In this paper recent experimental work on rat liver is discussed which is considered to indicate that a primary function of vitamin E in vivo may be to inhibit the oxidation of selenide-containing proteins present in mitochondria and in smooth endoplasmic reticulum. On the basis of molecular model building studies, it is also suggested that the well-known nutritional relationships between vitamin E and dietary polyunsaturated lipids may be due to the occurrence within normal membranes of specific complexes between the vitamin and some of the molecules of polyunsaturated phospholipids. Without the vitamin, membranes may have an abnormally high permeability and they may be subject to degradation by endogenous phospholipases in vivo, as well as being abnormally susceptible to damage in vitro by dialuric acid and hydrogen peroxide.
