Abstract

Potential toxicity of cyanogenic glycosides arises from enzymatic degradation to produce hydrogen cyanide. Information on the metabolism of cyanogenic glycosides is available from in vitro, animal and human studies. In the absence of β-glucosidase enzymes from the source plant material, two processes appear to contribute to the production of cyanide from cyanogenic glycosides; the proportion of the glycoside dose that reaches the large intestine, where most of the bacterial hydrolysis occurs, and the rate of hydrolysis of cyanogenic glycosides to cyanohydrin and cyanide. Some cyanogenic glycosides, such as prunasin, are actively absorbed in the jejunum by utilising the epithelial sodium-dependent monosaccharide transporter (SGLT1). The rate of cyanide production from cyanogenic glycosides due to bacterial β-glycosidase activity depends on; the sugar moiety in the molecule and the stability of the intermediate cyanohydrin following hydrolysis by bacterial β-glucosidase. Cyanogenic glycosides with a gentiobiose sugar, amygdalin, linustatin, and neolinustatin, undergo a two stage hydrolysis, with gentiobiose initially being hydrolysed to glucose to form prunasin, linamarin and lotaustralin, respectively. While the overall impact of these metabolic factors is difficult to predict, the toxicity of cyanogenic glycosides will be less than the toxicity suggested by their theoretical hydrocyanic acid equivalents.

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