Antineoplastic effects of cassava-cyanide extract on human glioblastoma (LN229) cells.

Several natural compounds reduce tumour cell growth and metastasis by inducing programmed cell death. Cassava (Manihot esculenta Crantz) contains cyanogenic glycosides such as, linamarin and lotaustralin, can be enzymatically cleaved by linamarase to release hydrogen cyanide (HCN), which can have therapeutic benefits against hypertension, asthma, and cancer. We have developed a technology for isolating bio-active principles from cassava leaves.The present study is designed to analyze the cytotoxic effect of cassava cyanide extract (CCE) against human glioblastoma cells (LN229). The treatment of CCE demonstrated a dose dependent toxicity on glioblastoma cells. At higher concentration tested, the CCE (400 µg/mL) was found to be cytotoxic, reducing the cell viability to 14.07 ± 2.15% by negatively influencing the mitochondrial activity, and lysosomal and cytoskeletal integrity. Coomassie's brilliant blue staining confirmed cells' morphological aberration after 24 h of treatment with CCE. Moreover, DCFH-DA assay and Griess reagent showed an increase in ROS but a decrease in RNS production at a concentration of CCE. Flow cytometry analysis revealed that CCE interfered with G0/G1, S, and G2/M stages of the cell cycle of glioblastoma, and Annexin/PI staining indicated a dose-dependent increase in cell death, confirming the toxic nature of CCE on LN229 cells. These findings suggest that cassava cyanide extract has potential as an antineoplastic agent against glioblastoma cells, which is an aggressive and difficult-to-treat type of brain cancer. However, it is important to note that the study was conducted in vitro, and further research is necessary to assess the safety and efficacy of CCE in vivo. Additionally, it is essential to establish the optimal dose and potential side effects before considering its use as a therapeutic agent.

Poisonous plants for ruminants in the dairy region of Pernambuco, Northeastern Brazil / Plantas tóxicas para ruminantes na bacia leiteira de Pernambuco, Nordeste do Brasil

A survey carried out in the dairy region of Pernambuco was conducted to determine the most important poisonous plants for ruminants in the region. A total of 95 farmers from 19 municipalities were interviewed and the grazing areas of ruminants were inspected. According to the survey, the most important poisonous plants for ruminants were Manihot esculenta, Palicourea aeneofusca, Brachiaria decumbens, Indigofera suffruticosa, Ricinus communis and Cestrum axillare. Less reported classes of poisonous plants included nephrotoxic plants and plants that cause abortions or congenic malformations. Psychotria hoffmannseggiana, Psychotria colorata and Psychotria capitata were reported by farmers as the cause of sudden death in cattle. These plants should be better investigated to evaluate their importance as the cause of cattle deaths.(AU)

Neste estudo prospectivo, realizou-se um levantamento sobre a ocorrência das principais plantas tóxicas e a ocorrência de intoxicações por plantas em ruminantes na bacia leiteira de Pernambuco. Para isso, foram entrevistados 95 produtores rurais de 19 municípios e as áreas de pastagem de ruminantes foram inspecionadas. De acordo com o levantamento, as plantas tóxicas mais importantes para ruminantes foram Manihot esculenta, Palicourea aeneofusca, Brachiaria decumbens, Indigofera suffruticosa e Ricinus communis. As classes menos importantes de plantas tóxicas incluíram plantas nefrotóxicas e plantas que causam abortos e malformações congênitas. Psychotria hoffmannseggiana, Psychotria colorata e Psychotria capitata foram relatadas por produtores rurais como a causa de mortes súbitas em bovinos. Essas plantas devem ser investigadas melhor para avaliar sua importância como a causa de mortes de bovinos.(AU)

Preclinical and clinical research on the toxic and neurological effects of cassava (Manihot esculenta Crantz) consumption.

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 some neurological disorders, including motor impairment, cognitive deterioration, and symptoms that characterize tropical ataxic neuropathy and spastic epidemic paraparesis (Konzo). These alterations that are associated with the consumption of cassava or its derivatives have been reported in both humans and experimental animals. The present review discusses and integrates preclinical and clinical evidence that indicates the toxic and neurological effects of cassava and its derivatives by affecting metabolic processes and the central nervous system. An exhaustive review of the literature was performed using specialized databases that focused on the toxic and neurological effects of the consumption of cassava and its derivatives. We sought to provide structured information that will contribute to understanding the undesirable effects of some foods and preventing health problems in vulnerable populations who consume these vegetables. Cassava contains cyanogenic glycosides that contribute to the development of neurological disorders when they are ingested inappropriately or for prolonged periods of time. Such high consumption can affect neurochemical and neurophysiological processes in particular brain structures and affect peripheral metabolic processes that impact wellness. Although some vegetables have high nutritional value and ameliorate food deficits in vulnerable populations, they can also predispose individuals to the development of neurological diseases.

Plants with neurotoxic potential in undernourished subjects.

The consumption by humans of plants with potential to induce neurological disorders is widespread, but overt disease surfaces only when the subject's toxic threshold is exceeded. Excessive intake arising from food dependency in the setting of hunger, chronic undernutrition, vitamin deficiency, inadequate detoxication, or other individual susceptibility, can trigger acute encephalopathy (lychee, ackee fruits), sub-acute spastic paraparesis (grasspea, cassava root/leaves) or ataxic neuropathy (cassava root flour). While these disorders are very rarely encountered in high-income countries, they are not only common among impoverished populations but also often occur as outbreaks that impact a significant proportion of an affected community. Unfamiliarity with the adverse effects of plant toxins has sometimes led to the mistaken attribution of nutritional neurotoxic disease to a neurotropic viral or synthetic pesticidal etiology. The combination of human population growth, food and water insecurity, poverty and, with climate change, increased dependency on environmentally tolerant plants with neurotoxic potential, predictably may result in an increased prevalence of nutritional neurotoxic disorders, especially in certain parts of Africa and Asia.

Detoxification of Cassava Leaves by Thermal, Sodium Bicarbonate, Enzymatic, and Ultrasonic Treatments.

Cassava leaves are a valuable source of protein but the cyanogenic potential limits their use as food and feed. Four different treatments were investigated to detoxify cassava leaves. Thermal (55 °C for 6 hr), sodium bicarbonate (0.4% NaHCO3 , 55 °C for 6 hr), enzymatic (0.32% Multifect® GC Extra, 4 hr), and ultrasonic treatments (500 W, 35 kHz, 55 °C, 0.25 hr) reduced the total cyanide (µg HCN equivalents per g fresh leaf or ppm) content by 90%, 93%, 82%, and 84% while the cyanide content reduction in the respective controls was 85%, 90%, 79%, and 84%, respectively. The sodium bicarbonate treatment was found to be the most effective treatment. Therefore, it was further optimized by varying time and temperature. A significant effect on the cyanide content was observed by changing the incubation time while no significant effect of temperature was noticed. Nevertheless, extended incubation time during sodium bicarbonate treatment reduced ascorbic acid content by 7% and 39% when leaves were incubated with sodium bicarbonate for 0.5 hr and 48 hr, respectively. PRACTICAL APPLICATION: Cyanogenic glucosides are the major toxic compound in cassava leaves, which limits their use as food and feed. The methods proposed in this study can be used to detoxify cassava leaves, which are generally considered as an inferior by-product. Hence, detoxified cassava leaves may contribute to fulfil world protein demand in an eco-sustainable way.

Konzo: a distinct neurological disease associated with food (cassava) cyanogenic poisoning.

Epidemics of neurodegenerative diseases putatively caused by food toxins have been reported in the tropics with no clear understanding of their pathogenetic mechanisms. These diseases include the disease named Konzo that has been well documented in sub-Sahara Africa, mostly among children and women of childbearing age. Outbreaks of Konzo have occurred in the Democratic Republic of Congo, Mozambique, Tanzania, Central African Republic, Angola, Cameroun, and most recently in Zambia. The main clinical picture consists of a symmetrical, permanent and irreversible spastic paraparesis (motor neuron disease) with no signs of sensory or genitourinary impairments. Recently, cognitive impairments and neurodevelopmental delays have been reported among school-aged and very young children. The exact pathogenetic mechanisms of the disease remain unknown. Epidemiological studies consistently show an association between outbreaks of the disease and chronic dietary reliance on insufficiently processed cyanogenic cassava (manioc or tapioca). Biochemical and toxicological studies suggest that the metabolites of linamarin (α-Hydroxyisobutyronitrile ß-D-glucopyranoside, the main cassava cyanogen), notably cyanide (mitochondrial toxin), thiocyanate (AMPA chaotropic agent), and cyanate (protein carbamoylating agent) may play an important role in the pathogenesis of Konzo. Experimental data suggest that thiol-redox and protein- folding mechanisms may also be perturbed. Factors of susceptibility including genetics, poor nutrition, poverty and dietary cyanogen exposure, or their interactions have been suggested. Serological studies have ruled out the role of retroviruses such as the human lymphotropic viruses HIV-I/II or HTLV-I/II. Because there is no cure for Konzo, prevention of the disease remains of paramount importance. Prospects for cognitive rehabilitation still need to be explored and tested.

Effects of acetone cyanohydrin, a derivative of cassava, on motor activity and kidney and liver function in Wistar rats. / Efecto de la acetona cianohidrina, un derivado de la yuca, sobre la actividad motora y la función renal y hepática en ratas Wistar.

INTRODUCTION: Acetone cyanohydrin (ACH) is a toxic substance present in cassava roots (Manihot esculenta Crantz) which results from enzymatic hydrolysis of linamarin. Long-term consumption is associated with 2 neurological disorders: konzo and tropical ataxic neuropathy. Previous studies have evaluated behavioural alterations linked to ACH consumption, but the toxic effects of this substance on physiological processes remain unknown. METHOD: 32 male Wistar rats were assigned to 4 experimental groups (n=8 per group): a vehicle group (0.3mL saline solution, IP) and 3 ACH groups (PubChem CID: 6406) dosed at 10, 15, and 20mM/24h for 28 days. We evaluated spontaneous motor activity with the open field test and motor coordination with the rotarod and forced swimming tests at 0, 7, 14, 21, and 28 days of treatment. At the end of the assessment period (day 28), blood samples were collected by transcardiac puncture to evaluate kidney and liver function. RESULTS: ACH caused alterations in locomotor activity and promoted both lateral swimming and spinning in the forced swimming test at 21 and 28 days of treatment. Furthermore, it led to an increase in the levels of the parameters of kidney and liver function in a concentration-dependent manner, except for glucose and total bilirubin. CONCLUSION: Our results suggest that long-term consumption of this toxic compound present in cassava roots may be potentially dangerous for vulnerable subjects.

Pancreatitis crónica. Algunos aspectos históricos relevantes / Chronic pancreatitis. Some important historical aspects

Desde la antigüedad había llamado la atención el aumento de tamaño y dureza que, en ocasiones, presentaba la estructura abdominal que recibió el nombre de páncreas. Portal en 1803 describió por primera vez los signos clínicos de la pancreatitis crónica. En 1815 Fleischman especuló sobre el posible papel del consumo exagerado de alcohol. Comfort en 1946 acuñó el término «pancreatitis crónica recidivante» y 6 años más tarde refirió lo que se llamaría pancreatitis hereditaria. Zuidema en 1959 definió la pancreatitis tropical y 2 años después Sarles puntualizó sobre otra forma de pancreatitis que en 1995 Yoshida denominaría pancreatitis autoinmune. La pancreatitis del surco era descrita en 1970 por Potet. En 1984 se definió la pancreatitis obstructiva y en 1987 Ammann refirió la pancreatitis idiopática. En este artículo se hace un recuerdo histórico de los pioneros que supieron valorar determinadas características que permitieron definir diferentes formas de pancreatitis crónicas

Since ancient times the increase of size and hardness sometimes presented by the abdominal structure known as the pancreas has attracted attention. Portal was the first to describe the clinical signs of chronic pancreatitis in 1803. In 1815, Fleischman speculated about the potential role of excessive alcohol consumption. Comfort coined the term "chronic relapsing pancreatitis" in 1946 and described hereditary pancreatitis 6 years later. Zuidema defined tropical pancreatitis in 1959 and 2 years later Sarles described another form of pancreatitis to which Yoshida gave the name autoimmune pancreatitis in 1995. Groove pancreatitis was described by Potet in 1970. Obstructive pancreatitis was defined in 1984 and Ammann identified idiopathic pancreatitis 3 years later. This article gives a historical account of the pioneers who developed the knowledge of how to assess the characteristics that allowed the different forms of chronic pancreatitis to be defined

Chronic pancreatitis. Some important historical aspects. / Pancreatitis crónica. Algunos aspectos históricos relevantes.

Since ancient times the increase of size and hardness sometimes presented by the abdominal structure known as the pancreas has attracted attention. Portal was the first to describe the clinical signs of chronic pancreatitis in 1803. In 1815, Fleischman speculated about the potential role of excessive alcohol consumption. Comfort coined the term "chronic relapsing pancreatitis" in 1946 and described hereditary pancreatitis 6 years later. Zuidema defined tropical pancreatitis in 1959 and 2 years later Sarles described another form of pancreatitis to which Yoshida gave the name autoimmune pancreatitis in 1995. Groove pancreatitis was described by Potet in 1970. Obstructive pancreatitis was defined in 1984 and Ammann identified idiopathic pancreatitis 3 years later. This article gives a historical account of the pioneers who developed the knowledge of how to assess the characteristics that allowed the different forms of chronic pancreatitis to be defined.

Dietary cyanogen exposure and early child neurodevelopment: An observational study from the Democratic Republic of Congo.

BACKGROUND: Dietary cyanogen exposure from ingesting bitter (toxic) cassava as a main source of food in sub-Saharan Africa is related to neurological impairments in sub-Saharan Africa. We explored possible association with early child neurodevelopmental outcomes. METHODS: We undertook a cross-sectional neurodevelopmental assessment of 12-48 month-old children using the Mullen Scale of Early Learning (MSEL) and the Gensini Gavito Scale (GGS). We used the Hopkins Symptoms Checklist-10 (HSCL-10) and Goldberg Depression Anxiety Scale (GDAS) to screen for symptoms of maternal depression-anxiety. We used the cyanogen content in household cassava flour and urinary thiocyanate (SCN) as biomarkers of dietary cyanogen exposure. We employed multivariable generalized linear models (GLM) with Gamma link function to determine predictors of early child neurodevelopmental outcomes. RESULTS: The mean (SD) and median (IQR) of cyanogen content of cassava household flour were above the WHO cut-off points of 10 ppm (52.18 [32·79]) and 50 (30-50) ppm, respectively. Mean (SD) urinary levels of thiocyanate and median (IQR) were respectively 817·81 (474·59) and 688 (344-1032) µmole/l in mothers, and 617·49 (449·48) and 688 (344-688) µmole/l in children reflecting individual high levels as well as a community-wide cyanogenic exposure. The concentration of cyanide in cassava flour was significantly associated with early child neurodevelopment, motor development and cognitive ability as indicated by univariable linear regression (p < 0.05). After adjusting for biological and socioeconomic predictors at multivariable analyses, fine motor proficiency and child neurodevelopment remained the main predictors associated with the concentration of cyanide in cassava flour: coefficients of -0·08 to -.15 (p < 0·01). We also found a significant association between child linear growth, early child neurodevelopment, cognitive ability and motor development at both univariable and multivariable linear regression analyses coefficients of 1.44 to 7.31 (p < 0·01). CONCLUSION: Dietary cyanogen exposure is associated with early child neurodevelopment, cognitive abilities and motor development, even in the absence of clinically evident paralysis. There is a need for community-wide interventions for better cassava processing practices for detoxification, improved nutrition, and neuro-rehabilitation, all of which are essential for optimal development in exposed children.

Experimental poisoning by cassava wastewater in sheep / Intoxicação experimental por manipueira em ovinos

The processing of Manihot esculenta (cassava) tubers yield different by-products, including cassava wastewater, which is the liquid pressed out of the tuber after it has been mechanically crushed. Cyanide poisoning after ingestion of cassava wastewater has been reported in ruminants and pigs in Northeastern Brazil. With the aim of studying its toxicity, cassava wastewater was administered orally to six sheep at doses of 0.99, 0.75, 0.70, 0.63, and 0.5 mg of hydrocyanic acid kg-1 body weight, which corresponded to 14.2, 10.6, 9.8, 8.89, and 7.1 mL of wastewater kg-1. On the second day, the sheep received a volume of wastewater which corresponded to 0.46, 0.34, 0.31, 0.28, and 0.23 mg of HCN kg-1. A sheep used as control received 9.9 mL of water kg-1 BW. Sheep that received from 0.75 to 0.99 mg kg-1 of HCN on the first day exhibited severe clinical signs of poisoning, and the sheep that received 0.63 and 0.5 mg kg-1 exhibited mild clinical signs. All sheep were successfully treated with sodium thiosulfate. On the second day, only the sheep that received 0.46 mg kg-1 and 0.34 mg kg-1 exhibited mild clinical signs and recovered spontaneously. The concentration of HCN in the wastewater was 71.69±2.19 μg mL-1 immediately after production, 30.56±2.45 μg mL-1 after 24 hours, and 24.25±1.28 μg mL-1 after 48 hours. The picric acid paper test was strongly positive 5 minutes after production; moderately positive 24 hours after production, and negative 48 hours after production. We conclude that cassava wastewater is highly toxic to sheep if ingested immediately after production, but rapidly loses toxicity in 24-48 hours.(AU)

O processamento dos tubérculos de Manihot esculenta (mandioca) produzem diferentes subprodutos, incluindo a manipueira, líquido que escorre das raízes da mandioca depois de ter sido mecanicamente prensada. A intoxicação por cianeto após a ingestão de manipueira tem sido relatada em ruminantes e suínos no Nordeste do Brasil. Com o objetivo de estudar sua toxicidade, administrou-se manipueira por via oral a seis ovelhas em doses de 0,99, 0,75, 0,70, 0,63 e 0,5 mg de peso corporal de ácido cianídrico kg-1, correspondendo a 14,2, 10,6, 9,8, 8,89 e 7,1 mL de manipueira kg-1 de peso corporal. No segundo dia, as ovelhas receberam um volume de manipueira que correspondeu a 0,46, 0,34, 0,31, 0,28 e 0,23 mg de HCN kg-1. Uma ovelha usada como controle recebeu 9,9 mL de água kg-1 de peso corporal. Ovelhas que receberam doses de 0,75 a 0,99 mg kg-1 de HCN no primeiro dia exibiram sinais clínicos graves de intoxicação e as ovelhas que receberam 0,63 e 0,5 mg kg-1 exibiram sinais clínicos leves. Todas as ovelhas foram tratadas com sucesso com tiossulfato de sódio. No segundo dia, apenas as ovelhas que receberam 0,46 mg kg-1 e 0,34 mg kg-1 apresentaram sinais clínicos leves e se recuperaram espontaneamente. A concentração de HCN na manipueira foi de 71,69 ± 2,19 μg mL-1 imediatamente após a produção, 30,56 ± 2,45 μg mL-1 após 24 horas e 24,25 ± 1,28 μg mL-1 após 48 horas. O teste de papel picrosódico foi fortemente positivo 5 minutos após a produção; moderadamente positivo 24 horas após a produção e negativo 48 horas após a produção. Concluímos que a manipueira é altamente tóxica para ovinos se ingeridas imediatamente após a produção, mas rapidamente perdem toxicidade em 24-48 horas.(AU)

Contribution of hippocampal area CA1 to acetone cyanohydrin-induced loss of motor coordination in rats. / Participación del área CA1 del hipocampo en la incoordinación motora inducida por acetonacianohidrina en la rata.

INTRODUCTION: Some vegetable foodstuffs contain toxic compounds that, when consumed, favour the development of certain diseases. Cassava (Manihot esculenta Crantz) is an important food source, but it contains cyanogenic glucosides (linamarin and lotaustralin) that have been associated with the development of tropical ataxic neuropathy and konzo. In rats, intraperitoneal administration of acetone cyanohydrin (a metabolite of linamarin) produces neurological disorders and neuronal damage in the hippocampus. However, it is unknown whether hippocampal area CA1 plays a role in neurological disorders associated with acetone cyanohydrin. METHOD: A total of 32 male Wistar rats 3 months old were assigned to 4 groups (n=8 per group) as follows: vehicle (1µl physiological saline), and 3 groups with acetone cyanohydrin (1µl of 10, 15, and 20mM solution, respectively). The substances were microinjected intrahippocampally every 24hours for 7 consecutive days, and their effects on locomotor activity, rota-rod and swim tests were assessed daily. On the fifth day post-treatment, rats underwent further assessment with behavioural tests to identify or rule out permanent damage induced by acetone cyanohydrin. RESULTS: Microinjection of acetone cyanohydrin 20mM resulted in hyperactivity, motor impairment, and reduced exploration from the third day of treatment. All concentrations of acetone cyanohydrin produced rotational behaviour in the swim test from the first day of microinjection. CONCLUSION: The hippocampal area CA1 is involved in motor alterations induced by microinjection of acetone cyanohydrin, as has been reported for other cassava compounds.

The Metabolic Effects of Consumption of Yellow Cassava (Manihot esculenta Crantz) on Some Biochemical Parameters in Experimental Rats.

The metabolism of yellow cassava (variety TMS 01/1368) was investigated in male albino rats fed a diet containing yellow cassava for 7 to 28 days. There were significant increases (P < 0.05) in total and free cyanide and thiocyanate in the sera and urine samples of the experimental rats compared with the control, significant increases (P < 0.05) in serum glucose, alanine aminotransaminase, aspartate aminotransaminase, and alkaline phosphatase levels of the experimental rats compared with the control, significant decreases (P < 0.05) in serum albumin of the experimental rats compared with the control, but no significant differences (P > 0.05) in the serum total proteins of the experimental rats compared with the control. The experimental rats treated for 7, 14, 21, or 28 days exhibited body weight decreases of 5.11%, 11.10%, 19.16%, and 24.18%, respectively, whereas the control group showed 9.17% gain in body weight. Total and free cyanide concentrations were detected in the liver, kidney, and heart of most of the rats in both the experimental and control groups, except for free cyanide in the control group that was not detected. Metabolism of the yellow cassava variety in experimental rats was capable of exposing the animals to cyanide, underscoring the need for its proper processing before consumption by humans.

The management of cassava toxicity and its changing sociocultural context in the Kei Islands, eastern Indonesia.

Over a period of 150 years the Kei Islands have undergone environmental change, from rainforest to dryland savanna woodland. This has been accompanied by a shift in starch staple from sago, tubers, and grain to cassava. We show how this has been an effective ecological adaptation with social ramifications, not least the adoption of bitter cassava as a cultural identity marker. One of the problems of bitter cassava diets where people have become dependent upon them in poor parts of the Old World tropics are the effects of toxicity. We show how through a combination of factors and strategies this has not been a major issue in the Kei Islands, and how through a government-assisted agricultural project, attempts are being made to build upon this successful transition. The viability of present trends are evaluated.

Assessment of cassava toxicity in patients with tropical chronic pancreatitis.

BACKGROUND AND AIM: There have been conflicting reports on the role of cassava ingestion in tropical pancreatitis (TCP). In this study we aimed to estimate cyanogens detoxifying enzyme rhodanese, thiocyanate and sulfur containing amino acids in cassava consumer as well as cassava non-consumer TCP patients and healthy controls and compare the same. METHODS: Eighty-six TCP patients and 90 healthy controls were recruited. Serum rhodanese, thiocyanate, plasma amino acids, urinary inorganic sulfate/creatinine were measured. RESULTS: There was significant reduction in serum rhodanese activity in both cassava consumer- and non-consumer TCP patients as compared to controls but no significant difference between cassava consumer- and non-consumer TCP patients was observed. Serum thiocyanate was significantly lower in cassava consumer TCP patients as compared to cassava consumer controls but not significantly different from cassava non-consumer TCP patients. Plasma methionine, cysteine and urinary inorganic sulfate / creatinine ratio was significantly lower in both cassava consumer and non-consumer TCP patients as compared to controls but were comparable among cassava consumers and non-consumers. CONCLUSIONS: Significant reduction in rhodanese activity with concomitant decrease in sulfur containing amino acids and antioxidants such as glutathione suggests that TCP patients are at higher risk of defective detoxification of cyanogens. However there was no difference between cassava consumers and non-consumers. Low levels of sulfur amino acids may contribute to the development of pancreatitis.

Konzo: from poverty, cassava, and cyanogen intake to toxico-nutritional neurological disease.

Konzo is a distinct neurological entity with selective upper motor neuron damage, characterized by an abrupt onset of an irreversible, non-progressive, and symmetrical spastic para/tetraparesis. Despite its severity, konzo remains a neglected disease. The disease is associated with high dietary cyanogen consumption from insufficiently processed roots of bitter cassava combined with a protein-deficient diet. Epidemics occur when these conditions coincide at times of severe food shortage. Up to 1993, outbreaks in poor rural areas in Africa contributed to more than 3,700 cases of konzo. The number of affected people is underestimated. From unofficial reports, the number of cases was estimated to be at least 100,000 in 2000, in contrast to the 6,788 cases reported up to 2009 from published papers.

Strategies for elimination of cyanogens from cassava for reducing toxicity and improving food safety.

Toxicity of cassava arises due to the presence of the cyanoglucosides linamarin and lotaustralin which are hydrolysed by endogenous enzyme linamarase to acetonecyanohydrin (ACN) and cyanide (CN) which are toxic. Major research efforts to eliminate/reduce cyanoglucosides have focused on (i) development of acyanogenic cassava varieties by breeding; (ii) controlling its metabolism; and (iii) processing to remove cyanogens. The cyanoglucoside (CNG) content in cassava is genetically controlled and cultivars may be classified as low (<50 µg/g), medium (50-100 µg/g) and high CN (>100 µg CN eq./g) varieties. Molecular techniques for reducing tuber CNG have focused on development of transgenic plants with reduced expression of cyt P 450 in leaves, or increased expression of hydroxynitrilelyase in tuber. For immediate solution, CNG content can be reduced using several processing methods. Traditional methods used for processing include boiling, drying, parboiling and drying, baking, steaming, frying and preparation of flour. These processes result in CN losses ranging from 25% to 98%. The cyanogen level in the final product is influenced both by the tuber CNG and the method of processing. In order to achieve safe levels of 10 µg/g in cassava products, new methods of processing, especially for cassava containing more than 250 µg CN eq./g, remains a challenging problem.

The retail market for fresh cassava root tubers in the European Union (EU): the case of Copenhagen, Denmark--a chemical food safety issue?

BACKGROUND: A number of retail shops in Copenhagen sell fresh cassava roots. Cassava roots contain the toxic cyanogenic glucoside linamarin. A survey was made of the shop characteristics, origin of the roots, buyers, shop owner's knowledge of toxicity levels, and actual toxicity levels. RESULTS: Shops selling fresh cassava were shown mostly to be owned by persons originating in the Middle East or Afghanistan, buyers were found to predominantly be of African origin, and sellers' knowledge concerning the potential toxicity was found to be very restricted. Seventy-six per cent of the roots purchased had a total cyanogenic potentials (CNp) above the 50 mg HCN equivalents kg(-1) dry weight (d.w.) proposed as acceptable by an EU working group. Two of 25 roots purchased had CNp higher than 340 mg HCN eq. kg(-1) d.w. CONCLUSION: The EU has previously made risk assessments concerning cassava and cyanogenic compounds. In the light of the conclusions drawn, the EU needs to make decisions about how to deal with the regulation and control of fresh cassava roots imported to the European food market. Also cassava root products and cassava leaves should be considered.

Quantificação de cianeto total nas etapas de processamento das farinhas de mandioca dos grupos seca e d'água / Total cyanide quantification in processing stages of cassava flour from dry and water groups

O objetivo deste trabalho foi quantificar a concentração de cianeto total durante as etapas de produção da farinha de mandioca dos grupos seca e d'água. Em relação à farinha seca, a concentração de cianeto total na raiz de mandioca diminuiu de 160±11,8 mg HCN/kg para 149±12,3 mg HCN/kg após a trituração, 68±2,5 mg HCN/kg após a prensagem e chegando a 5±0,2 mg HCN/kg no produto final, após o processo de torração. Na produção da farinha d'água, a raiz de mandioca apresentava teor de cianeto total de 321±21,6 mg HCN/kg e durante o processo de fermentação da raiz, o teor de cianeto total nas primeiras 24 horas de fermentação era de 297±2,7 mg HCN/kg chegando a 64±2,3 mg HCN/kg após 96 horas em repouso no tanque. Após trituração e prensagem da massa fermentada, os valores diminuíram para 50±0,6 e 36±0,4 mg HCN/kg, respectivamente, obtendo-se no produto final a concentração de 9±0,1 mg HCN/kg, sendo evidenciado a eficiência do processo de destoxificação em ambos os processamentos.

The aim of this work was to quantify the total cyanide concentration during the production stages of cassava flour from dry and water groups. In relation to dry flour, the total cyanide concentration in the cassava root reduced from 160±11.8 mg HCN/kg to 149±12.3 mg HCN/kg after grinding, 68±2.5mg HCN/kg after pressing and 5±0.2 mg HCN/kg was obtained in the final product after the roasting process. For the water flour production, the cassava root showed 321±21.6 mg HCN/kg total cyanide content, and during the fermentation process, the total cyanide content for the first 24-hour fermentation was from 297±2.7 mg HCN/kg reaching 64±2.3 mg HCN/kg after resting in a pool for 96 hours. After grinding and pressing the fermented roots, the values lowered to 50±0.6 and 36±0.4 mg HCN/kg, respectively. A concentration of 9±0.1 mg HCN/kg was obtained in the final product, evidencing the detoxification process efficiency in both processings.

Plantas tóxicas para ruminantes e eqüídeos no Norte Piauiense / Toxic plants for ruminants and equidae in Northern Piauí

Este trabalho teve por objetivo realizar um levantamento sobre as plantas tóxicas para ruminantes e equídeos na Mesorregião Norte do Piauí. Foram feitas 71 entrevistas a médicos veterinários, engenheiros agrônomos, técnicos agrícolas e produtores de 16 municípios, entrevistando pelo menos quatro pessoas por município. As plantas comprovadamente tóxicas que foram apontadas com maior frequência na região estudada foram Ipomoea asarifolia, que causa intoxicações em pequenos ruminantes em todas as áreas visitadas. Stryphnodendron coriaceum pelas mortes que ocasiona é, aparentemente, a planta que causa maiores perdas econômicas na mesorregião estudada. Enterolobium contortisiliquum também foi citada como causa importante de sinais digestivos, abortamentos e fotossensibilização em bovinos da região. Os entrevistados confirmaram a ocorrência de surtos de intoxicação em bovinos por Thiloa glaucocarpa no inicio do período chuvoso. Manihot spp. e Piptadenia macrocarpa são plantas cianogênicas apontadas como causa de mortes superagudas em bovinos. Outras plantas relatadas como tóxicas pelos entrevistados, mas sem que haja comprovação de sua toxicidade, foram Buchenavia tomentosa, Caesalpinia sp., Brunfelsia sp., Luetzelburgia sp., Hybantus ipecaconha, Phisalys angulata e Spondias luta. De acordo com os entrevistados os frutos de Buchenavia tomentosa causam sinais digestivos e abortos em caprinos, ovinos e bovinos. Produtores relatam surtos de intoxicação em caprinos que apresentam sinais digestivos e morte após a ingestão de favas de Luetzelburgia sp. Brunfelsia sp. é relatada como causa de alterações nervosas, no começo das chuvas, quando os animais ingerem as folhas e flores e os asininos são aparentemente mais afetados. Os frutos de Spondias luta foram mencionados como causa de diarréia em caprinos. Experimentos não publicados demonstraram a toxicidade de Brunfelsia sp. em ovinos e de Luetzelburgia sp. como causa de sinais digestivos e mortes em caprinos.

The objective of this study was to survey toxic plants for ruminants and equidae in northern Piauí. Seventy one persons were interviewed, including farmers, veterinary practitioners, agronomists, and agrarian technicians from 16 municipalities, performing at least four interviews in each municipality. The most common plant mentioned as a cause of poisoning was Ipomoea asarifolia, which is a well known cause of tremogenic disease in ruminants. Stryphnodendron coriaceum which causes digestive signs was referred as a common cause of death, and is probably the plant that causes most cattle deaths in the region. Enterolobium contortisiliquum was also mentioned as a frequent cause of digestive signs, abortion and photosensitization in cattle. Outbreaks of nephrosis caused by Thiloa glaucocarpa are frequent at the beginning of the raining season. Poisoning by the cyanogenic plants Manihot spp. e Piptadenia macrocarpa are a cause of peracute deaths. Other plants mentioned as toxic were Buchenavia tomentosa, Caesalpinia sp., Brunfelsia sp., Luetzelburgia sp., Hybantus ipecaconha, Phisalys angulata, and Spondias luta. Farmers report that goats are poisoned by the ingestion of the pods of Luetzelburgia sp., which causes digestive signs and death. The ingestion of the fruits of Buchenavia tomentosa is associated with digestive signs and and abortion in ruminants. Brunfelsia sp. is mentioned as a cause of nervous signs at the start of the raining season and donkeys are apparently more affected. The consumption of the fruits of Spondias luta are associated with diarrhea in goats. Recent unpublished experiments demonstrated the toxicity of Brunfelsia sp. as a cause of nervous signs and of Luetzelburgia sp. as a cause of digestive signs in goats. Experiments with other plants are necessary to confirm their toxicity.