VITAMIN E AND SELENIUM PROTECTION FROM IN VIVO LIPID PEROXIDATION*

Some of the vitamins and many of the metals that are being considered at this symposium interact in lipid peroxidation. Some of these interactions have been studied in vivo. Measurement of in vivo lipid peroxidation in the rat is accomplished by gas chromatographic analysis of pentane, a minor peroxidation product that is exhaled in the breath. In the rat, lipid peroxidation is proportional to dietary polyunsaturated lipids when the animal is deficient in antioxygenic agents. The chain-breaking antioxidant vitamin E is the main protector against in vivo lipid peroxidation. Dietary selenium, through its involvement in the biosynthesis of glutathione peroxidase, functions in a secondary antioxygenic role as a hydroperoxide reducer. In rats fed a vitamin E-deficient diet, injection of some hydroperoxides, iron, or vitamin C leads to initiation of in vivo lipid peroxidation, apparently by decomposing hydroperoxides to free radicals. Carbon tetrachloride, a toxic halogenated hydrocarbon, is metabolized by liver microsomes and initiates in vivo lipid peroxidation in the liver. These examples show that practical information on interactions involving in vivo lipid peroxidation can be obtained by studies that use the pentane method.