On the existence and significance of lipid peroxides in vitamin E-deficient animals

Abstract

1. A micro-adaptation of the iodimetric method has been used to determine lipid peroxides in the tissues of vitamin E-deficient rats and chicks.2. No increases in lipid peroxide were found in liver, kidney or adipose tissue of rats with nutritional liver necrosis due to deficiency of vitamin E and selenium. When liver necrosis was induced by giving rats a casein diet and silver acetate solution to drink, the peroxide value of the adipose tissue was not increased.3. Degeneration of the testes of vitamin E-deficient rats was not accompanied by a rise in the peroxide value of the tissue lipids.4. There was an increase in cathepsin activity of the kidneys of rats displaying the phenomenon of renal autolysis (post mortem), but there was no increase in lipid peroxide content.5. No rise in lipid peroxide was found in dystrophic chick breast muscle, in cerebellum, brain and adipose tissue of chicks with encephalomalacia nor in the liver of chicks with exudative diathesis.6. In rat liver, kidney, testis and leg muscle, peroxide values in the range 10–40 µ-equiv./g lipid were found, and these values were not altered either by a substantial change in the degree of unsaturation of the dietary lipid or by the addition of vitamin E to the diet. Dietary addition of N, N'-diphenyl-p-phenylenediamine (DPPD) or 6-ethoxy-1, 2-dihydro-2,2,4-trime-thylquinoline (ethoxyquin) also failed to affect the peroxide value of liver. The possibility that lipid peroxide is a normal metabolite of these tissues is discussed.7. Peroxide values of rat adipose tissue were never found to be greater than 40 µ-equiv./g lipid and were readily decreased by the addition of vitamin E to the diet or by a decrease in the unsaturation of the dietary lipid. The peroxide content of this tissue may depend upon the up-take of peroxidized dietary lipid.8. The conclusion from this study of true lipid peroxides in animal tissues is that the biological role of vitamin E is not connected with lipid peroxidation in vivo, in agreement with our previous studies on the metabolism of the fatty acid substrates of peroxidation and of α-tocopherol and other postulated biological antioxidants.