Effects of Long-Term Low-Dose Cyanide Administration to Rats

Soto-Blanco, Benito; Marioka, Paulo César; Górniak, Silvana Lima

doi:10.1006/eesa.2002.2189

Cited by 34 publications

(20 citation statements)

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“…The tumor inhibition without causing acute poisoning in animals was only possible due to cyanide act promoting the inhibition of cytochrome C oxidase, an enzyme directly involved in mitochondrial respiration, thus promoting a decrease in ATP levels and resulting in cellular injury or establishing cell death, depending on its concentration 8,10 . However, due to unavoidable exposure to cyanide, living organisms have developed a selfdefense mechanism by conversion of cyanide to thiocyanate by the transfer of sulfur from the sulfane sulfur group (sulfur donors) for the cyanide by the rhodanese mitochondrial enzyme 10,11 .…”

Section: Discussionmentioning

confidence: 99%

“…However, due to unavoidable exposure to cyanide, living organisms have developed a selfdefense mechanism by conversion of cyanide to thiocyanate by the transfer of sulfur from the sulfane sulfur group (sulfur donors) for the cyanide by the rhodanese mitochondrial enzyme 10,11 . A feature present in cancer cells is the residual activity of rhodanese 12 , due to a defi ciency of sulfane sulfur, which makes transport and biosynthesis of sulfur from sulfane not occur satisfactorily in such cells.…”

Section: Discussionmentioning

confidence: 99%

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

Ramalho

Aydos²,

Schettert³

et al. 2013

Acta Cir. Bras.

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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.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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

Ramalho

Aydos²,

Schettert³

et al. 2013

Acta Cir. Bras.

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“…Another study (Soto-Blanco et al, 2002b) seems to point to cyanide being considerably more toxic (causing CNS damages) at least when given to weanling rats. However, it should be noted that this study lacks statistic evidence and the high peak concentrations (as a result of gavage dosing) might have influenced the results of this three month study.…”

Section: Terms Of Referencementioning

confidence: 99%

Opinion of the Scientific Panel on contaminants in the food chain [CONTAM] related to cyanogenic compounds as undesirable substances in animal feed

2007

EFSA Journal

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SUMMARYHydrogen cyanide (HCN) is formed following the enzymatic hydrolysis of cyanogenic glycosides, which are produced as secondary metabolites by various plant species. In the intact plant these cyanogenic compounds are stored separated from hydrolytic enzymes. Crushing of plant materials either by technical processes or by chewing by animals obliterates this separation and initiates the enzymatic hydrolysis of cyanogenic compounds, resulting ultimately in the formation of HCN. Hydrolysis to release HCN can also be accomplished by microorganisms in the digestive tract.

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“…La DL50 oral en ratas es 8,5 mg/kg para el cianuro de hidrógeno, 6,4 mg/kg para cianuro de sodio, 10 mg/ kg para cianuro de potasio, 39 mg/kg para cianuro de calcio (24) .…”

Section: En Animales De Experimentaciónunclassified

“…No se observa efectos adversos en el proceso reproductivo ni durante la lactancia en ratas preñadas y lactantes alimentadas hasta con 500 mg de cianuro por kg; el desarrollo, peso del producto al nacer, consumo de alimento y crecimiento no son significativamente diferentes de los controles (24,27) .…”

Section: En Animales De Experimentaciónunclassified

Toxicidad del cianuro. Investigación bibliográfica de sus efectos en animales y en el hombre

Ramírez

2011

An Fac med

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REVISIÓN La prevención, el mejor antídotoResumen 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 'no clasificables como carcinógenos humanos'. 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. Palabras clave: Cianuros; exposición ocupacional; acciones tóxicas; neurotóxicos. AbstractCyanide, 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 minimum 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 "not classifiable as human carcinogen". 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.

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Effects of Long-Term Low-Dose Cyanide Administration to Rats

Cited by 34 publications

References 35 publications

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

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

Opinion of the Scientific Panel on contaminants in the food chain [CONTAM] related to cyanogenic compounds as undesirable substances in animal feed

Toxicidad del cianuro. Investigación bibliográfica de sus efectos en animales y en el hombre

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