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Pathological changes in growing dogs fed on a balanced cassava (Manihot esculenta Crantz) diet.
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Studies were carried out to determine the effects of the toxic principle linamarin, a cyanogenic glucoside, in a diet containing cassava (Manihot esculenta Crantz) in the form of gari fed to growing dogs for 14 weeks. There were three groups of dogs, each comprising six animals. One group was fed on
Preclinical and clinical research on the toxic and neurological effects of cassava (Manihot esculenta Crantz) consumption.
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Cassava (Manihot esculenta Crantz) is a tropical plant that is used as fresh food, processed food, or raw material for the preparation of flours with high nutritional value. However, cassava contains cyanogenic glycosides, such as linamarin and lotaustralin, that can trigger severe toxic effects and
Constituents and secondary metabolite natural products in fresh and deteriorated cassava roots.
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A phytochemical analysis of cassava (Manihot esculenta Crantz) fresh roots and roots suffering from post-harvest physiological deterioration (PPD) has been carried out. The first isolation and identification of galactosyl diacylglycerides from fresh cassava roots is reported, as well as
Chronic consumption of cassava juice induces cellular stress in rat substantia nigra.
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Objectives
Cassava (Manihot esculenta Crantz) contains cyanogenic glycosides (linamarin and lotaustralin) that have been associated with neurological disorders in humans and rats. In basal ganglia, the dopaminergic neurons of substantia nigra pars compacta (SNpc)Changes of cyanide content and linamarase activity in wounded cassava roots.
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When cassava (Manihot esculenta Crantz) root was cut into blocks and incubated under laboratory conditions, the blocks showed more widespread and more even symptoms of physiological deterioration than those under natural conditions. Thus, the tissue block system has potential for biochemical studies
The targets of acetone cyanohydrin neurotoxicity in the rat are not the ones expected in an animal model of konzo.
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Konzo is a neurotoxic motor disease caused by excess consumption of insufficiently processed cassava. Cassava contains the cyanogenic glucoside linamarin, but konzo does not present the known pathological effects of cyanide. We hypothesized that the aglycone of linamarin, acetone cyanohydrin, may be
Toxic models of upper motor neuron disease.
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Although neurotoxic models for progressive degeneration of both the anterior horn cell and the Betz cell do not exist, (neuro)lathyrism and neurocassavism (konzo) are examples of self limiting neurotoxic disorders that predominantly target the Betz cell. Both disorders are caused by the continuous
Cyanide in human disease: a review of clinical and laboratory evidence.
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Experimental cyanide exposure in animals causes demyelination and circumstantial clinical and laboratory evidence suggest that there are human parallels. In Leber's hereditary optic atrophy there appears to be a defect in the conversion of cyanide to thiocyanate because of deficient rhodanese
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