Abstract
Cassava (Manihot esculenta Crantz) is an important dietary staple for more than 500 million people in developing countries. People eat 60% of the cassava produced and one third of the harvest feeds animals. All cultivars of cassava contain the cyanogenic glucoside, linamarin, but in different concentrations. The roots of those cultivars with high cyanogenic content are processed to reduce the level of linamarin, because linamarin is hydrolysed in the intestinal tract of both men and animals by microbial flora and HCN is released. Researchers have implicated the sublethal levels of HCN produced on ingestion in the development of a number of metabolic diseases in both man and animals when cassava-based diets are consumed over a long period of time but the release of HCN cannot fully explain the metabolic effects of ingested linamarin. A significant amount of linamarin remains intact and is excreted in the urine. It appears that the intact linamarin inhibits Na+K+ATPase causing electrolyte imbalance within the cell. This phenomenon is exacerbated by free radicals generated by the hypoxia/normoxia cycles created by cyanide released from linamarin, which cause lipid peroxidation and cell membrane damage. When the supply of endogenous thiosulphate is adequate, cyanide plays a very minor role in the development of lesions. The amount of damage is related to the quantity of linamarin routinely ingested at sublethal levels. There appears to be species differences in the rate of the development of diseases and the intensity.
International Journal of Food Sciences and Nutrition 03/1995; 46(1):65-93. DOI:10.3109/09637489509003387
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