0 Members and 2 Guests are viewing this topic.
"Cyanide" is a staple of crime fiction, often used synonymously with deadly poison. Many cyanide-containing compounds are indeed highly toxic, but many are not. Prussian blue, nominally Fe7(CN)18, a common pigment, is administered orally to counteract the effects of poisoning by thallium and Caesium-137.The most dangerous cyanides are hydrogen cyanide (HCN) and salts derived from it, such as potassium cyanide (KCN) and sodium cyanide (NaCN), among others. Also some compounds readily release HCN or the cyanide ion, such as trimethylsilyl cyanide (CH3)3SiCN upon contact with water and cyanoacrylates upon pyrolysis.Many thousands of organic compounds contain the CN group. These compounds are called nitriles. Generally, nitriles do not display the toxicity of HCN, NaCN, and KCN. In fact, the nitrile functional group is an integral component of numerous pharmaceutical drugs including cimetidine (Tagamet), verapamil (Isoptin), and citalopram (celexa). The reason for their diminished toxicity is that nitriles do not release the CN− ion, which permanently binds to and inhibits cytochrome c oxidase, the specific basis of the lethality of cyanide (see below). Nitriles can be released from the burning of some plastics and may be a source of cyanide toxicity.AbsorptionThe most usual route of absorption is by inhalation of hydrogen cyanide gas, which can be formed from alkaline cyanides and certain complex cyanides by the action of acid. Hydrogen cyanide poisoning is also common as a result of smoke inhalation after house fires.Ingestion is equally dangerous, although this route of absorption is usually deliberate (suicidal or criminal).Absorption through the skin as an aqueous solution is low. Potassium or sodium cyanide can pass through the skin easily as a DMSO solution, though this is rare.Mechanism of toxicityCyanide is an irreversible enzyme inhibitor. Cyanide ions bind to the iron atom of the enzyme cytochrome c oxidase (also known as aa3) in the fourth complex in the mitochondrial membrane in the mitochondria of cells. This denatures the enzyme, and the final transport of electrons from cytochrome c oxidase to oxygen cannot be completed. As a result, the electron transport chain is disrupted, meaning that 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.Plants contain an alternative pathway for respiration in their mitochondria. The alternate oxidase is not as efficient as the normal pathway, but immune to cyanide. As a result, plants are insensitive to concentrations of cyanide that are lethal to animals, and a few species (e.g. the Giant Bamboo in its shoots) are known to contain cyanides. Interestingly, the Golden Bamboo Lemur is able to consume Giant Bamboo shoots containing many times the lethal dose of cyanide for humans and most other animals, with no ill effects. The reason for its immunity is not yet understood.Clinical symptomsIt is difficult to give dose figures in this section due to the rapid metabolism of cyanide in the human body. Animal studies are of little help, as different species have widely different sensitivities to cyanide: it is quite possible that there is also a considerable range of sensitivity among human individuals. The Regulatory information section below may give some guidance.Acute poisoningInhalation of high concentrations of cyanide causes a coma with seizures, apnea and cardiac arrest, with death following in a matter of minutes.At lower doses, loss of consciousness may be preceded by general weakness, giddiness, headaches, vertigo, confusion, and perceived difficulty in breathing. At the first stages of unconsciousness, breathing is often sufficient or even rapid, although the state of the victim progresses towards a deep coma, sometimes accompanied by pulmonary edema, and finally cardiac arrest. Skin colour goes pink from high blood oxygen saturation.Chronic exposureExposure to lower levels of cyanide over a long period (e.g., after use of cassava roots as a primary food source in tropical Africa) results in increased blood cyanide levels, which can result in weakness and a variety of symptoms, including permanent paralysis.