Hostname: page-component-848d4c4894-nr4z6 Total loading time: 0 Render date: 2024-06-03T15:31:07.531Z Has data issue: false hasContentIssue false
  • English
  • Français

Serum enzyme changes, muscular dystrophy and erythrocyte abnormalities in lambs fed on diets containing cod-liver oil and maize oil, and the therapeutic effect of vitamin E

Published online by Cambridge University Press:  09 March 2007

J. W. Boyd
J. W. Boyd
Affiliation:
Biochemistry Department, ARC Institute of Animal Physiology, Babraham, Cambridge
Rights & Permissions [Opens in a new window]

Abstract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. Lambs fed on skim milk containing either maize oil or cod-liver oil or both were observed for signs of muscular dystrophy, changes in serum enzymes and increases in the susceptibility of red cells to haemolysis by peroxide (peroxide haemolysis).

2. Four lambs fed on the milk containing cod-liver oil, and not receiving α-tocopheryl acetate injections, developed acute muscular dystrophy, but no abnormal changes occurred in peroxide haemolysis, packed cell volume or haemoglobin concentration in the blood. Marked increases occurred in the aspartate transaminase, alanine transaminase and glutamate dehydrogenase, and in lactate dehydrogenase isoenzyme activities of the serum, presumably due to leakage from the degenerating tissues. One lamb given weekly injections of 100 mg α-tocopheryl acetate remained clinically normal and maintained normal serum enzyme levels. Treatment of dystrophic animals with 200 mg α-tocopheryl acetate by injection produced prompt clinical recovery and an exponential decline in the raised serum enzyme activities.

3. In the five lambs fed on the skim-milk containing maize oil, muscular dystrophy did not occur. Small but significant increases occurred, however, in serum aspartate transaminase and glutamate dehydrogenase activities. In all five animals peroxide haemolysis was greatly increased, but in only two did packed cell volume and haemoglobin values fall slightly below the lower limit of normal (mean − 2 × SD). Injections of 100–200 mg α-tocopheryl acetate neither prevented nor cured the abnormally high levels of serum enzymes and peroxide haemolysis, although a change in the diet was followed by a gradual return to normal. In one lamb given massive doses of α-tocopherol by mouth, peroxide haemolysis was not reduced. Large amounts of α-tocopherol added in vitro to erythrocytes from the lamb did, however, prevent peroxide haemolysis.

4. Peroxide haemolysis did not increase in any of three lambs fed on skim milk containing both maize oil and cod-liver oil, although two of them, which were given much larger amounts of cod-liver oil than the third, developed muscular dystrophy with elevated serum enzyme levels.

5. Peroxide haemolysis in lambs is evidently not a measure of vitamin E deficiency. It is suggested that increased peroxide haemolysis in lambs, like encephalomalacia in chicks, depends on the fatty acid composition of the unsaturated lipids in the diet.

Type
Research Article
Information
British Journal of Nutrition , Volume 22 , Issue 3 , September 1968 , pp. 411 - 422
Copyright
Copyright © The Nutrition Society 1968

References

Boyd, J. W. (1962). Res. vet. Sci. 3, 256.CrossRefGoogle Scholar
Boyd, J. W. (1964). Res. vet. Sci. 5, 419.CrossRefGoogle Scholar
Boyd, J. W. (1966). Biochim. biophys. Acta 113, 302.CrossRefGoogle Scholar
Boyd, J. W. (1967). Biochim. biophys. Acta 132, 221.CrossRefGoogle Scholar
Century, B. & Horwitt, M. K. (1959). Proc. Soc. exp. Biol. Med. 102, 375.CrossRefGoogle Scholar
Century, B. & Horwitt, M. K. (1960). J. Nutr. 72, 357.CrossRefGoogle Scholar
Century, B., Witting, L. A., Harvey, C. C. & Horwitt, M. K. (1961). J. Nutr. 75, 341.CrossRefGoogle Scholar
Century, B., Witting, L. A., Harvey, C. C. & Horwitt, M. K. (1963). Am. J. clin. Nutr. 13, 362.CrossRefGoogle Scholar
Dam, H., Nielsen, G. K., Prange, I. & Søndergaard, E. (1958). Nature, Lond. 182, 802.CrossRefGoogle Scholar
De Gier, J. & Van Deenen, L. L. M. (1964). Biochim. biophys. Acta 84, 294.Google Scholar
Gaddum, J. H. (1945). Nature, Lond. 156, 463.CrossRefGoogle Scholar
Green, J., Diplock, A. T., Bunyan, J., McHale, D. & Muthy, I. R. (1967). Br. J. Nutr. 21, 69.CrossRefGoogle Scholar
Harris, P. L. & Embree, N. D. (1963). Am. J. clin. Nutr. 13, 385.CrossRefGoogle Scholar
Hassan, H., Hashim, S. A., Van Itallie, T. B. & Sebrell, W. H. (1966). Am. J. clin. Nutr. 19, 147.CrossRefGoogle Scholar
Hopkins, L. L. Jr, Pope, A. L. & Baumann, C. A. (1964). J. Anim. Sci. 23, 674.CrossRefGoogle Scholar
Horwitt, M. K. (1960). Am. J. clin. Nutr. 8, 451.CrossRefGoogle Scholar
Horwitt, M. K., Century, B. & Zeman, A. A. (1963). Am. J. clin. Nutr. 12, 99.CrossRefGoogle Scholar
Horwitt, M. K., Harvey, C. C., Duncan, G. D. & Wilson, W. C. (1956). Am. J. clin. Nutr. 4, 408.CrossRefGoogle Scholar
Kuttler, K. L. & Marble, D. W. (1960). Am. J. vet. Res. 21, 437.Google Scholar
Mohrhauer, H. & Holman, R. T. (1963). J. Nutr. 81, 67.CrossRefGoogle Scholar
Paulson, G. D., Pope, A. L. & Baumann, C. A. (1966). Proc. Soc. exp. Biol. Med. 122, 321.CrossRefGoogle Scholar
Rose, C. S. & György, P. (1952). Am. J. Physiol. 168, 414.CrossRefGoogle Scholar
Thafvelin, B. (1960). Nature, Lond. 188, 1169.CrossRefGoogle Scholar
Wieme, R. J. & Herpol, J. E. (1962). Nature, Lond. 194, 287.CrossRefGoogle Scholar
Witting, L. A., Harvey, C. C., Century, B. & Horwitt, M. K. (1961). J. Lipid Res. 2, 412.CrossRefGoogle Scholar