title: Vitamin E differentially regulates the expression of peroxiredoxin-1 and -6 in alveolar type II cells.
abstract: Vitamin E is the primary lipophilic antioxidant in mammals. Lack of vitamin E may lead to an increase of cytotoxic phospholipid-peroxidation products (PL-Ox). However, we could previously show that alimentary vitamin E-depletion in rats did not change the concentrations of dienes, hydroperoxides, and platelet-activating factor-related oxidation products in alveolar type II cells (TII cells). We hypothesized that vitamin E deficiency increases the activity of enzymes involved in the degradation of PL-Ox. Degradation of PL-Ox may be catalyzed by phospholipase A2, PAF-acetylhydrolase, or peroxiredoxins (Prx's). Alimentary vitamin E deficiency in rats increased the expression of Prx-1 at the mRNA and protein levels and the formation of Prx-SO3, but it did not change the expression of Prx-6 or the activity of phospholipase A2 and PAF-acetylhydrolase in TII cells. H2O2-induced oxidative stress in isolated TII cells activated protein kinase Calpha (PKCalpha) and increased the expression of Prx-1 and Prx-6. Inhibition of PKCalpha in isolated TII cells by long-time incubation with PMA inhibited PKCalpha and Prx-1 but not Prx-6. We concluded that the expression of Prx-1 and -6 is selectively regulated in TII cells; PKCalpha regulates the expression of Prx-1 but not Prx-6. Prx-6 expression may be closely linked to lipid peroxidation.
authors.affiliation: Klinik für Neonatologie, Universitätsmedizin-Berlin, Charité Campus Mitte, D-10098 Berlin, Germany.
authors.forename: Angelika
authors.initials: A
authors.lastname: Tölle
authors.forename: Michael
authors.initials: M
authors.lastname: Schlame
authors.forename: Nico
authors.initials: N
authors.lastname: Charlier
authors.forename: Florian
authors.initials: F
authors.lastname: Guthmann
authors.forename: Bernd
authors.initials: B
authors.lastname: Rüstow
mesh_terms: D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D004789:Enzyme Activation / Q000187:drug effects; D005786:Gene Expression Regulation / Q000187:drug effects*; D006861:Hydrogen Peroxide / Q000494:pharmacology; D015227:Lipid Peroxidation / Q000187:drug effects*; D016676:Macrophages, Alveolar; D018384:Oxidative Stress; D010544:Peroxidases / Q000235:genetics / Q000378:metabolism*; D054464:Peroxiredoxins; D010741:Phospholipases A / Q000378:metabolism; D054467:Phospholipases A2; D011493:Protein Kinase C / Q000378:metabolism; D051571:Protein Kinase C-alpha; D011650:Pulmonary Alveoli / Q000201:enzymology* / Q000254:growth & development; D012333:RNA, Messenger; D051381:Rats; D017208:Rats, Wistar; D014810:Vitamin E / Q000494:pharmacology*; D014811:Vitamin E Deficiency
chemical_list: D000975:Antioxidants; D012333:RNA, Messenger; D014810:Vitamin E; D006861:Hydrogen Peroxide; D010544:Peroxidases; D054464:Peroxiredoxins; D011493:Protein Kinase C; D051571:Protein Kinase C-alpha; D010741:Phospholipases A; D054467:Phospholipases A2; D043203:1-Alkyl-2-acetylglycerophosphocholine Esterase