1426 Nickel potassium cyanide Nickel potassium cyanide is a chemical compound of nickel, potassium and cyanide. Nickel is a chemical compound with the atomic number 28. It is found abundantly in nature in laterite ore minerals, such as limonite, garnierite, and pentlandite. Nickel has a biological role and is found in certain enzymes, including urease, hydrogenase, methylcoenzyme M reductase, and carbon monoxide dehydrogenase. (L40, L41) 14220-17-8 61717 C4K2N4Ni 239.875060 White powder. Oral (L96) ; inhalation (L96) ; dermal (L96) Nickel is known to substitute for other essential elements in certain enzmes, such as calcineurin. It is genotoxic, and some nickel compounds have been shown to promote cell proliferation. Nickel has a high affinity for chromatin proteins, particularly histones and protamines. The complexing of nickel ions with heterochromatin results in a number of alterations including condensation, DNA hypermethylation, gene silencing, and inhibition of histone acetylation, which have been shown to disturb gene expression. Nickel has also been shown to alter several transcription factors, including hypoxia-inducible transcription factor, activating transcription factor, and NF-KB transcription factor. There is also evidence that nickel ions inhibit DNA repair, either by directly inhibiting DNA repair enzymes or competing with zinc ions for binding to zinc-finger DNA binding proteins, resulting in structural changes in DNA that prevent repair enzymes from binding. Nickel ions can also complex with a number of cellular ligands including amino acids, peptides, and proteins resulting in the generation of oxygen radicals, which induce base damage, DNA strand breaks, and DNA protein crosslinks. 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. (L41, A40, L97) Nickel is absorbed mainly through the lungs and gastrointestinal tract. Once in the body it enters the bloodstream, where it binds to albumin, L-histidine, and _2-macroglobulin. Nickel tends to accumulate in the lungs, thyroid, kidney, heart, and liver. Absorbed nickel is excreted in the urine, wherease unabsorbed nickel is excreted in the faeces. Cyanide is rapidly alsorbed through oral, inhalation, and dermal routes 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. (L41, L96) LD50: 275 mg/kg (Oral, Mouse) (L507) 1, carcinogenic to humans. (L135) Intermediate Inhalation: 0.0002 mg/m3 (Nickel) (L134) Chronic Inhalation: 0.00009 mg/m3 (Nickel) (L134) The most common harmful health effect of nickel in humans is an allergic reaction. This usually manifests as a skin rash, although some people experience asthma attacks. Long term inhahation of nickel causes chronic bronchitis and reduced lung function, as well as damage to the naval cavity. Ingestion of excess nickel results in damage to the stomach, blood, liver, kidneys, and immune system, as well as having adverse effects on reproduction and development. 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. (L41, L96, L97) Symptoms of nickel poisoning include headache, nausea, vomiting, dizziness, irritability, and difficulty sleeping, followed by chest pains, sweating, rapid heart beat, and a dry cough. 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, L42) Excess exposure to nickel is usually handled by preventing further exposure and symptomatic treatment. Nickel poisoning may also be treated using chelation therapy with sodium diethyldithiocarbamate. 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. (L42, L97) 2009-06-19T21:58:45Z 2014-12-24T20:23:52Z Serum albumin (P02768) Alpha-2-macroglobulin (P01023) Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L41, L96) 30071 Nickel potassium cyanide true Thiosulfate sulfurtransferase (Q16762) 3-mercaptopyruvate sulfurtransferase (P25325) (L96) Serum albumin (P02768) Alpha-2-macroglobulin (P01023) (L41) [K+].[K+].[Ni++].[C-]#N.[C-]#N.[C-]#N.[C-]#N C4K2N4Ni InChI=1S/4CN.2K.Ni/c4*1-2;;;/q4*-1;2*+1;+2 InChIKey=LXWJYIBQIPSFSE-UHFFFAOYSA-N 240.9596 239.875057664 Exogenous Solid 55617