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The effect of dietary fibre sources on aflatoxicosis in the weanling male rat

Published online by Cambridge University Press:  09 March 2007

D. L. Frape ,
B. J. Wayman  and
Mary G. Tuck
D. L. Frape
Affiliation:
The Priory, Church Yard, Mildenhall, Suffolk IP28 7EE
B. J. Wayman
Affiliation:
Dalgety Spillers Ltd., Research & Technology Centre, Station Road, Cambridge CB1 2JN
Mary G. Tuck
Affiliation:
Dalgety Spillers Ltd., Research & Technology Centre, Station Road, Cambridge CB1 2JN
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Abstract

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1. Two experiments with male weanling rats were conducted in which they received individually and restrictedly either a basal semi-purified diet containing starch as the principal carbohydrate or the same diet to which mixed aflatoxins were added in quantities providing from 0·13 to 0·4 mg aflatoxin B1 /kg diet. Various natural ingredients, or semi-purified sources of dietary fibre were substituted for a portion of the starch in the basal diet containing aflaloxin. The diets were fed for 13–14 weeks after which the rats were given ad lib. a commercial rodent diet until they were killed at 109 weeks of age.

2. Two further experiments were conducted in which twenty-four rats in each experimentreceived the basal diet plus aflatoxin, or diets in which a portion of the starch was replaced by gum arabic or by wheat offal. After 13 or more weeksthe absorption, retention and excretion of 14C-labelled aflaloxin B1 was measured in each rat.

3. The addition of gum arabic or wheat bran to the diet decreased the effects of the toxin in the first two experiments, but as measured by several characteristics, only wheat bran provided an effect which persisted during the period when neither it nor the toxin was given. The effects included an apparent reduction in tumour incidence. The change in the content of starch in the basal diet, occurring as a consequence of adding the test ingredients is also considered to be an associated cause of the effects observed

4. In comparison to starch, wheat offal increased the total 14C in the faeces and the proportion of the total found during the first 48 h after dosing. Rats receiving starch excreted more 14C in their urine and retained more 14C in their livers. The differences between gum arabic and starch were not significant as measured by 14C excretion and retention. Liver size as a proportion of carcass weight was less in rats receiving wheat offal or gum arabic, and rats receiving wheat offal had a lower incidence of fat-loaded hepatocytes.

5. The interaction of dietary toxins, or drugs, with the ingredient composition of diet may affect animal response even when the diets are adequate and similar in nutrient composition. This may be of significance both in drug-safety studies and in animal production.

Type
Papers on General Nutrition
Information
British Journal of Nutrition , Volume 46 , Issue 2 , September 1981 , pp. 315 - 326
Copyright
Copyright © The Nutrition Society 1981

References

Alfin-Slater, R. B., Aftergood, L. & Wells, P. (1975). J. Am. Oil Chem. Soc. 52, 266.CrossRefGoogle Scholar
Butler, W. H. & Neal, G. E. (1973). Cancer Res. 33, 2878.Google Scholar
Dickerson, J. W. T., Basu, T. K. & Parke, D. V. (1971). Proc. Nutr. Soc. 30, 27A.Google Scholar
Frape, D. L., Wayman, B. J. & Tuck, M. G. (1979). J. Agric. Sci., Camb. 93, 133.CrossRefGoogle Scholar
Frape, D. L., Wayman, B. J. & Wilkinson, J. (1981 a). Nutr. Rep. Int. 23(1), 163.Google Scholar
Frape, D. L., Wayman, B. J. & Wilkinson, J. (1981 b). Nutr. Rep. Int. 23(1), 171.Google Scholar
Frape, D. L., Wilkinson, J. & Chubb, L. G. (1970). Lab. Anim. 4, 67.CrossRefGoogle Scholar
McLean, A. E. M. & McLean, E. K. (1967). Proc. Nutr. Soc. 26, xiii.Google Scholar
McLean, A. E. M. & McLean, E. K. (1969). Br. med. Bull. 25, 278.CrossRefGoogle Scholar
McLean, A. E. M. & Marshall, A. (1971). Br. J. exp. Path 52, 322.Google Scholar
Madhavan, T. V. & Goplan, C. (1965). Archs. Path. 80, 123.Google Scholar
Ness, A. T., Dickerson, H. C. & Pastewka, J. V. (1965). Clinica chimica Acta, 12, 532.CrossRefGoogle Scholar
Newberne, P. M., Chan, W-C. M. & Rogers, A. E. (1974). Toxic. appl. Pharmac. 28, 200.CrossRefGoogle Scholar
Newberne, P. M., Harrington, D. H. & Wogan, G. N. (1966). Lab. Invest. 15, 962.Google Scholar
Owen, D. E., Munday, K. A., Taylor, T. G. & Turner, M. R. (1975). Proc. Nutr. Soc. 34, 16A.Google Scholar
Patterson, D. S. P. (1973). Food & Cosmet. Toxicol. 11, 287.CrossRefGoogle Scholar
Patterson, D. S. P. & Allcroft, R. (1970). Food & Cosmet. Toxicol. 8, 43.CrossRefGoogle Scholar
Ranhotra, G. S., Loewe, R. J. & Puyat, L. V. (1977). J. Fd. Sci. 42, 1587.CrossRefGoogle Scholar
Riottot, M., Sacquet, E., Mejean, C. & Leprince, C. (1975). Nutr. Rep. Int. 12, 1.Google Scholar
Rogers, A. E. & Newberne, P. M. (1971). Nature, Lond. 229, 62.CrossRefGoogle Scholar
Wicks, A. C. B., Yeates, J. & Heaton, K. W. (1978). Scand. J. Gastroenterol. 13, 289.CrossRefGoogle Scholar
Wise, A., Suzangar, M., Messripour, M. & Mohammade, J. (1978). Br. J. Nutr. 40, 397.CrossRefGoogle Scholar
Wogan, G. N., Paglialunga, S. & Newberne, P. M. (1974). Food & Cosmet. Toxicol. 12, 681.CrossRefGoogle Scholar
Wogan, G. N. & Pong, R. S. (1970). Ann. N.Y. Acad. Sci. 174, 623.CrossRefGoogle Scholar
Yacowitz, H., Fleischman, A. I. & Kritchevsky, D. (1976). 2nd Jt. Mtg. Am. Inst. Nutr., Am. Soc. Clin. Nutr., Nutr. Soc. Can. 26, Abstr. 39.Google Scholar
Yoskikura, H.(1974). Nature, Lond. 252, 71.CrossRefGoogle Scholar