title: HDL and vitamin E in plasma and the expression of SR-BI on lung cells during rat perinatal development.
abstract: Vitamin E is the most important lipophilic antioxidant, and beneficial effects on oxidant-caused injuries have been reported. Neonates are at high risk of oxidative injury in the lung and other organs because of a low vitamin E concentration, but the optimal timing of the application, a safe application form, and the optimal dosage of vitamin E are not known at present. We recently showed that alveolar type II cells take up vitamin E preferentially from high-density lipoprotein (HDL), probably by means of the candidate HDL receptor, scavenger receptor class B type I (SR-BI; Kolleck et al. Free Rad Biol Med 27; 882-890, 1999). Therefore, both the HDL-bound vitamin E in plasma and the expression of SR-BI on alveolar type II cells may determine the supply of the cells with vitamin E. We show here that the plasma level of vitamin E, total and HDL cholesterol, and the ratio of vitamin E to polyunsaturated fatty acids and to total fatty acids decrease during fetal rat development, reaching the minimum at the postconceptual day 21 (day -1). These parameters increase thereafter to about the same levels as in adult rats. SR-BI is not detectable until day -1 on fetal lung cells, but the expression during the postnatal phase follows the same pattern as the plasma lipid constituents. We conclude that the ability of alveolar type II cells to take up vitamin E develops perinatally in mature neonates. This aspect also has to be considered when the optimal timing of supplementation for the protection of preterm neonates with vitamin E against oxidative lung injury is established.
authors.affiliation: Department of Neonatology, University Hospital Charité, Humboldt University, 10098 Berlin, Germany.
authors.forename: I
authors.initials: I
authors.lastname: Kolleck
authors.forename: W
authors.initials: W
authors.lastname: Witt
authors.forename: H
authors.initials: H
authors.lastname: Wissel
authors.forename: P
authors.initials: P
authors.lastname: Sinha
authors.forename: B
authors.initials: B
authors.lastname: Rüstow
mesh_terms: D000818:Animals; D000831:Animals, Newborn; D018955:CD36 Antigens / Q000378:metabolism*; D005333:Fetus; D007150:Immunohistochemistry; D008075:Lipoproteins, HDL / Q000097:blood*; D008099:Liver / Q000378:metabolism; D008168:Lung / Q000378:metabolism*; D016676:Macrophages, Alveolar / Q000378:metabolism; D008565:Membrane Proteins; D051381:Rats; D011971:Receptors, Immunologic; D018110:Receptors, Lipoprotein / Q000378:metabolism*; D051116:Receptors, Scavenger; D051122:Scavenger Receptors, Class B; D013997:Time Factors; D014810:Vitamin E / Q000097:blood*
chemical_list: D018955:CD36 Antigens; D008075:Lipoproteins, HDL; D008565:Membrane Proteins; D011971:Receptors, Immunologic; D018110:Receptors, Lipoprotein; D051116:Receptors, Scavenger; C454739:Scarb1 protein, mouse; C495125:Scarb1 protein, rat; D051122:Scavenger Receptors, Class B; D014810:Vitamin E