Abstract
Investigation of the dietary interaction between cyanide and selenium in the chick, whereby cyanide alleviates selenium toxicity, suggests that cyanide alters metabolic reductive potential. Cyanide enhances the elimination of selenium as dimethyl selenide, the formation of which requires both reducing equivalents and methyl groups. Even when the methionine supply is adequate, meeting the need for the methyl groups, the interaction can be lost if there is a deficiency of certain micronutrients or an excess of vitamin K. Cyanide reduces liver glycogen, implying greater emphasis on anaerobic metabolism through inhibition of cytochrome oxidase. This may increase reductive potential but may also result in increased free radical production, processes that can be modified by levels of micronutrients. There is no evidence that an excess of sulphur amino acids can markedly enhance cyanide detoxification, although, for reasons that are not yet clear, cystine may be beneficial. However, the balance of dietary amino acids may be more critical than had been realized, because an excess of alanine appears to exacerbate cyanide toxicity.
Published Version
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