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Cyanide poisoning occurs because cyanide inhibits the enzyme cytochrome c oxidase, which is one of the enzymes that enable cells to use oxygen. Antidotes for cyanide poisoning tend to focus on binding the cyanide ion so that this inhibition stops. The liver is capable of metabolizing cyanide as well, to take care of any small residual amounts remaining.There are several ways to accomplish this.

Nitrites and/or 4-dimethylaminophenol both convert hemoglobin to methemoglobin, which binds tightly with cyanide. This causes problems of its own, though ... methemoglobin cannot carry oxygen, and it's necessary to convert a lot of hemoglobin to methemoglobin to be sure there's an excess to bind all the cyanide, which leaves the person treated with methemoglobinemia ... which then must be treated separately (usually by treatment with methylene blue).

Thiosulfates react with cyanide to convert it to thiocyanide, which is much less toxic. However, the reaction does not occur quickly in the body, so this treatment must be supplemented with one of the others (usually nitrates/4-DMAP).

Cyanide is present in one form of vitamin B12, so treatment with the cyanideless form hydroxocobalamin will bind cyanide in the harmless cyanocobalamin.

Cobalt ions in general will bind cyanide, but cyanocobalt complexes are themselves generally toxic, so this is not necessarily much of an improvement. It is fast, though, and is sometimes used (in the form of the dicobalt EDTA complex) in cases of severe cyanide poisoning. Administration with glucose helps mitigate the toxic effects of the cyanocobalt complexes.

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Sigurd Nolan

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3y ago

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