Effects of vitamin E deficiency on total polyunsaturated fatty acids in rats and chicks.

The hypothesis that vitamin E acts mainly as a physiological antioxidant suggests that, in its absence, loss of many types of oxidizable substances may occur. Considerable importance has been attached, in this connexion, to the polyunsaturated fatty acids (PUFA), because of their chemical structure and because of their biochemical role in structural elements of the cell. Pritchard & Singh (1960) found marked decreases (50-75 yo) in the PUFA content of heart, liver, adrenals and plasma (but not brain) of vitamin E-deficient rats, although Bernhard (1958) had previously reported no great change in PUFA content of brain, liver, lung, spleen and depot fat when vitamin E-deficient female rats were given vitamin E. Our recent studies on the metabolism of [14C]a-tocopherol in the vitamin E-deficient rat (Green, Diplock, Bunyan, McHale & Muthy, 1967) and chick (Diplock, Bunyan, McHale & Green, 1967) led us to conclude that lipid peroxidation is not a causal process in the aetiology of vitamin E deficiency disease. Consequently, we would not expect there to be a general loss of tissue PUFA in the deficient animal, contrary to the findings of Pritchard & Singh (1960) and in agreement with Bernhard (1958). In this paper we describe our experiments on PUFA in vitamin E-deficient tissues.