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The effect of dietary fats on the composition of the liver endoplasmic reticulum and oxidative drug metabolism

Published online by Cambridge University Press:  09 December 2008

Catherine T. Hammer
Affiliation:
Department of Biochemistry, The Medical College of St Bartholomew's Hospital, Charterhouse Square, LondonECIM 6BQ
E. D. Wills
Affiliation:
Department of Biochemistry, The Medical College of St Bartholomew's Hospital, Charterhouse Square, LondonECIM 6BQ
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Abstract

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1. The dependence of the rate of oxidative demethylation in the liver endoplasmic reticulum on the fatty acid composition of the endoplasmic reticulum has been studied by varying the lipid content of the diet.

2. The rate of oxidative demethylation was markedly dependent on the percentage of linoleic acid (18:2) incorporated into the membrane. Feeding diets containing (g/kg) 100 coconut oil, 100 lard or 100 maize oil caused respectively the incorporation of 7.6, 10.3 and 25.1% linoleic acid (18:2) and a demethylation rate of 3.26, 3.15 and 5.03 nmol formaldehyde/min per mg protein. Feeding 100 g herring oil/kg diet caused incorporation of only 5.1% C18:2 but also 27.2% ωw3 unsaturated fatty acids, including 8.7% eicosapentaenoic acid (20:5) and 17.0% docosahexaenoic acid (22.6) and caused a very high rate of oxidative demethylation (6.53 nmol formaldehyde/min per mg protein).

3. Destruction of the polyunsaturated fatty acids in herring oil by irradiation with 400 krad caused incorporation of a smaller quantity of ωw3 unsaturated acids into the endoplasmic reticulum and decreased the rate of oxidative demethylation (4.83 nmol formaldehyde/min per mg protein).

4. The inductive effects of phenobarbitone on oxidative demethylation were partially dependent on changes in the fatty acid composition of the endoplasmic reticulum. Phenobarbitone (100 mg/kg) increased the percentage of C18:2 from 25.1 to 29.4% in rats given a maize-oil diet, increased the percentage of C20:5 from 8.7 to 10.3% in rats given a herring-oil diet and decreased the percentage of arachidonic acid (20:4) and C22:6 in rats given a lard, maize-oil, herring-oil or irradiated-herring-oil diet.

5. Intraperitoneal α-tocopherol (50 mg/kg) increased the percentage of C20:4 from 11.1 to 13.1% in rats given a lard diet and from 5.9 to 7.3% in rats given a herring-oil diet.

6. It is concluded that dietary C18:2 is an important factor in the regulation of the rate of oxidative demethylation in the liver endoplasmic reticulum but this may be replaced effectively by dietary C20:5 ω3 and C22:6 ω3 acids. Oxidative demethylation is regulated by changes in the fatty acid composition of the membranes of the liver endoplasmic reticulum.

Type
Papers of direct relevance to Clinical and Human Nutrition
Copyright
Copyright © The Nutrition Society 1979

References

Chapman, D. (1973). In Form and Function of Phospholipids p.117, (Ansell, G. B., Hawthorne, J. N. and Dawson, R. M. C., editors). Amsterdam: Elsevier.Google Scholar
Davison, S. C. & Wills, E. D. (1974). Biochem. J. 142, 19.CrossRefGoogle Scholar
Diplock, A. T., Bunyan, J., Green, J. & Edwin, E. E. (1961). Biochem. J. 79, 105.CrossRefGoogle Scholar
Fouts, J.R. & Rogers, L.A. (1965). J. Pharmac. exp. Ther. 147, 112.Google Scholar
Fricke, H., Hart, E.J. & Smith, H.P. (1938). J. chem Phys. 6, 229.CrossRefGoogle Scholar
Hammer, C.T. & Wills, E.D. (1979). Int. J. Rad. Biol. (In the Press.)Google Scholar
Ingelman-Sundberg, M. (1977). Biochim. biophys. Acta 488, 225.CrossRefGoogle Scholar
Ingelman-Sundberg, M. & Gustafsson, J. (1975). Biochem. Soc. Trans. 3, 977.CrossRefGoogle Scholar
Kamath, S. A. & Rubin, E. (1972). Biochem. biophys. Res. Commun. 49, 52.CrossRefGoogle Scholar
Lambert, L. & Wills, E. D. (1977 a). Biochem. Pharmac. 26, 1417.CrossRefGoogle Scholar
Lambert, L. & Wills, E. D. (1977 b). Biochem. Pharmac. 26, 1423.Google Scholar
Lu, A. Y. H., Junk, K. W. & Coon, M. J. (1969). J. biol. Chem. 244, 3714.CrossRefGoogle Scholar
Lucy, J. A. (1972). Ann. N. Y. Acad. Sci. 203, 4.CrossRefGoogle Scholar
May, H. E. & McCay, P. B. (1968). J. biol. Chem. 243, 2288.CrossRefGoogle Scholar
Morrison, W. R. & Smith, L. M. (1964). J. Lipid Res. 5, 600.CrossRefGoogle Scholar
Recknagel, R. O. & Ghoshal, A. K. (1966). In Biochemical Pathology p. 132, (Farber, E. and Magee, P. N., editors). Baltimore: Williams & Wilkins.Google Scholar
Remmer, H. & Merker, H. J. (1965). Ann N. Y. Acad. Sci. 123, 79.CrossRefGoogle Scholar
Rowe, L. & Wills, E. D. (1976). Biochem. Pharmac. 25, 175.Google Scholar
Strobel, H. W., Lu, A. Y. H., Heidema, J. & Coon, M. J. (1970). J. Biol. Chem. 245, 4851.CrossRefGoogle Scholar
Tappel, A. L. (1962). Vitam. Horm. 20, 493.CrossRefGoogle Scholar
Victoria, E. J. & Barber, A. A. (1969). Lipids 4, 582.CrossRefGoogle Scholar
Wills, E. D. (1971). Biochem. J. 123, 983.CrossRefGoogle Scholar