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2143. Not-so-sweet potato
NATURAL PRODUCTS
455
2142. A surfeit of lysine Acheampong-Mensah, D. K. & Hill, D. C. (1970). Effect of excess dietary lysine on the weanling rat. Nutr. Rep. Int. 2, 9. Last month we referred to teratogenic malformations induced in chicks by the amino acid lysine (Cited in F.C.T. 1971,9, 309), and toxic effects due to an excess of dietary lysine have been reported by several authors. As little as 0.4 ~ lysine was toxic to week-old chicks, but the effect could be corrected by arginine (ibid 1969, 7, 457). An increase in kidney arginase accompanied the toxic effect (Nutrition Reviews 1968, 26, 89). Recent work on weanling rats (Cited in F.C.T. 1971,9, 137) indicated that, in this species, somewhat higher concentrations of lysine (7-10~o) were required to produce signs of toxicity. The present report deals further with the problem of lysine toxicity in weanling rats and investigates the action of arginine and the levels of arginase in this species. Weanling rats were fed for l wk on a basal (10~) casein diet and then transferred to diets containing casein and various amino acids. Dietary levels of 3~o lysine with 10~o casein or 6 ~o lysine with 20 ~ casein were required to produce a significant drop in weight gain, but the toxicity was slightly increased when the diet was deficient in arginine. Conversely, the toxicity of lysine could be relieved by supplementing the diets with arginine although in neither case was the interaction between lysine and arginine effects significant. Deficiencies of methionine, tyrosine and threonine did not accentuate the toxicity of lysine. There was no evidence for an increase in liver arginase activity; rather a consistent, if small, decrease was indicated. Arginase activity was elevated when the dietary protein level was increased and this was paralleled by an increase in urea excretion. A small rise in urea excretion was also observed with high levels of lysine, but this did not require any increase in arginase activity. It is clear that, in the rat, lysine toxicity is comparatively mild and can be moderated by arginine supplementation. This is probably a general effect, rather than a reflection of a specific or close relationship between lysine and arginine metabolism such as appears to exist in the chick. This conclusion is supported by the markedly different effect of lysine on arginase activity in the two species.
2143. Not-so-sweet potato Wilson, B. J., Yang, D. T. C. & Boyd, M. R. (1970). Toxicity of mould-damaged sweet potatoes (Ipomoea batatas). Nature, Lond. 227, 521. We are fast collecting a wide variety of moulds which produce toxic metabolites in foodstuffs, the most notorious being the aflatoxin producers (Cited in F.C.T. 1970, 8, 695). The present study stemmed from an outbreak of a fatal disease among beef cattle in Georgia, an incident in which the consumption of mouldy sweet-potato tubers was implicated. As in earlier cases of cattle poisoning associated with mouldy sweet potatoes, the cattle which died in this outbreak were found to have marked respiratory-tract lesions. Among the moulds found on the offending tubers were Penicillium, Aspergillus and Fusarium spp., none of them toxic per se, as far as could be seen from tests in mice of extracts of cultures of the fungal isolates. Residues of ether extracts from the infected vegetables were dark-brown to yellow oils, often with a pungent odour. Mice given 30-50 mg of this material by stomach tube developed generalized illness, followed within a few hours by progressively laboured respiration, with death occurring within 8-24 hr, preceded by brief convulsions. At necropsy there was gross and microscopic evidence of lung oedema FOOD 9/3--I
456
NATURAL PRODUCTS
with pleural exudates. Moreover, there were often toxic cell changes in the liver, spleen and kidneys. Thin-layer chromatography of the extractive using Ehrlich reagent revealed three main constituents: Ipomeamarone, the corresponding alcohol ipomeamaronol, and a third Ehrlich-positive compound which proved to be responsible for the respiratory-tract lesions but caused no liver damage when administered to mice. These compounds were produced experimentally by inoculating sweet-potato slices with a pure culture of Fusariumjavanicum. Perhaps the most alarming aspect of this investigation was the discovery that all three toxins described were found, together with related metabolites, in extracts of sweet potatoes showing only minor blemishes and bought from the food-produce markets in Nashville, Tennessee. The toxins were not removed by the normal processes of baking and boiling, ethereal extracts from tubers cooked in this way remaining toxic to mice. 2144. A trio on tannins
Glick, Z. & Joslyn, M. A. (1970). Food intake depression and other metabolic effects of tannic acid in the rat, J. Nutr. 100, 509. Glick, Z. & Joslyn, M. A. (1970). Effect of tannic acid and related compounds on the absorption and utilization of proteins in the rat. J. Nutr. 100, 516. Tamir, Musha & Alumot, Eugenia (1970). Carob tannins--growth depression and levels of insoluble nitrogen in the digestive tract of rats. J. Nutr. 100, 573. Considerable quantities of naturally-occurring tannins present in tea, coffee and other foods are consumed by man in his daily diet, and vegetable tannins found in carobs may be present in animal feeds. Various grades of tannic acid have been used in barium enemas and as food additives, and their toxicity has already been reported (Cited in F.C.T. 1967, 5, 244; ibid 1969, 7, 364). Reduced growth rates in young weanling rats fed diets containing tannins and related phenolics (ibid 1970, 8, 116) have been attributed to the unpalatability of the diet and the ability of tannins to bind with proteins. The work now described concerns the effects of tannic acid and related compounds and of the hydrolysable and condensed tannins found respectively in green and ripe carobs on growth and faecal excretion of nitrogen in young rats. Glick & Joslyn (first paper cited above) measured the food intake and growth of weanling rats fed laboratory diets containing 4, 5 or 8 ~ tannic acid for periods up to 36 days. When compared with values in control animals, growth and food intake were depressed, particulady in animals receiving 8 ~ tannic acid. Similar initial depressions in growth were seen in pair-fed controls, but their subsequent weight gain was greater than that of test animals, suggesting that some toxic effect occurred in addition to the unpalatability of the diet. Supplementing the diets with methionine or choline did not prevent similar weight-gain depression, but additional casein in the diet slightly improved the growth of the test animals. The same workers (second paper cited above) subsequently studied the faecal excretion of nitrogen in rats fed diets containing up to 8 ~o tannic acid, 10 ~o gallic acid or 5 ~ of other vegetable tannins. Attempts were made to identify the source of the increased faecal nitrogen by the use of diets supplemented with 14C-labelled casein and by proteolytic enzyme assays of the intestinal contents and pancreas. In rats receiving tannic acid, grape-seed tannins or quebracho tannins in their diet, a significant increase in faecal nitrogen was observed. This increase was not, however, accompanied by an increase in the excretion of 14C from the labelled casein, suggesting that ingested casein was not a major source of the high faecal nitrogen levels, which were more probably derived in these animals from enzyme
455
2142. A surfeit of lysine Acheampong-Mensah, D. K. & Hill, D. C. (1970). Effect of excess dietary lysine on the weanling rat. Nutr. Rep. Int. 2, 9. Last month we referred to teratogenic malformations induced in chicks by the amino acid lysine (Cited in F.C.T. 1971,9, 309), and toxic effects due to an excess of dietary lysine have been reported by several authors. As little as 0.4 ~ lysine was toxic to week-old chicks, but the effect could be corrected by arginine (ibid 1969, 7, 457). An increase in kidney arginase accompanied the toxic effect (Nutrition Reviews 1968, 26, 89). Recent work on weanling rats (Cited in F.C.T. 1971,9, 137) indicated that, in this species, somewhat higher concentrations of lysine (7-10~o) were required to produce signs of toxicity. The present report deals further with the problem of lysine toxicity in weanling rats and investigates the action of arginine and the levels of arginase in this species. Weanling rats were fed for l wk on a basal (10~) casein diet and then transferred to diets containing casein and various amino acids. Dietary levels of 3~o lysine with 10~o casein or 6 ~o lysine with 20 ~ casein were required to produce a significant drop in weight gain, but the toxicity was slightly increased when the diet was deficient in arginine. Conversely, the toxicity of lysine could be relieved by supplementing the diets with arginine although in neither case was the interaction between lysine and arginine effects significant. Deficiencies of methionine, tyrosine and threonine did not accentuate the toxicity of lysine. There was no evidence for an increase in liver arginase activity; rather a consistent, if small, decrease was indicated. Arginase activity was elevated when the dietary protein level was increased and this was paralleled by an increase in urea excretion. A small rise in urea excretion was also observed with high levels of lysine, but this did not require any increase in arginase activity. It is clear that, in the rat, lysine toxicity is comparatively mild and can be moderated by arginine supplementation. This is probably a general effect, rather than a reflection of a specific or close relationship between lysine and arginine metabolism such as appears to exist in the chick. This conclusion is supported by the markedly different effect of lysine on arginase activity in the two species.
2143. Not-so-sweet potato Wilson, B. J., Yang, D. T. C. & Boyd, M. R. (1970). Toxicity of mould-damaged sweet potatoes (Ipomoea batatas). Nature, Lond. 227, 521. We are fast collecting a wide variety of moulds which produce toxic metabolites in foodstuffs, the most notorious being the aflatoxin producers (Cited in F.C.T. 1970, 8, 695). The present study stemmed from an outbreak of a fatal disease among beef cattle in Georgia, an incident in which the consumption of mouldy sweet-potato tubers was implicated. As in earlier cases of cattle poisoning associated with mouldy sweet potatoes, the cattle which died in this outbreak were found to have marked respiratory-tract lesions. Among the moulds found on the offending tubers were Penicillium, Aspergillus and Fusarium spp., none of them toxic per se, as far as could be seen from tests in mice of extracts of cultures of the fungal isolates. Residues of ether extracts from the infected vegetables were dark-brown to yellow oils, often with a pungent odour. Mice given 30-50 mg of this material by stomach tube developed generalized illness, followed within a few hours by progressively laboured respiration, with death occurring within 8-24 hr, preceded by brief convulsions. At necropsy there was gross and microscopic evidence of lung oedema FOOD 9/3--I
456
NATURAL PRODUCTS
with pleural exudates. Moreover, there were often toxic cell changes in the liver, spleen and kidneys. Thin-layer chromatography of the extractive using Ehrlich reagent revealed three main constituents: Ipomeamarone, the corresponding alcohol ipomeamaronol, and a third Ehrlich-positive compound which proved to be responsible for the respiratory-tract lesions but caused no liver damage when administered to mice. These compounds were produced experimentally by inoculating sweet-potato slices with a pure culture of Fusariumjavanicum. Perhaps the most alarming aspect of this investigation was the discovery that all three toxins described were found, together with related metabolites, in extracts of sweet potatoes showing only minor blemishes and bought from the food-produce markets in Nashville, Tennessee. The toxins were not removed by the normal processes of baking and boiling, ethereal extracts from tubers cooked in this way remaining toxic to mice. 2144. A trio on tannins
Glick, Z. & Joslyn, M. A. (1970). Food intake depression and other metabolic effects of tannic acid in the rat, J. Nutr. 100, 509. Glick, Z. & Joslyn, M. A. (1970). Effect of tannic acid and related compounds on the absorption and utilization of proteins in the rat. J. Nutr. 100, 516. Tamir, Musha & Alumot, Eugenia (1970). Carob tannins--growth depression and levels of insoluble nitrogen in the digestive tract of rats. J. Nutr. 100, 573. Considerable quantities of naturally-occurring tannins present in tea, coffee and other foods are consumed by man in his daily diet, and vegetable tannins found in carobs may be present in animal feeds. Various grades of tannic acid have been used in barium enemas and as food additives, and their toxicity has already been reported (Cited in F.C.T. 1967, 5, 244; ibid 1969, 7, 364). Reduced growth rates in young weanling rats fed diets containing tannins and related phenolics (ibid 1970, 8, 116) have been attributed to the unpalatability of the diet and the ability of tannins to bind with proteins. The work now described concerns the effects of tannic acid and related compounds and of the hydrolysable and condensed tannins found respectively in green and ripe carobs on growth and faecal excretion of nitrogen in young rats. Glick & Joslyn (first paper cited above) measured the food intake and growth of weanling rats fed laboratory diets containing 4, 5 or 8 ~ tannic acid for periods up to 36 days. When compared with values in control animals, growth and food intake were depressed, particulady in animals receiving 8 ~ tannic acid. Similar initial depressions in growth were seen in pair-fed controls, but their subsequent weight gain was greater than that of test animals, suggesting that some toxic effect occurred in addition to the unpalatability of the diet. Supplementing the diets with methionine or choline did not prevent similar weight-gain depression, but additional casein in the diet slightly improved the growth of the test animals. The same workers (second paper cited above) subsequently studied the faecal excretion of nitrogen in rats fed diets containing up to 8 ~o tannic acid, 10 ~o gallic acid or 5 ~ of other vegetable tannins. Attempts were made to identify the source of the increased faecal nitrogen by the use of diets supplemented with 14C-labelled casein and by proteolytic enzyme assays of the intestinal contents and pancreas. In rats receiving tannic acid, grape-seed tannins or quebracho tannins in their diet, a significant increase in faecal nitrogen was observed. This increase was not, however, accompanied by an increase in the excretion of 14C from the labelled casein, suggesting that ingested casein was not a major source of the high faecal nitrogen levels, which were more probably derived in these animals from enzyme