Hostname: page-component-586b7cd67f-t7czq Total loading time: 0 Render date: 2024-11-27T13:35:28.486Z Has data issue: false hasContentIssue false
  • English
  • Français

On the postulated peroxidation of unsaturated lipids in the tissues of vitamin E-deficient rats

Published online by Cambridge University Press:  09 March 2007

J. Bunyan ,
J. Green ,
Elspeth A. Murrell ,
A. T. Diplock  and
M. A. Cawthorne
J. Bunyan
Affiliation:
Walton Oaks Experimental Station, Vitamins Ltd, Tadworth, Surrey
J. Green
Affiliation:
Walton Oaks Experimental Station, Vitamins Ltd, Tadworth, Surrey
Elspeth A. Murrell
Affiliation:
Walton Oaks Experimental Station, Vitamins Ltd, Tadworth, Surrey
A. T. Diplock
Affiliation:
Walton Oaks Experimental Station, Vitamins Ltd, Tadworth, Surrey
M. A. Cawthorne
Affiliation:
Walton Oaks Experimental Station, Vitamins Ltd, Tadworth, Surrey
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. The micro-iodimetric method has been used to study some factors affecting the concentration of lipid peroxides in the adipose tissue of vitamin E-deficient rats.

2. Cod-liver oil methyl esters (CLOME) or maize oil methyl esters (MOME) with peroxide values ranging from 3 to 330 μ-equiv./g were given by mouth to vitamin E-deficient rats deprived of food before and after the dose. Lipid peroxides did not accumulate in the adipose tissue of these rats.

3. Experiments with dietary CLOME and MOME of varying peroxide values (2–230 μ-equiv./g) showed that exogenous lipid peroxide accumulates in the adipose tissue when the rats received these lipids at 10% in the diet for 4 weeks, but not if the dietary concentration was only 4% or if the diet with 10% lipid was given for 5 days only.

4. Rats were given dietary CLOME for 4 weeks. Their adipose tissue was then found to contain about 50 μ-equiv. lipid peroxide/g. They were divided into three groups. One group was given a fat-free diet and, after 10 days, the adipose tissue concentration of lipid peroxide had decreased to about 10 μ-equiv./g. The other groups were given the fat-free basal diet supplemented with vitamin E or DPPD (N,N′-diphenyl-p-phenylenediamine). Neither supplement significantly affected the rate of disappearance of the peroxides from the adipose tissue.

5. It was shown that neither α-tocopherol nor DPPD reacted with the lipid peroxides of CLOME or MOME in vitro, at room temperature or even after 65 h at 37°.

6. It was concluded that unsaturated lipids do not become peroxidized after incorporation into the adipose tissue of vitamin E-deficient rats. Lipid peroxides taken up from the diet into the adipose tissue are not of fleeting existence, having a half-life of about 6 days. Dietary vitamin E probably prevents the accumulation of exogenous lipid peroxides in the adipose tissue by reinforcing the barrier to their absorption in the gut.

7. These studies provide further evidence that current concepts of lipid peroxidation in vitamin E-deficient animals are incorrect. In fact, vitamin E-deficient animals have low concentrations of peroxide in their adipose tissue, unless they have received large amounts of unsaturated lipid for long periods, and the role of vitamin E in controlling this concentration is not due to any effect on peroxidation in vivo.

Type
Research Article
Information
British Journal of Nutrition , Volume 22 , Issue 1 , February 1968 , pp. 97 - 110
Copyright
Copyright © The Nutrition Society 1968

References

Aaes-Jorgensen, E. (1949). Int. Congr. Biochem. I.Cambridge.Abstr. Commun. p. 57.Google Scholar
Brown, R. G., Button, G. M. & Smith, J. T. (1967). J. Nutr. 91, 99.CrossRefGoogle Scholar
Bunyan, J., McHale, D. & Green, J. (1963). Br. J. Nutr. 17, 391.CrossRefGoogle Scholar
Bunyan, J., Murrell, E. A., Green, J. & Diplock, A. T. (1967). Br. J. Nutr. 21, 475.CrossRefGoogle Scholar
Carpenter, M. P. (1967). Fedn Proc. Fedn Am. Socs exp. Biol. 26, 475.Google Scholar
Christensen, F., Dam, H., Prange, I. & Søndergaard, E. (1958). Acta pharm. tox. 15, 181.CrossRefGoogle Scholar
Dam, H. (1962). Vitams Horm. 20, 527.CrossRefGoogle Scholar
Dam, H. & Granados, H. (1945). Acta physiol. scand. 10, 162.CrossRefGoogle Scholar
Diplock, A. T., Bunyan, J., McHale, D. & Green, J. (1967). Br. J. Nutr. 21, 103.CrossRefGoogle Scholar
Emmel, V. M. & LaCelle, P. L. (1961). J. Nutr. 75, 335.CrossRefGoogle Scholar
Filer, L. J., Rumery, R. E. & Mason, K. E. (1946). Trans. 1st Conf. on Biological Antioxidants, p. 67. New York.Google Scholar
Folkers, K., Smith, J. L. & Moore, H. W. (1965). Fedn Proc. Fedn Am. Socs exp. Biol. 24, 79.Google Scholar
Ghoshal, A. K. & Recknagel, R. O. (1965). Life Sciences 4, 1521.CrossRefGoogle Scholar
Green, J., Diplock, A. T., Bunyan, J., McHale, D. & Muthy, I. (1967). Br. J. Nutr. 21, 69.CrossRefGoogle Scholar
Guha, A. & Roels, O. A. (1965). Biochim. biophys. Acta 111, 364.CrossRefGoogle Scholar
Kokatnur, M. G., Bergan, J. G. & Draper, H. H. (1966). Proc. Soc. exp. Biol. Med. 123, 254.CrossRefGoogle Scholar
Kummerow, F. A. (1964). Fedn Proc. Fedn Am. Socs exp. Biol. 23, 1053.Google Scholar
MacGee, J. (1959). Analyt. Chem. 31, 298.CrossRefGoogle Scholar
Marcos, T. N., Fodor, G. P., Kovacs, V. V. & Katonai, B. (1966). J. Nutr. 90, 219.CrossRefGoogle Scholar
Martin, A. J. P. & Moore, T. (1939). J. Hyg. Camb. 39, 643.Google Scholar
Mason, K. E., Dam, H. & Granados, H. (1946). Anat. Rec. 94, 265.CrossRefGoogle Scholar
O'Brien, P. J. & Frazer, A. C. (1966). Proc. Nutr. Soc. 25, 9.CrossRefGoogle Scholar
Slater, E. C. (1962). Vitams Horm. 20, 521.CrossRefGoogle Scholar
Tappel, A. L. (1962). In Lipids and their Oxidation, p. 387. [Schultz, H. W., editor.] Westport, Connecticut: The Avi Publishing Co., Inc.Google Scholar
Tappel, A. L. (1965). Fedn Proc. Fedn Am. Socs exp. Biol. 24, 73.Google Scholar
Witting, L. A. (1965). Fedn Proc. Fedn Am. Socs exp. Biol. 24, 912.Google Scholar
Wright, A. S., Crowne, R. S. & Hathway, D. E. (1965). Biochem. J. 95, 98.CrossRefGoogle Scholar