title: Vitamin E and selenium deficiency induces expression of the ubiquinone-dependent antioxidant system at the plasma membrane.
abstract: We have used a model of dietary deficiency that leads to a chronic oxidative stress to evaluate responses that are adaptations invoked to boost cellular defense systems. Long-Evans hooded rats were fed with a diet lacking vitamin E (E) and selenium (Se) for 7 wk from weaning leading to animals deficient in both nutrients (-E -Se). In the absence of an electron donor, liver plasma membranes from these rats were more sensitive to lipid peroxidation, although they contained 40% greater amounts of ubiquinone than the plasma membranes from rats consuming diets with sufficient vitamin E and Se (+E +Se). The incubation of plasma membranes with NAD(P)H resulted in protection against peroxidation, and this effect was more pronounced in -E -Se membranes. Deficiency was accompanied by a twofold increase in redox activities associated with trans plasma membrane electron transport such as ubiquinone reductase and ascorbate free radical reductase. Staining with a polyclonal antibody against pig liver cytochrome b5 reductase, which acts as one ubiquinone reductase in the plasma membrane, showed an increased expression of the enzyme in membranes from -E -Se rats. Little DT-diaphorase activity was measured in +E +Se plasma membranes, but this activity was dramatically increased in -E -Se plasma membranes. No such increase was found in liver cytosols, which contained elevated activity of calcium-independent phospholipase A2. Thus, ubiquinone-dependent antioxidant protection in +E +Se plasma membranes is based primarily on NADH-cytochrome b5 reductase, whereas additional protection needed in -E -Se plasma membranes is supported by the increase of ubiquinone levels, increased expression of the cytochrome b5 reductase, and translocation of soluble DT-diaphorase to the plasma membrane. Our results indicate that, in the absence of vitamin E and Se, enhancement of ubiquinone-dependent reductase systems can fulfill the membrane antioxidant protection.
authors.affiliation: Departamento de Biología Celular, Facultad de Ciencias, Universidad de Córdoba, Spain.
authors.forename: F
authors.initials: F
authors.lastname: Navarro
authors.forename: P
authors.initials: P
authors.lastname: Navas
authors.forename: J R
authors.initials: JR
authors.lastname: Burgess
authors.forename: R I
authors.initials: RI
authors.lastname: Bello
authors.forename: R
authors.initials: R
authors.lastname: De Cabo
authors.forename: A
authors.initials: A
authors.lastname: Arroyo
authors.forename: J M
authors.initials: JM
authors.lastname: Villalba
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000378:metabolism*; D002462:Cell Membrane / Q000378:metabolism*; D003579:Cytochrome Reductases / Q000032:analysis; D042966:Cytochrome-B(5) Reductase; D003600:Cytosol / Q000201:enzymology; D004579:Electron Transport; D010450:Endopeptidases / Q000032:analysis; D015227:Lipid Peroxidation; D008099:Liver / Q000378:metabolism; D008297:Male; D009243:NAD / Q000378:metabolism; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000032:analysis; D009249:NADP / Q000378:metabolism; D010084:Oxidation-Reduction; D018384:Oxidative Stress / Q000502:physiology*; D010741:Phospholipases A / Q000032:analysis; D054467:Phospholipases A2; D011808:Quinone Reductases / Q000032:analysis; D051381:Rats; D020318:Rats, Long-Evans; D012643:Selenium / Q000172:deficiency*; D014451:Ubiquinone / Q000378:metabolism*; D014811:Vitamin E Deficiency / Q000378:metabolism*
chemical_list: D000975:Antioxidants; D009243:NAD; D014451:Ubiquinone; D009249:NADP; D003579:Cytochrome Reductases; D042966:Cytochrome-B(5) Reductase; D016660:NAD(P)H Dehydrogenase (Quinone); D011808:Quinone Reductases; D010741:Phospholipases A; D054467:Phospholipases A2; D010450:Endopeptidases; D012643:Selenium