Sodium Cyanide

Sodium Cyanide Brokermet




Sodium cyanide is a poisonous compound with the formula NaCN. It is a white, water-soluble solid. Cyanide has a high affinity for metals, which leads to the high toxicity of this salt. Its main application, in gold mining, also exploits its high reactivity toward metals. It is a moderately strong base.

When treated with acid, it forms the toxic gas hydrogen cyanide:

NaCN + H2SO4 → HCN + NaHSO4

Sodium Cyanide Brokermet SL

Sodium Cyanide Properties

Sodium Cyanide Brokermet SL

Industrial uses for Sodium Cyanide

Sodium cyanide is used mainly to extract gold and other precious metals in mining industry. This application exploits the high affinity of gold(I) for cyanide, which induces gold metal to oxidize and dissolve in the presence of air (oxygen) and water, producing the salt sodium gold cyanide (or gold sodium cyanide) and sodium hydroxide:

4 Au + 8 NaCN + O2 + 2 H2O → 4 Na[Au(CN)2] + 4 NaOH

A similar process uses potassium cyanide (KCN, a close relative of sodium cyanide) to produce potassium gold cyanide (KAu(CN)2). Few other methods exist for this extraction process.

Sodium Cyanide Brokermet SL

Several commercially significant chemical compounds are derived from cyanide, including cyanuric chloride, cyanogen chloride, and many nitriles. In organic synthesis, cyanide, which is classified as a strong nucleophile, is used to prepare nitriles, which occur widely in many chemicals, including pharmaceuticals. Illustrative is the synthesis of benzyl cyanide by the reaction of benzyl chloride and sodium cyanide.

 Being highly toxic, sodium cyanide is used to kill or stun rapidly such as in widely illegal cyanide fishing and in collecting jars used by entomologists.

Sodium cyanide, like other soluble cyanide salts, is among the most rapidly acting of all known poisons. NaCN is a potent inhibitor of respiration, acting on mitochondrial cytochrome oxidase and hence blocking electron transport. This results in decreased oxidative metabolism and oxygen utilization. Lactic acidosis then occurs as a consequence of anaerobic metabolism. An oral dosage as small as 200–300 mg can be fatal.

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