Tissue α-tocopherol status during late fetal and early neonatal life of the guinea-pig

Abstract

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...

Vitamin E: pharmacokinetics of parenteral products and its effect on swine reproduction

“…reported greater plasma a-tocopherol concentration of the neonate than in the dam. showed lower liver tocopherol concentration in the newborn than in the dam, whereas Kelly et al (1992) reported greater liver a-tocopherol concentration in the neonatal guinea pig than in the dam.…”

“…The levels of plasma |8-apolipoprotein, which transports tocopherol, are low in the human fetus (Kayden, 1983) and as a result may limit the capacity for transport of vitamin E across the placenta. Kelly et al (1992) reported that significant tocopherol storage takes place in the fetal liver of guinea pigs by the end of gestation. They concluded that the newborn guinea pig utilized liver stores to increase plasma tocopherol concentration after birth.…”

Vitamin E in young turkeys: a reassessment of the requirement

“…Increases in lung aTOC with dietary VE supplementation have been described for cattle (Arnold etal., 1993), chicks (Sheehy et al, 1991), guinea pigs (Kelly et al, 1992), monkeys (f\/lachlin and Gabriel, 1982), pigs (Asghar ef a!., 1991a; Chung ef 400, and 600 mg/sheep) (Hidiroglou and Charmley, 1990 and sheep (Hidiroglou, 1986(Hidiroglou, , 1987Karpinski and Hidiroglou, 1990;) responded slowly to parenteral administration of VE, suggesting either saturation of the tissue, or a slow uptake of the VE by the pancreas. Similar results were reported by Batra and Hidiroglou (1994) after intramuscular injection of VE to pigs.…”

“…Lehmann (1981) used platelets to indicate the aTOC status of rats, whereas Mino et al (1981) used RBC aTOC to indicate the aTOC status of VE-deficient rats. Kelly et al (1992) found that RBC aTOC was the best indicator of VE status of guinea pigs during the perinatal period. Finally, RBC hemolysis has been used as the most sensitive indicator of aTOC status, especially in VE deficiency, for different species (Rose and Gyorgy, 1950;Horwitt etal., 1972;Mino et al, 1981;Stevenson and Jones, 1989;Eicher et al, 1994).…”

“…This suggests an inefficient absorption of nutrients (Sell et al, 1991, ISU, Ames, lA 50011, personal communication), including qTOC, early in life. Third, liver has been proposed as the main organ with capacity to store aTOC for short periods of time (Bieri, 1972;Kelly et al, 1992). If that is the case, liver would mobilize its aTOC stores, i.e., at times of intense metabolic activity, to be used by organs and tissues that need the protecting antioxidant capacities of aTOC.…”