Cassava toxicity

Osuntokun BO. 1973. Atoxic neuropathy associated with high cassava diets in West Africa. In Nestel B, MacIntyre R, eds. Chronic Cassava Toxicity. 127-138. 

RoslingH. 1987. Cassava toxicity and food security. Prepared for UNICEF African Household Food Security Program, lsted. Uppsala, Sweden Tryck kontakt. 1-40. 

H. Rosling, Cassava Toxicity and Food Security, Report for UNICEF, Uppsala, Tryck Kontakt, 1988. 

De Bruijn, G.H. (1973) The cyanogenic character of cassava (Manihot esculenta), in Chronic Cassava Toxicity (eds B. Nestel and R. MacIntyre). International Development Research Centre, Ottawa, Canada, pp. 43 8. 

I. Ramirez, M. Cruz and J. Varea, Endemic cretinism in the Andean region New methodological approaches, "Cassava toxicity and thyroid research and public health issues", F. Delange, R. Ahluwalia eds.. International Development Research Center Publ., Ottawa (1983),... 

Ramirez I. Cruz M, Varea J. Endemic cretinism in the Andean region new methodological approaches. In Delange F, Ahluwalia R. Eds. Cassava toxicity and thyroid research and public health issues. Ottowa IDRC. 1983 73-76. 

New Methodological Approaches. In, Cassava Toxicity and Thyroid Research in Public Health Issues. 1983. 73. 

Linamurin is the principal cyanogenic glycoside in cassava its toxicity is due to hydrolysis by intestinal microflora releasing free cyanide (Padmaja and Panikkar 1989). Rabbits (Oryctolagus cuniculus) fed 1.43 mg linamurin/kg BW daily (10 mg/kg BW weekly) for 24 weeks showed effects similar to those of rabbits fed 0.3 mg KCN/kg BW weekly. Specihc effects produced by linamurin and KCN included elevated lactic acid in heart, brain, and liver reduced glycogen in liver and brain and marked depletion in brain phospholipids (Padmaja and Panikkar 1989). 

Oral exposure to cyanide usually results from accidental, homicidal, or suicidal ingestion of cyanide salts. Sodium cyanide and potassium cyanide are the most frequently studied cyanide compounds. Copper cyanide, potassium silver cyanide, silver cyanide, and calcium cyanide are other compounds that humans could encounter through oral or dermal exposure. Cassava roots and certain fruit pits contain compounds that can be broken down to form cyanide. Cassava roots form the staple diet of some populations in Africa, Central and South America, and Asia. However, it must be noted that cassava roots are notoriously deficient in protein and other nutrients and contain many other compounds, in addition to cyanide, that could be responsible for some of the observed toxic effects. Thiocyanate is a metabolite of cyanide that is formed in the body after exposure to cyanide compounds. When possible, all oral exposures are expressed as mg CN/kg/day. 

The nervous system is the most sensitive target for cyanide toxicity, partly because of its high metabolic demands. High doses of cyanide can result in death via central nervous system effects, which can cause respiratory arrest. In humans, chronic low-level cyanide exposure through cassava consumption (and possibly through tobacco smoke inhalation) has been associated with tropical neuropathy, tobacco amblyopia, and Leber s hereditary optic atrophy. It has been suggested that defects in the metabolic conversion of cyanide to thiocyanate, as well as nutritional deficiencies of protein and vitamin B12 and other vitamins and minerals may play a role in the development of these disorders (Wilson 1965). 

Developmental Effects. No studies were located regarding developmental effects in humans after any route of exposure and in animals after inhalation and dermal exposure. However, studies in rats (Singh 1981) and hamsters (Frakes et al. 1986a) fed a cassava diet suggested that cyanide may have teratogenic and fetotoxic effects at maternally toxic doses, but Singh (1981) indicated that the results... 

Reproductive Toxicity. No data were located regarding reproductive effects of cyanide in humans. One animal study reported increased resorptions in rats following oral exposure to a cassava diet (Singh 1981). Because some human populations use cassava roots as the main source of their diet, further... 

Jatrophagospiifolia L. var. delgans Muel. J. curcas L. Hong Ma Feng Shu (Sweet cassava) (seed) Phytotoxin, curcin, curcasin, arachidic, linoleic acid, myristic acid, oleic acid, palmitic acid, stearic acid.50 The herb (seed) is toxic. Seed oil emetic, laxative, purgative, treat skin ailments. 

Cyanide has many sources natural (plant-Cassava), industrial (cyanide salts and nitriles), and accidental (fires). The target organ is the brain death is from respiratory arrest. Cyanide blocks cytochrome a-a3 (cytochrome oxidase) in mitochondria. The toxic level is 1 mg mL-1 in blood. Treatment involves giving dicobalt edetate (chelation). Alternatively, by giving NaNCb, levels of methemoglobin are increased, and this binds cyanide. Detoxication is catalyzed by the enzyme rhodanese, and this pathway may be increased by giving NaS207. 

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