Princess Bugar
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PRINCESS BUGAR
The Effects of Cassava Cyanide on the Antioxidant (Glutathione) Status and Some Clinically Important Enzymes of Rats. (P.N. Okafor, V.O. Anyanwu and H.O. Onyema (2010). The Effects of Cassava Cyanide on the Antioxidant (Glutathione) Status and Some Clinically Important Enzymes of Rats. Journal of Pharmacology and Toxicology. Vol.5(7):389-395, 2010 ISSN 1816-496X / DOI: 10.3923/jpt.2006.40.46 © 2010 Academic Journals Inc.)
The effects of cassava cyanide on the antioxidant (glutathione) status and some clinically important enzymes were investigated biochemically in male albino wistar rats fed for 28 days with cassava diet containing 54.6 mg CN kg- DM and 10% protein supplement.
Cassava diet Glutathione status Clinical important enzymes Rats
Locale Animal house of University of Nigeria Nsukka Respondents Twenty male albino rats of the wistarstrain Design StatisticaAnalysis Statistical tool Student T-test
Analysis of the urinary and serum cyanide and thiocyanate of the test and control rats showed a statistically significant difference (p<0.05) between the test and the control. The mean serum and urinary cyanide were 2.92=0.53 and 8.21+6.32 ug mL-- after 7 days and 3.80+0.67 and 11.08+0.54 ug mL-' after 28 days, respectively. Mean serum and urinary thiocyanate were 16.73+0.42 and 19.90+1.35 ug mL-1 after 7 days and 18.14+0.18 and 36.59+1.87 ug mL- after 28 days, respectively. Depletion in whole blood glutathione level by 47.3 and 89% (after 7 and 28 days, respectively) compared to that of the control was also observed. Increases in plasma activity of aspartate aminotrasferase (90%), alanine aminotrasferase (88.5%) and alkaline phosphatse (49%) were also measured after 28 days of the feeding experiment. There was elevation in blood glucose of the test animals, while the levels of protein and albumin remain within the normal range for both test and control animals.
The results from this study cleanly show that exposure to cassava cyanide has effect on the antioxidant status of animals ingesting cassavabased foods as evidenced by glutathione (antioxidant) depletion in whole blood of rats fed cassava diet containing 54.6 mg HCN equivalent kg-1 at 9% protein supplementation.
From this study, another implication of cyanide detoxification is decreased concentration of the qlutathione of the body. This could be in part due to reduced synthesis of this important biological compound. In this connection cysteine a sulphur-containing amino acid needed for cyanide detoxification in the body (Nagahara et al., 1999) is the limiting amino acid in glutathione synthesis.
Total cyanide content of cassava food products in Australia.Journal of Food Composition and Analysis. (Anna E. Burns a, J. Howard Bradbury b, Timothy R. Cavagnaro a,c, Roslyn M. Gleadow (2011). Total cyanide content of cassava food products in Australia.Journal of Food Composition and Analysis.)
The aim of this study was to determine the amounts of cyanogens present in cassava products in Melbourne and Canberra, Australia, and the possibility of deleterious effects as a result of consumption of high cyanide products.
Cassava Starchy tuberous food Hydrogen cyanide
Locale Research School of Biology, Australian National University, Canberra, ACT Respondents Cassava food products of Australia Design Experimental Design or True experimentation Statistical tool *One-way ANOVA *Tukey t-tests
Procedure Duplicate or triplicate 100 mg samples of cassava products were
added to a small plastic bottle, a buffer/enzyme paper was added, followed by 1 mL of 1 M pH 6 phosphate buffer, a picrate paper and a screw cap lid. The bottles were allowed to stand overnight at 30 8C, the picrate papers were removed from the plastic support and 5.0 mL of water added to elute the colour. The absorbance was measured in a spectrophotometer at 510 nm and the total cyanide content in mg HCN equivalents/ kg fresh weight = ppm calculated by multiplying the absorbance by 396 (Egan et al., 1998; Bradbury et al., 1999). This gives an accurate total cyanide analysis down to a minimum of 1 ppm total cyanide (Haque and Bradbury, 2002; Bradbury, 2009). The cyanide present is primarily linamarin (Jørgensen et al., 2005). The assay used here measures both linamarin and acetone cyanohydrin, but the concentration of the latter is extremely small compared to linamarin. Any HCN released from acetone cyanohydrin is of relevance to human health, as it breaks down completely in the alkaline condition in the gut to give CN (Bradbury, 2009). The amount of lotaustralin and free cyanide (HCN and CN) is negligible (Jørgensen et al., 2005). Food was tested in the form that it is normally consumed, with cyanide expressed on a fresh weight (or ‘as consumed’) basis.
This survey revealed a wide range of cyanide concentrations in commonly available cassava-based products in Australia. As the negative impacts of excess cyanide consumption are well known, it is clear that careful regulation of the importation of cassava products may be necessary to monitor and control the amount of total cyanogens in ready-to-eat food products
However, we note a very significant reduction in total cyanide content of a recent sample of cassava chips to 7 ppm, which is below the safe limit, and shows the importance of the development of enforceable standards (Kolind-Hansen and Brimer, 2009). Apart from this sample, the toxicity of all samples of cassava chips and frozen cassava roots was much greater than the FSANZ limit of 10 ppm. Frozen roots are usually boiled, baked or fried before consumption, which can reduce the concentration of total cyanide in these products by 10–75% (Nambisan and Sundaresan, 1985; Montagnac et al., 2009b), but may not reduce the concentration below the safe limit. Consumption of such cyanide-containing products, therefore, poses a health risk, especially to consumers who are unaware of the need for detoxification of cassava Based on the results presented here it is strongly advisable that the maximum 10 ppm safe level for total cyanide in cassava products introduced by FSANZ (FSANZ, 2009) be monitored to ensure that cassava chips will be safe, as shown by the most recent result given in Table 2, and that frozen cassava root parenchyma will also be safe in Australia.
Carbamoylation correlates of cyanate neuropathy and cyanide poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity (Kimani et al.(2013). Carbamoylation correlates of cyanate neuropathy and cyanide
poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity.SpringerPlus , 2:647 Page 8 of 8.)
We sought to elucidate the protein carbamoylation patterns associated with cyanate neuropathy relative to cyanide poisoning.
Carbamoylation Cyanate Cyanide Neuropathy Proteomics
Locale Center for Research on Occupational & Environmental Toxicology, OHSU, Portland Subject Young adult male Heterozygous rats Design Experimental Design or True Experimentation Statistical tool Correlation
Procedure We hypothesized that under a diet deficient in sulfur amino acids (SAA), the carbamoylation pattern associated with cyanide poisoning is similar to that of cyanate neuropathy. Male rats (6–8 weeks old) were fed a diet with all amino acids (AAA) or 75%-deficiency in SAA and treated with 2.5 mg/kg/body weight (bw) NaCN, or 50 mg/kg/bw NaOCN, or 1 μl/g/bw saline, for up to 6 weeks. Albumin and spinal cord proteins were analyzed using liquid chromatography mass spectrometry (LC-MS/MS). Only NaOCN induced motor deficits with significant levels of carbamoylation. At Day 14, we found a diet-treatment interaction effect on albumin carbamoylation (p = 0.07). At Day 28, no effect was attributed to diet (p = 0.71). Mean number of NaCN-carbamoylated sites on albumin was 47.4% higher relative to vehicle (95% CI:16.7-86.4%). Only NaOCN carbamoylated spinal cord proteins, prominently, under SAA-restricted diet. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclic-nucleotide 3'-phosphodiesterase. Under SAA deficiency, chronic but not acute cyanide toxicity may share biomarkers and pathogenetic similarities with cyanate neuropathy. Prevention of carbamoylation may protect against the neuropathic effects of cyanate.
Cassava is a carbohydrate-enriched and cyanogenic crop with a very low content in proteins and only 12% content in SAA, which are needed for humans to detoxify cyanide. The carbamoylation and neurotoxicity effects of cyanate may be influenced by diet with an exacerbating effect of dietary deficiency in sulfur amino acids. Cyanate hits proteins that are important in maintaining the shape and organization of the cytoskeleton, and hence, supporting mechanisms of neuronal survival. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclicnucleotide 3'-phosphodiesterase
The aforementioned pattern of protein susceptibility to carbamoylation should inform such studies to elucidate the exact pathways and mechanisms leading to cyanate neuropathy (Han et al. 2013). Studies on the biomarkers and mechanisms of food (cassava) associated neurological diseases should consider the potential role of cyanate and its carbamoylation effects as endpoints of interest both at the experimental, clinical, and public health standpoints.
Motor impairments induced by microinjection of linamarin in the dorsal hippocampus of Wistar rats (E. Rivadeneyra-Domínguez a,∗, J.F. Rodríguez-Landa (2016). Motor impairments induced by microinjection of linamarin in the dorsal hippocampus of Wistar rats.Neuroligia. Vol. 31(8):516—522. )
This study aimed to determine the effects of intrahippocampal microinjection of linamarin on spontaneous motor activity (locomotor activity test) and motor coordination (rotarod and forced swimming tests) in Wistar rats.
Cassava Linamarin Tropical ataxic neuropathy Konzo Lateral swimming Motor impairment
Locale Universidad Veracruzana Respondents 32 three-month-old male Wistar rats Design Experimental design or True experimentation Statistical tool 2-way repeated measures ANOVA, post hocStudent—Newman—Keuls test
Procedure Male Wistar rats (3 months old), were assigned to 4 groups (n = 8 per group) as fol- lows: a vehicle-control group (receiving injectable solution 1 μl) and three groups receiving linamarin (10, 15, and 20 mM). The substances were microinjected intrahippocampally (CA1) every 24 hours for 7 consecutive days, and their effects on locomotor activity, rotarod, and swim tests were assessed daily.
Microinjection of linamarin into the dorsal hippocampus of the rat is associ- ated with impaired motor coordination, suggesting that the dorsal hippocampus, among other brain structures, may be affected by the neurological changes associated with inappropriate consumption of cassava in humans. The toxicity of the cyanogenic compounds of cassava mainly affects the brain structures involved in memory processing and integration, emotions, control of autonomic functions, smell, and motor function such as the thalamus, the piriform cortex, the hypothalamus, and the hippocampus Similarly, rats receiving treat- ment with cassava root juice (with a linamarin concentration of 0.30 mg/2 mL) also developed such motor alterations as poor motor coordination and lateral swimming,17 which microinjections of either linamarin or a vehicle to assess the effects of linamarin on behaviour.
The increase in these 2 types of behaviour suggests that linamarin microinjections into the dorsal hippocampus induced neuronal damage, thereby preventing the consolidation of visuospatial memory in a process that may be linked to the apparent state of ‘locomotor hyperactivity’. This hypothesis is supported by the fact that intact experimental animals or those receiving the vehicle display a gradual decrease in locomotor activity and vertical behaviour after performing the locomo- tor activity test several times,25 as occurred in our vehicle group. One possible explanation is that rats learn about which becomes familiar, resulting in a decreased need for exploration spontaneous motor activity. However, rats treated with linamarin show hippocampal damage, which is likely to impair learning and memory consolidation. If this the case, rat would not recognize the conditions of the cage and wood therefore explore as with new or unknown setting. We should highlight that increased locomotor activity over reapeated sessions of the lovomotor activity test has also been observed in rats undergoing dorsal hippocampus microinjection or neurotoxix cycad derivatives or receiving cassava root juice rally.
The Effects of Cassava Cyanide on the Antioxidant (Glutathione) Status and Some Clinically Important Enzymes of Rats. (P.N. Okafor, V.O. Anyanwu and H.O. Onyema (2010). The Effects of Cassava Cyanide on the Antioxidant (Glutathione) Status and Some Clinically Important Enzymes of Rats. Journal of Pharmacology and Toxicology. Vol.5(7):389-395, 2010 ISSN 1816-496X / DOI: 10.3923/jpt.2006.40.46 © 2010 Academic Journals Inc.)
The effects of cassava cyanide on the antioxidant (glutathione) status and some clinically important enzymes were investigated biochemically in male albino wistar rats fed for 28 days with cassava diet containing 54.6 mg CN kg- DM and 10% protein supplement.
Cassava diet Glutathione status Clinical important enzymes Rats
Locale Animal house of University of Nigeria Nsukka Respondents Twenty male albino rats of the wistarstrain Design StatisticaAnalysis Statistical tool Student T-test
Analysis of the urinary and serum cyanide and thiocyanate of the test and control rats showed a statistically significant difference (p<0.05) between the test and the control. The mean serum and urinary cyanide were 2.92=0.53 and 8.21+6.32 ug mL-- after 7 days and 3.80+0.67 and 11.08+0.54 ug mL-' after 28 days, respectively. Mean serum and urinary thiocyanate were 16.73+0.42 and 19.90+1.35 ug mL-1 after 7 days and 18.14+0.18 and 36.59+1.87 ug mL- after 28 days, respectively. Depletion in whole blood glutathione level by 47.3 and 89% (after 7 and 28 days, respectively) compared to that of the control was also observed. Increases in plasma activity of aspartate aminotrasferase (90%), alanine aminotrasferase (88.5%) and alkaline phosphatse (49%) were also measured after 28 days of the feeding experiment. There was elevation in blood glucose of the test animals, while the levels of protein and albumin remain within the normal range for both test and control animals.
The results from this study cleanly show that exposure to cassava cyanide has effect on the antioxidant status of animals ingesting cassavabased foods as evidenced by glutathione (antioxidant) depletion in whole blood of rats fed cassava diet containing 54.6 mg HCN equivalent kg-1 at 9% protein supplementation.
From this study, another implication of cyanide detoxification is decreased concentration of the qlutathione of the body. This could be in part due to reduced synthesis of this important biological compound. In this connection cysteine a sulphur-containing amino acid needed for cyanide detoxification in the body (Nagahara et al., 1999) is the limiting amino acid in glutathione synthesis.
Total cyanide content of cassava food products in Australia.Journal of Food Composition and Analysis. (Anna E. Burns a, J. Howard Bradbury b, Timothy R. Cavagnaro a,c, Roslyn M. Gleadow (2011). Total cyanide content of cassava food products in Australia.Journal of Food Composition and Analysis.)
The aim of this study was to determine the amounts of cyanogens present in cassava products in Melbourne and Canberra, Australia, and the possibility of deleterious effects as a result of consumption of high cyanide products.
Cassava Starchy tuberous food Hydrogen cyanide
Locale Research School of Biology, Australian National University, Canberra, ACT Respondents Cassava food products of Australia Design Experimental Design or True experimentation Statistical tool *One-way ANOVA *Tukey t-tests
Procedure Duplicate or triplicate 100 mg samples of cassava products were
added to a small plastic bottle, a buffer/enzyme paper was added, followed by 1 mL of 1 M pH 6 phosphate buffer, a picrate paper and a screw cap lid. The bottles were allowed to stand overnight at 30 8C, the picrate papers were removed from the plastic support and 5.0 mL of water added to elute the colour. The absorbance was measured in a spectrophotometer at 510 nm and the total cyanide content in mg HCN equivalents/ kg fresh weight = ppm calculated by multiplying the absorbance by 396 (Egan et al., 1998; Bradbury et al., 1999). This gives an accurate total cyanide analysis down to a minimum of 1 ppm total cyanide (Haque and Bradbury, 2002; Bradbury, 2009). The cyanide present is primarily linamarin (Jørgensen et al., 2005). The assay used here measures both linamarin and acetone cyanohydrin, but the concentration of the latter is extremely small compared to linamarin. Any HCN released from acetone cyanohydrin is of relevance to human health, as it breaks down completely in the alkaline condition in the gut to give CN (Bradbury, 2009). The amount of lotaustralin and free cyanide (HCN and CN) is negligible (Jørgensen et al., 2005). Food was tested in the form that it is normally consumed, with cyanide expressed on a fresh weight (or ‘as consumed’) basis.
This survey revealed a wide range of cyanide concentrations in commonly available cassava-based products in Australia. As the negative impacts of excess cyanide consumption are well known, it is clear that careful regulation of the importation of cassava products may be necessary to monitor and control the amount of total cyanogens in ready-to-eat food products
However, we note a very significant reduction in total cyanide content of a recent sample of cassava chips to 7 ppm, which is below the safe limit, and shows the importance of the development of enforceable standards (Kolind-Hansen and Brimer, 2009). Apart from this sample, the toxicity of all samples of cassava chips and frozen cassava roots was much greater than the FSANZ limit of 10 ppm. Frozen roots are usually boiled, baked or fried before consumption, which can reduce the concentration of total cyanide in these products by 10–75% (Nambisan and Sundaresan, 1985; Montagnac et al., 2009b), but may not reduce the concentration below the safe limit. Consumption of such cyanide-containing products, therefore, poses a health risk, especially to consumers who are unaware of the need for detoxification of cassava Based on the results presented here it is strongly advisable that the maximum 10 ppm safe level for total cyanide in cassava products introduced by FSANZ (FSANZ, 2009) be monitored to ensure that cassava chips will be safe, as shown by the most recent result given in Table 2, and that frozen cassava root parenchyma will also be safe in Australia.
Carbamoylation correlates of cyanate neuropathy and cyanide poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity (Kimani et al.(2013). Carbamoylation correlates of cyanate neuropathy and cyanide
poisoning: relevance to the biomarkers of cassava cyanogenesis and motor system toxicity.SpringerPlus , 2:647 Page 8 of 8.)
We sought to elucidate the protein carbamoylation patterns associated with cyanate neuropathy relative to cyanide poisoning.
Carbamoylation Cyanate Cyanide Neuropathy Proteomics
Locale Center for Research on Occupational & Environmental Toxicology, OHSU, Portland Subject Young adult male Heterozygous rats Design Experimental Design or True Experimentation Statistical tool Correlation
Procedure We hypothesized that under a diet deficient in sulfur amino acids (SAA), the carbamoylation pattern associated with cyanide poisoning is similar to that of cyanate neuropathy. Male rats (6–8 weeks old) were fed a diet with all amino acids (AAA) or 75%-deficiency in SAA and treated with 2.5 mg/kg/body weight (bw) NaCN, or 50 mg/kg/bw NaOCN, or 1 μl/g/bw saline, for up to 6 weeks. Albumin and spinal cord proteins were analyzed using liquid chromatography mass spectrometry (LC-MS/MS). Only NaOCN induced motor deficits with significant levels of carbamoylation. At Day 14, we found a diet-treatment interaction effect on albumin carbamoylation (p = 0.07). At Day 28, no effect was attributed to diet (p = 0.71). Mean number of NaCN-carbamoylated sites on albumin was 47.4% higher relative to vehicle (95% CI:16.7-86.4%). Only NaOCN carbamoylated spinal cord proteins, prominently, under SAA-restricted diet. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclic-nucleotide 3'-phosphodiesterase. Under SAA deficiency, chronic but not acute cyanide toxicity may share biomarkers and pathogenetic similarities with cyanate neuropathy. Prevention of carbamoylation may protect against the neuropathic effects of cyanate.
Cassava is a carbohydrate-enriched and cyanogenic crop with a very low content in proteins and only 12% content in SAA, which are needed for humans to detoxify cyanide. The carbamoylation and neurotoxicity effects of cyanate may be influenced by diet with an exacerbating effect of dietary deficiency in sulfur amino acids. Cyanate hits proteins that are important in maintaining the shape and organization of the cytoskeleton, and hence, supporting mechanisms of neuronal survival. Proteins targets included myelin basic and proteolipid proteins, neurofilament light and glial fibrillary acidic proteins, and 2', 3' cyclicnucleotide 3'-phosphodiesterase
The aforementioned pattern of protein susceptibility to carbamoylation should inform such studies to elucidate the exact pathways and mechanisms leading to cyanate neuropathy (Han et al. 2013). Studies on the biomarkers and mechanisms of food (cassava) associated neurological diseases should consider the potential role of cyanate and its carbamoylation effects as endpoints of interest both at the experimental, clinical, and public health standpoints.
Motor impairments induced by microinjection of linamarin in the dorsal hippocampus of Wistar rats (E. Rivadeneyra-Domínguez a,∗, J.F. Rodríguez-Landa (2016). Motor impairments induced by microinjection of linamarin in the dorsal hippocampus of Wistar rats.Neuroligia. Vol. 31(8):516—522. )
This study aimed to determine the effects of intrahippocampal microinjection of linamarin on spontaneous motor activity (locomotor activity test) and motor coordination (rotarod and forced swimming tests) in Wistar rats.
Cassava Linamarin Tropical ataxic neuropathy Konzo Lateral swimming Motor impairment
Locale Universidad Veracruzana Respondents 32 three-month-old male Wistar rats Design Experimental design or True experimentation Statistical tool 2-way repeated measures ANOVA, post hocStudent—Newman—Keuls test
Procedure Male Wistar rats (3 months old), were assigned to 4 groups (n = 8 per group) as fol- lows: a vehicle-control group (receiving injectable solution 1 μl) and three groups receiving linamarin (10, 15, and 20 mM). The substances were microinjected intrahippocampally (CA1) every 24 hours for 7 consecutive days, and their effects on locomotor activity, rotarod, and swim tests were assessed daily.
Microinjection of linamarin into the dorsal hippocampus of the rat is associ- ated with impaired motor coordination, suggesting that the dorsal hippocampus, among other brain structures, may be affected by the neurological changes associated with inappropriate consumption of cassava in humans. The toxicity of the cyanogenic compounds of cassava mainly affects the brain structures involved in memory processing and integration, emotions, control of autonomic functions, smell, and motor function such as the thalamus, the piriform cortex, the hypothalamus, and the hippocampus Similarly, rats receiving treat- ment with cassava root juice (with a linamarin concentration of 0.30 mg/2 mL) also developed such motor alterations as poor motor coordination and lateral swimming,17 which microinjections of either linamarin or a vehicle to assess the effects of linamarin on behaviour.
The increase in these 2 types of behaviour suggests that linamarin microinjections into the dorsal hippocampus induced neuronal damage, thereby preventing the consolidation of visuospatial memory in a process that may be linked to the apparent state of ‘locomotor hyperactivity’. This hypothesis is supported by the fact that intact experimental animals or those receiving the vehicle display a gradual decrease in locomotor activity and vertical behaviour after performing the locomo- tor activity test several times,25 as occurred in our vehicle group. One possible explanation is that rats learn about which becomes familiar, resulting in a decreased need for exploration spontaneous motor activity. However, rats treated with linamarin show hippocampal damage, which is likely to impair learning and memory consolidation. If this the case, rat would not recognize the conditions of the cage and wood therefore explore as with new or unknown setting. We should highlight that increased locomotor activity over reapeated sessions of the lovomotor activity test has also been observed in rats undergoing dorsal hippocampus microinjection or neurotoxix cycad derivatives or receiving cassava root juice rally.
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