The a-tocopherol content of a number of different fetal, neonatal and maternal guinea-pig tissues was determined and compared with plasma and erythrocyte a-tocopherol values. During late gestation, the fetal liver appears to act as a storage site for a-tocopherol, the majority of which is released immediately following birth. In contrast, lung and brain vitamin E levels are relatively constant over the final period of gestation and during early neonatal life. The ontogeny of a-tocopherol in brain and lung was similar to that for erythrocytes while plasma a-tocopherol content varied considerably and did not accurately reflect tissue a-tocopherol status. Surprisingly, fetal and maternal lung a-tocopherol concentrations were similar at all time-points considered, whereas fetal liver a-tocopherol status was always considerably greater than maternal liver a-tocopherol content. These results, if representative of the human fetus, suggest that preterm infants may not have tissue a-tocopherol concentrations as low as previously assumed and that during the perinatal period erythrocyte a-tocopherol content is a more accurate indicator of tissue a-tocopherol concentration than plasma a-tocopherol content.Vitamin E: Fetus: Chronic lung disease: Prematurity : Guinea-pigThe newborn infant has low circulating levels of vitamin E (Dju et al. 1958;Mino et al. 1977; Kelly et al. 1990b). In term neonates, plasma vitamin E concentrations increase rapidly following the feeding of colostrum which contains high concentrations of vitamin E (Ostrea et al. 1986). In sick preterm infants, deprived of colostrum because of intense management of their respiratory insufficiency, plasma vitamin E concentrations rise much more slowly (Bell et al. 1979;Gross & Gabriel, 1985;Kelly et al. 1990h). These observations have led a number of workers to suggest that the preterm neonate is born with low concentrations of vitamin E, both circulating and in the tissues, and that is why these infants are particularly sensitive to oxidative stress. In particular, association has been made between deficiency of vitamin E and chronic lung disease (Ehrenkranz et al. 1982), intraventricular haemorrhage (Chiswick et al. 1983;Speer et al. 1984) and retinopathy of prematurity (Owens & Owens, 1949; Johnston et al. 1974;Hittner et al. 1981).Vitamin E is situated primarily in membranes of cells, where it protects polyunsaturated fatty acids from free-radical-induced oxidative damage (Mason & Filer, 1947;McCay et al. 1972). Knowledge of membrane vitamin E concentration is, therefore, important when investigating the role of this vitamin in neonatal diseases. Due to ethical and practical difficulties of working with sick preterm infants, little information is available regarding vitamin E status of their tissues. From the few studies available it appears that the human fetus has low tissue concentrations of vitamin E, and these only increase following initiation of feeding at birth (Dju & Mason, 1952;Dju et a[. 1958;Mino et a!. 1977).Recently, Mino et al. (1985) suggest...