L135) Cobalt(II) cyanide is used as a catalyst and in the preparation of cyanide complexes. (L483) Chronic Inhalation: 0.0001 mg/m3 (Cobalt) (L134) Intermediate Oral: 0.01 mg/kg/day (Cobalt) (L134) Exposure to high amount of cobalt can cause heart, lung, kidney, and liver damage. Skin contact is known to result in contact dermatitus. Cobalt may also have mutagenic and carcinogenic effects. 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. (L29, L30, L96, L97) Cobalt inhalation can cause asthma-like breathing problems. Skin contact is known to result in contact dermatitis, which is characterized by irritation and rashes. Ingesting large amounts of cobalt may cause nausea and vomiting. 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. (L2090, L29, L96, L97) Treatment of cobalt poisoning is symptomatic. 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. (L29, L97) 2009-06-19T21:58:43Z 2014-12-24T20:23:49Z Serum albumin (P02768) Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (A39, L96) Cobalt(II) cyanide true Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L96) Serum albumin (P02768) (A39) N#C[Co]C#N C2CoN2 InChI=1S/2CN.Co/c2*1-2; InChIKey=XAWSBNBFMQAZCE-UHFFFAOYSA-N 110.968 110.939348204 Exogenous Solid 19529144