Anaerobic cyanides oxidation with bimetallic modulation of biological toxicity and activity for nitrite reduction.

Cyanide is a typical toxic reducing agent prevailing in wastewater with a well-defined chemical mechanism, whereas its exploitation as an electron donor by microorganisms is currently understudied. Given that conventional denitrification requires additional electron donors, the cyanide and nitrogen can be eliminated simultaneously if the reducing HCN/CN- and its complexes are used as inorganic electron donors. Hence, this paper proposes anaerobic cyanides oxidation for nitrite reduction, whereby the biological toxicity and activity of cyanides are modulated by bimetallics. Performance tests illustrated that low toxicity equivalents of iron-copper composite cyanides provided higher denitrification loads with the release of cyanide ions and electrons from the complex structure by the bimetal. Both isotopic labeling and Density Functional Theory (DFT) demonstrated that CN--N supplied electrons for nitrite reduction. The superposition of chemical processes reduces the biotoxicity and enhances the biological activity of cyanides in the CN-/Fe3+/Cu2+/NO2- coexistence system, including complex detoxification of CN- by Fe3+, CN- release by Cu2+ from [Fe(CN)6]3-, and NO release by nitrite substitution of -CN groups. Cyanide is the smallest structural unit of C/N-containing compounds and serves as a probe to extend the electron-donating principle of anaerobic cyanides oxidation to more electron-donor microbial utilization.

A benzothiophene-based fluorescent probe with dual-functional to polarity and cyanide for practical applications in living cells and real water samples.

Polarity is a significant intracellular environmental parameter associated with cancer, while cyanide (CN-) is known to be highly toxic to humans. In this work, we designed a dual-functional fluorescent probe (TPABT) for simultaneous detection of polarity and CN-. As a polarity sensor, the probe exhibits NIR emission at 766 nm in 1,4-dioxane (non-polar solvent), whose emission intensity is 71-fold stronger than that in water (polar solvent). Meanwhile, the fluorescence intensity and quantum yield are linearly related to solvent polarity, confirming the polarity response ability of TPABT. For cell polarity detection, low cytotoxicity and polarity sensitivity of probe enable the applications for differentiating cancer cells (HeLa, 4TI) from normal cells (HUV, 3 T3) and monitoring the polarity changes of 4TI cells. As a CN- sensor, TPABT displays a turn-on fluorescence at 640 nm upon the addition of CN-, with advantages of anti-interference, response in aqueous media and low detection limit (22 nM). Additionally, we further explored the practical applications of TPABT for CN- determination in three types of real water samples (drinking water, tap water and lake water) and living cells. Notably, TPABT responses to polarity and CN- in two independent fluorescence channels of 766 and 640 nm, respectively, ensuring the dual functions for polarity and CN- sensing. Consequently, this multi-responsive fluorescent probe TPABT is promising to diagnose polarity-related diseases and detect CN- in real environments.

Bacterial tolerance and detoxification of cyanide, arsenic and heavy metals: Holistic approaches applied to bioremediation of industrial complex wastes.

Cyanide is a highly toxic compound that is found in wastewaters generated from different industrial activities, such as mining or jewellery. These residues usually contain high concentrations of other toxic pollutants like arsenic and heavy metals that may form different complexes with cyanide. To develop bioremediation strategies, it is necessary to know the metabolic processes involved in the tolerance and detoxification of these pollutants, but most of the current studies are focused on the characterization of the microbial responses to each one of these environmental hazards individually, and the effect of co-contaminated wastes on microbial metabolism has been hardly addressed. This work summarizes the main strategies developed by bacteria to alleviate the effects of cyanide, arsenic and heavy metals, analysing interactions among these toxic chemicals. Additionally, it is discussed the role of systems biology and synthetic biology as tools for the development of bioremediation strategies of complex industrial wastes and co-contaminated sites, emphasizing the importance and progress derived from meta-omic studies.

Mercury cyanide complexes and their relevance as environmental contaminants.

This review addresses the formation and relevance of mercury cyanide complexes as environmental contaminants. Gold extraction is traditionally carried out through the process of mercury amalgamation (Hg) due to its simplicity and low cost. However, this process is inefficient, capturing only about 30% of the gold present in the processed material. Additionally, mercury is toxic, mobile, and capable of accumulating in aquatic ecosystems, leading to its prohibition in several countries. As an alternative, cyanidation has been widely used in gold extraction. However, the frequent combination of Hg amalgamation with cyanidation can result in the formation of mercury cyanide complexes, which can be released into local water bodies, potentially impacting human health and the environment. This article reviews the existing knowledge of these complexes and highlights the remaining gaps in understanding their environmental behavior. It also emphasizes the need to address concerns related to the formation of these complexes and seek solutions to minimize their negative impacts. Furthermore, the article highlights the lack of updates in the literature regarding the impacts of cyanidation and the limited availability of comprehensive information on the topic. It is essential to conduct updated research in this area to advance knowledge and promote safer and more responsible practices in the mining industry.

Problemas diagnósticos de la intoxicación por cianuro derivada de la ingesta de almendras amargas / Difficulties in the diagnosis of cyanide poisoning following consumption of bitter almonds

Los casos de intoxicación por ingesta de cianuro en niños son raros. La almendra amarga contiene amigdalina y se descompone tras su ingesta, produciendo ácido cianhídrico que bloquea el uso celular del oxígeno, lo que ocasiona afectación de órganos diana. Presentamos un caso de sospecha de intoxicación por cianuro en un niño de 3 años tras ingesta de almendras amargas. El diagnóstico de sospecha se estableció con base en la clínica gastrointestinal y neurológica y en el hallazgo gasométrico de acidosis metabólica con hiperlactacidemia y anión GAP aumentado, lo cual es muy específico de esta entidad. No se pudieron determinar los niveles de cianuro en ningún laboratorio habitual de España, tampoco en el Instituto Toxicológico Nacional y Ciencias Forenses sin disponer de orden judicial. Ante la clínica inespecífica y las dificultades para determinar la concentración de cianuro en sangre, debe ofrecerse tratamiento precoz y antídoto específico ante la sospecha de intoxicación por cianuro (AU)

Cyanide poisoning in children is rare. Bitter almonds contain amygdalin, and hydrolysis of this compound following ingestion yields hydrocyanic acid, which inhibits cellular oxygen use and therefore causes target organ damage. We present a case of suspected cyanide poisoning in a child aged 3 years after the ingestion of bitter almonds. The diagnosis was based on the gastrointestinal and neurological symptoms and the detection of metabolic acidosis with hyperlacticaemia and a high anion gap, which are highly specific for this type of poisoning. Blood cyanide levels could not be measured in any clinical laboratory in Spain, and it was also not possible to do it in the National Institute of Toxicology and Forensic Sciences without a court order. Given the non-specific symptoms and the difficulty of measuring the concentration of cyanide in blood, treatment should be initiated early with administration of specific antidote if cyanide poisoning is suspected. (AU)

Intoxicación por cianuro y accidente cerebrovascular en fosa posterior: reporte de un caso y revisión de la literatura / Cyanide poisoning and cerebrovascular accident in the posterior fossa: a case report and review of the literature

La intoxicación por cianuro y el accidente cerebrovascular (ACV) en fosa posterior es una asociación que genera un paradigma trascendental y desafiante en el escenario clínico actual, presentando un trasfondo fisiopatológico intrincado aún sin establecer. La muerte fatal por cianuro está suscrita a infarto de miocardio, embolismo pulmonar o disritmia ventricular, entre otras. Cuando existe injuria del sistema nervioso central (SNC) podemos encontrar compromiso a nivel de núcleos de la base de cráneo; sin embargo, es inusual el ACV en fosa posterior, más aún en paciente joven y sin secuelas neurológicas importantes posteriores a la intoxicación. Es menester, intentar proporcionar los elementos necesarios para fomentar la sospecha clínica, alcanzar un diagnóstico oportuno y un óptimo tratamiento; ya que, es excepcionalmente raro y complejo este tipo de presentación clínica. (AU)

Cyanide poisoning and stroke in posterior fossa is an association that generates a transcendental and challenging paradigm in the current clinical setting, presenting an intricate pathophysiological background that has yet to be established. Fatal death from cyanide is subscribed to myocardial infarction, pulmonary embolism or ventricular dysrhythmia, among others. When there is injury to the central nervous system (CNS) we can find compromise at the level of the nuclei of the skull base; however, stroke in the posterior fossa is unusual, even more so in young patients and without significant neurological sequelae after intoxication. It is necessary to try to provide the necessary elements to promote clinical suspicion, achieve a timely diagnosis and optimal treatment; since this type of clinical presentation is exceptionally rare and complex. (AU)

Hidroxocobalamina no tratamento de intoxicações por cianeto / Hydroxocobalamin in the treatment of cyanide poisoning

CONTEXTO: A intoxicação por cianeto pode ser considerada uma intoxicação rara porém de extrema gravidade. A causa mais comum de exposição aguda ao cianeto é a inalação de fumaça em incêndios. Nos casos de intoxicação, além das medidas de suporte clínico, como suplementação de oxigênio, a terapia com antídotos deve ser realizada. Dentre os antídotos disponíveis (hidroxocobalamina, nitrito de amila, nitrito de sódio, tiossulfato de sódio, 4-dimetilaminofenol e edetato de dicobalto), a hidroxocobalamina é apontada como o antídoto de primeira linha. Atualmente, tais medicamentos não estão disponíveis no Brasil. EVIDÊNCIAS CIENTÍFICAS: Dentre as melhores evidências recuperadas, após buscas por revisões sistemáticas, encontram-se 4 estudos observacionais realizados na França, sendo um de delineamento prospectivo e os demais retrospectivos (um total de 345 pacientes estudados). A maioria dos pacientes foi exposta ao cianeto por inalação de fumaça em incêndios domésticos, exceto por um estudo que avaliou principalmente tentativas de suicídio com ingestão de cianeto. Como intervenção, os estudos preconizaram uma dose inicial de 5g de hidroxocobalamina em infusão de 15-30 min, a qual foi administrada em aproximadamente 20 min após o contato com o serviço de emergência ainda em âmbito pré-hospitalar, com a possibilidade de doses adicionais em pacientes não responsivos (até um total de 15g). Como resultados, a mortalidade variou de 28-42% considerando todos os indivíduos que receberam a hidroxocobalamina. Entre os indivíduos com intoxicação confirmada laboratorialmente, 33-36% vieram a falecer, sendo poupados até mesmo indivíduos com níveis plasmáticos potencialmente letais, nestes a morte ocorreu em 36-39% dos casos. A parada cardíaca se apresentou como uma complicação comum (38%). A presença de sequelas no momento da alta hospitalar foi de 10-14%, sendo confusão, perda de memória e síndrome cerebelar as mais comuns. A hidroxocobalamina apresentou um perfil de segurança favorável, apenas com incidência de efeitos adversos leves. Dentre eles, o mais comum foi a apresentação de coloração vermelho-rosa na pele e urina e, mais raramente, aumento da pressão arterial. Após a avaliação crítica com a proposta do sistema GRADE, as evidências de eficácia atualmente disponíveis foram classificadas com qualidade muito baixa e as evidências de segurança com qualidade moderada. DISCUSSÃO: A hidroxocobalamina se apresenta como um agente potencialmente efetivo no tratamento de intoxicações por cianeto. Suas evidências devem ser interpretadas com cautela devido às limitações de suas fontes. O delineamento descritivo não permite o testes das variadas hipóteses, sem, portanto, ser quantificada a influência do acaso sobre os resultados obtidos. Da mesma forma, a ausência de controles e ajustes estatísticos não afasta a influência de fatores de confusão, sendo esses, importantes fontes de viés nos estudos observacionais. Com os custos considerados nas análises econômicas, ela se apresenta também como uma opção potencialmente custo-efetiva e com baixo impacto orçamentário. Todavia, outros fatores além da qualidade das evidências, como as barreiras para a sua devida implementação, devem ser considerados na elaboração de uma recomendação sobre seu uso. DECISÃO FINAL: Após as considerações provenientes da Consulta Pública, os membros da CONITEC presentes na 40ª reunião do plenário do dia 08/09/2015 deliberaram, por unanimidade, recomendar a incorporação do Cloridrato de hidroxocobalamina na concentração de 5 g injetável no tratamento de intoxicações por cianeto. Foi assinado o Registro de Deliberação nº 149/2015. DECISÃO: Incorporar a hidroxocobalamina no tratamento de intoxicações por cianeto, no âmbito do Sistema Único de Saúde ­ SUS, dada pela Portaria nº 9 de 28 de janeiro de 2016 publicado no DOU nº 20 de 29 de janeiro de 2016.

Sulfane sulfur deficiency in malignant cells, increasing the inhibiting action of acetone cyanohydrin in tumor growth

PURPOSE: To demonstrate the irreversible poisoning action of the acetone cyanohydrin (AC) in malignant cells. METHODS: Thirty male Swiss mice were inoculated with 1x10³ Ehrlich tumor (ET) cells. The mice were divided into three groups (n=10): CG (saline); ACG1 (1.864 mg/Kg of AC) and ACG2 (2.796 mg/Kg of AC), treated every 48 hours from day 3 until day 13. On day 15 the mice were euthanized and the number of viable cells in ascites was determined. In the meantime, ET cells were incubated with AC (0.5, 1.0, 2.0 μg/mL). Cell viability and percentage of growth inhibition (PGI) were checked after one, two, three, four, 18 and 24 hours. RESULTS: There was reduction in volume and number of viable cells in ACG1 and ACG2 compared to CG. In ACG1 one of the animals did not present ascites. In ACG2 two mice did not present ascites and in CG none of the mice present ascites. The action of AC was dose and time dependent and there was no significant difference among the three doses. CONCLUSION: The acetone cyanohydrin promoted reduction of the tumor and also prevented tumor development in 20% of the treated animals.

Bases del manejo clínico de la intoxicación por humo de incendios «Docohumo Madrid 2010» / Basis for the clinical management of fire smoke poisoning «Docohumo Madrid 2010»

La intoxicación por humo es la principal causa de morbimortalidad en los incendios. El humo es una mezcla de partículas carbonáceas suspendidas en aire caliente y gases tóxicos. De todos ellos, el monóxido carbono (CO) y fundamentalmente el ácido cianhídrico (CNH) son los que van a provocar la anoxia tisular. Las manifestaciones clínicas de la intoxicación por humo son variables. Algunas de las manifestaciones potenciales podrían ser: irritación ocular, dolor de garganta, estridor laríngeo, disfagia, esputo carbonáceo, tos, disnea, laringoespasmo, broncoespasmo, síndrome coronario, coma, hipoxemia, acidosis láctica, cianosis y muerte. En la evaluación de estos enfermos la presencia de hollín en nariz, boca o esputo sugiere intoxicación grave. Niveles de lactato superiores a 10mmol/l indican cifras de cianuro mayores de 40micromol/l. La pulsicooximetría ha supuesto un avance importante para el diagnóstico, valoración y seguimiento de estos pacientes. En el tratamiento será indispensable valorar la necesidad de una intubación temprana. La administración de oxígeno al 100% será esencial. Como antídoto para el cianuro, el de primera elección es la hidroxicobalamina. Su administración ha de ser precoz. Los criterios de administración son: paciente que ha inhalado humo (restos de hollín en boca, faringe o esputo) y que tenga alteraciones neurológicas (confusión, coma, agitación, convulsiones) y además presenta una de las siguiente circunstancias: bradipnea, parada respiratoria, parada cardiorrespiratoria, shock, hipotensión, láctato >8mmol/l o acidosis láctica. Lógicamente el resto del manejo será convencional en función de síntomas o complicaciones (AU)ies

Poisoning by smoke is the main cause of morbidity and mortality in fires. Smoke is a mixture of carbonaceous particles suspended in hot air and toxic gases. Of these, carbon monoxide (CO) and primarily hydrocyanic acid (CNH), are those that provoke tissue anoxia. The clinical manifestations of smoke poisoning are variables. Some of the potential manifestations could be: eye irritation, sore throat, laryngeal stridor, dysphagia, carbonaceous sputum, cough, dyspnea, laryngospasm, bronchospasm, coronary syndrome, coma, hypoxemia, lactic acidosis, cyanosis and death. In the assessment of these patients the presence of soot in the nose, mouth or sputum suggests serious poisoning. Lactate levels higher than 10mmol/L indicates levels of cyanide major than 40micromole/L. The pulse co-oximetry has assumed an important step forward for the diagnosis, appraisal and monitoring of these patients. In the treatment it will be essential to assess the need of an early intubation. The administration of oxygen to the 100% will be essential. As an antidote to the cyanide, the first-choice is the hydroxocobalamin. Its administration has to be early. Its administration criteria are: patient who has inhaled smoke (remnants of soot in the mouth, pharynx or sputum) and has neurological disorder (confusion, coma, agitation, seizures) and also presents one of the following circumstances: bradypnea, respiratory arrest, cardiorespiratory arrest, shock, hypotension, lactate >8mmol/L or lactic acidosis. Logically, the rest of the management will be conventional depending on symptoms or complications (AU)

Bases para el manejo clínico de la intoxicación por humo de incendios / Fundamentals in the clinical management of intoxication due to smoke inhalation

La intoxicación por humo es la principal causa de morbimortalidad en los incendios. El humo es una mezcla de partículas carbonáceas suspendidas en aire caliente y gases tóxicos. De todos ellos, el monóxido carbono (CO) y fundamentalmente el ácido cianhídrico(CNH), son los que van a provocar la anoxia tisular. Las manifestaciones clínicas de la intoxicación por humo son variables. Algunas de las manifestaciones potenciales podrían ser: irritación ocular, dolor de garganta, estridor laríngeo, disfagia, esputo carbonáceo, tos, disnea, laringoespasmo, broncoespasmo, síndrome coronario, coma, hipoxemia,acidosis láctica, cianosis y muerte. En la evaluación de estos enfermos la presencia de hollín en nariz, boca o esputo sugiere intoxicación grave. Los valores delactato superiores a 10 mmol/L indican cifras de cianuro mayores de 40 micromol/L. Lapulsicooximetría ha supuesto un avance importante para el diagnóstico, valoración y seguimiento de estos pacientes. En el tratamiento será indispensable valorar la necesidad de una intubación temprana. La administración de oxígeno al 100% será esencial. Como antídoto para el cianuro, el de primera elección es la hidroxicobalamina. Su administración ha de ser precoz. Los criterios de administración son: paciente que ha inhalado humo (restos de hollín en boca, faringe o esputo) y que tenga alteraciones neurológicas (confusión, coma, agitación, convulsiones) y que además presenta una de las siguiente circunstancias: bradipnea, parada respiratoria, parada cardiorrespiratoria, shock, hipotensión, lactato 8 mmol/L o acidosis láctica. Logicamente, el resto del manejo será el convencional en función de síntomas o complicaciones (AU)

Intoxication due to smoke inhalation is the main cause of morbidity and mortality from fires. Smoke is a mixture of carbon particles suspended in hot air containing toxic gases. Carbon monoxide (CO) and cyanuric acid are the gases that are mainly responsible for tissue anoxia. The clinical signs of intoxication due to smoke inhalation vary. They may include eye irritation, sore throat, laryngeal stridor, dysphagia, soot in sputum, cough, breathlessness, laryngeal spasm,bronchospasm, coronary syndrome, coma, hypoxemia, lactic acidosis, cyanosis, and death. A finding of soot in the nostrils, mouth or sputum suggests severe intoxication. Lactate dehydrogenase levels over 10 mmol/L are indicative of cyanuric acid levels over 40 mmol/L. Pulse oximetry has represented an important advance for diagnosis, examination, and follow-up in this setting. The possible need for early intubation must be assessed and oxygen administration (at100%) is essential. The treatment of choice for cyanuric acid poisoning is hydroxocobalamin. This antidote must be administered promptly whenever a patient has inhaled smoke (soot in mouth, throat or sputum), shows neurologic signs(confusion, coma, agitation, convulsions), or has any of the following signs: bradypnea, respiratory arrest, cardiac arrest,shock, hypotension, lactate dehydrogenase over 8 mmol/L, or lactic acidosis. There after, management will be dictated by symptoms or complications (AU)

Toxicidad del cianuro: investigación bibliográfica de sus efectos en animales y en el hombre: [revisión] / Cyanide toxicity: bibliography research of its effects in animals and ma: [review]

Se llama cianuro al cianuro en sí, al cianuro de hidrógeno y a sus sales. Los cianuros existen en forma natural e industrialmente se les obtiene como sales. Aún a dosis bajas son compuestos letales en tiempo mínimo de exposición. El sistema nervioso es su órgano blanco primario. Luego de ingestión, inhalación o contacto se presentan efectos neurotóxicos graves y mortales en humanos y animales. La exposición ocupacional produce alteraciones tiroideas, cefalea, vértigo, vómito, náuseas, dermatitis y exposiciones altas; a corto tiempo, terminan en paro respiratorio y muerte. Algunos compuestos de cianuro en microcantidades son indispensables para la vida. Respecto a su poder carcinógeno, al cianuro se le considera en el grupo D de los æno clasificables como carcinógenos humanosÆ. Para aplicar mejor las medidas preventivas en el trabajo con cianuros, y en salud pública, es necesario conocer satisfactoriamente su acción tóxica sobre los animales y el hombre.

Cyanide, hydrogen cyanide and its salts are called cyanide. They exist in natural form and are obtained as salts in industry. At low doses they are lethal in mínimum exposure time. The nervous system is its primary target organ. After ingestion, contact or inhalation, serious neurotoxic effects appear in humans and animals. Occupational exposure can produce headache, vertigo, vomiting, nausea, thyroid gland alterations, and dermatitis. At high doses and in short time, cyanide exposure can end in death. In very low amounts some cyanide compounds are indispensable for life. Cyanide is located in group D ônot classifiable as human carcinogenõ. In order to apply preventive measures when working with cyanides and in public health, it is necessary to acknowledge cyanide toxic effects on men and animals.

Tratamiento con hidroxicobalamina para la intoxicación por cianuro: una causa rara de pseudohematuria / Treatment with hydroxocobalamin for cyanide poisoning: a rare cause of pseudohematuria

No disponible

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Fracaso renal agudo tras intento autolítico con sales de cianuro y mercurio. A propósito de un caso / No disponible

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Exposição cianídrica em suínos: Uma abordagem dos parâmetros toxicocinéticos utilizando o tiocianato como biomarcador / Cianidric exposition in swines: A bording of the toxicocinetics parameters using the tiocianato as biomarker

O objetivo do presente estudo foi verificar os efeitos sobre a cinética do cianeto, em suínos, em diferentes fases da vida, usando o tiocianato como biomarcador. Vinte e dois suínos, foram divididos em quatro grupos (60 dias da idade, 95 dias da idade, 80 dias do gestação e 21 dias de lactação), e receberam por via oral, a dose única de 3.0 mg /kg de peso vivo de cianeto do potássio (KCN). As concentrações do tiocianato no sangue foram medidas dentro de 24h. O tempo máximo (Tmax) e constante de eliminação (Kel) foram mais elevados em porcas lactantes (15 hs e 0.045, respectivamente); por ouro lado, a maior concentração do tiocianato (Cmax) foi observada nas fêmeas grávidas (161.8). A meia vida de eliminação (t1/2) e o volume da distribuição (Vd) foram mais elevados nas fêmeas adultas (41, 57 e 1.23, respectivamente). Contudo a área sob a curva (AUC) do tiocianato foi mais elevado nos animais novos (354183,28), e o clearance o mais baixo (0.007) nestes animais. Concluindo, os resultados do presente estudo, evidenciam que o metabolismo do cianeto, varia extremamente, considerando o estado fisiológico dos suínos fêmeas, e que são os animais novos, provavelmente, os mais sensíveis aos efeitos tóxicos, da exposição crônica as baixas doses do cianeto.

The aim of the present study was to determine the effects of the swine, in different periods of life on the toxicokinetics of cyanide using thiocyante as biomaker. Twenty and two swines, was divided into four groups (60 days of age, 95 days of age, sows with 80 days of gestation and lactating swine), were dosed orally with 3,0 mg/kg/ body weigth of potassium cyanide (KCN). Thiocyanate concentrations in blood were measured within 24h. The time of peak concentration (Tmax) and constant of elimination (Kel) were higher in lactating sows (15 hs and 0,045, respectively); on the other hand, the maximum plasma concentration (Cmax) of thiocyanate was observed in pregnant females (161,8). The elimination half life (t1/2) and volume of distribution (Vd) were higher in adult sows (41, 57 and 1,23, respectively). Whereas the clearance and the area under the curve (AUC) of thiocyanate was higher in young animals (354183,28) the clearance was lower (0,007) in these animals. In coclusion , the results of the present study evidence that the metabolism of cyanide varies greatly considering the physiologic state of female swine being the young animals probably more sensitive to the toxic effects of chronic exposure to low doses of cyanide.

Enfermedades neurológicas asociadas al consumo de variedades de mandioca con alto contenido en gluconitrilos / Neurological diseases associated with intake of cassava varieties with high gluconitrile content

Los alimentos vegetales contienen, con frecuencia, compuestos tóxicos. En condiciones normales, el procesamiento de dichos alimentos está adaptado para permitir su consumo seguro. Sin embargo, en determinadas circunstancias, estos tóxicos provocan la aparición de enfermedades, entre las que destacan las de tipo neurológico. Un caso importante es el de la mandioca o yuca, la principal fuente de fécula en múltiples regiones tropicales. La mandioca contiene los gluconitrilos linamarina y lotaustralina, cuya degradación genera cianuro. Datos epidemiológicos asocian el consumo de mandioca a hipotiroidismo y a 2 enfermedades neurológicas muy diferentes entre sí: la neuropatía atáxica tropical, una polineuropatía periférica que cursa con sordera sensitivoneural y atrofia óptica, y el konzo, una paraparesia espástica. La neuropatía atáxica tropical y el konzo se asocian a 2 patrones diferentes de consumo de mandioca. La neuropatía atáxica tropical es una enfermedad crónica, que se presenta en personas de más de 40 años en determinadas regiones de Nigeria en las que se da una dieta monótona predominada por la mandioca. El konzo es una enfermedad que afecta preferentemente a niños y mujeres y que aparece de forma abrupta en períodos de crisis alimentaria, en los que la mandioca se mantiene prácticamente como el único alimento disponible. La patogenia de ambas enfermedades sigue sin esclarecerse. Para la neuropatía atáxica tropical, su origen alimentario no está suficientemente demostrado. En el caso del konzo, el origen tóxico-nutricional y la vinculación con la mandioca parecen indudables; sin embargo, la hipótesis más simple, la que supone un papel causal del cianuro, no parece cierta (AU)

West Indian amblyopia

The visual fields of ten patients with West Indian amblyopia, but with no other sign of neurological disease, have been carefully charted. The scotomata found varied considerably in size, shape and density between the individuals in the group. They were scattered, and quite large with irregular margins, sometimes with small dense defects in their central areas and usually with very shelving edges; a connexion with the blind spot was often present and/or break-through to the periphery. The causative lesions are likely to be subchiasmal. There is a slight resemblance to the field defects in tobacco amblyopia, but as tobbaco does not seem to be a factor in our cases, cyanide poisoning may be the common factor.(Summary)

Observations on the cyanide content and toxicity of tropical pulses

The content of cyanogenetic glucosides in West Indian and other pulses was estimated by the release of hydrocyanic acid on hydrolysis. In the varieties of phaseolus lunatus (lima bean) examined, the CN content was under 20mg. per cent, and not of the order previously known to cause acute poisoning. Trace amounts were found in 5 other species, and a high content was found in a variety of vicia sativa seeds (common vetch). A comparison of hydrolytic procedures in ph. lunatus showed that whereas the cyanogenetic glucoside is stable on cooking the intact bean, neither human saliva nor dilute hydrochloric acid at 37oC was effective in releasing free HCN from beans crushed after cooking. Animal feeding tests of crushed uncooked beans showed that the toxicity of these varieties was unrelated to their CN content. Severe 'toxicity' of ph. vulgaris (kidney bean, red pea) in rats and guinea pigs was mainly, if not entirely, due to unpalatability, causing starvation. Palatability was much improved by cooking. Absorption and utilisation of other species were good when fed to rats, even at 50 per cent level. There was some evidence of pancreatic hypertrophy and of impaired absorption or utilization of vigna sp. (black-eye pea) and cajanus cajan (gungo pea) in guinea pigs. No neurological lesions were detected in rats in feeding tests of up to 6 month's duration (AU)