| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
RESEARCH COMMUNICATION |
a Departamento de Biología Celular, Facultad de Ciencias, Universidad de Córdoba, Spain
b Department of Foods and Nutrition, Purdue University, West Lafayette, Indiana, 47907 USA
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.—Navarro, F., Navas, P., Burgess, J. R., Bello, R. I., de Cabo, R., Arroyo, A., Villalba, J. M. Vitamin E and selenium deficiency induces expression of the ubiquinone-dependent antioxidant system at the plasma membrane. FASEB J. 12, 1665–1673 (1998)
Key Words: lipid peroxidation • oxidative stress • plasma membrane • ubiquinone • vitamin E and selenium deficiency
This article has been cited by other articles:
|
|
 |
|
  Z. Ungvari, C. Parrado-Fernandez, A. Csiszar, and R. de Cabo Mechanisms Underlying Caloric Restriction and Lifespan Regulation: Implications for Vascular Aging Circ. Res., March 14, 2008; 102(5): 519 - 528. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 D.-H. Hyun, S. S. Emerson, D.-G. Jo, M. P. Mattson, and R. de Cabo Calorie restriction up-regulates the plasma membrane redox system in brain cells and suppresses oxidative stress during aging PNAS, December 26, 2006; 103(52): 19908 - 19912. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 R. Buffenstein The Naked Mole-Rat: A New Long-Living Model for Human Aging Research J. Gerontol. A Biol. Sci. Med. Sci., November 1, 2005; 60(11): 1369 - 1377. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. L. GENOVA, M. M. PICH, A. BERNACCHIA, C. BIANCHI, A. BIONDI, C. BOVINA, A. I. FALASCA, G. FORMIGGINI, G. P. CASTELLI, and G. LENAZ The Mitochondrial Production of Reactive Oxygen Species in Relation to Aging and Pathology Ann. N.Y. Acad. Sci., April 1, 2004; 1011(1): 86 - 100. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Saito, Y. Yoshida, T. Akazawa, K. Takahashi, and E. Niki Cell Death Caused by Selenium Deficiency and Protective Effect of Antioxidants J. Biol. Chem., October 10, 2003; 278(41): 39428 - 39434. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. H. Audi, R. D. Bongard, Y. Okamoto, M. P. Merker, D. L. Roerig, and C. A. Dawson Pulmonary reduction of an intravascular redox polymer Am J Physiol Lung Cell Mol Physiol, June 1, 2001; 280(6): L1290 - L1299. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 P Klivenyi, E Karg, C Rozsa, R Horvath, S Komoly, I Nemeth, S Turi, and L Vecsei {alpha}-Tocopherol/lipid ratio in blood is decreased in patients with Leber's hereditary optic neuropathy and asymptomatic carriers of the 11778 mtDNA mutation J. Neurol. Neurosurg. Psychiatry, March 1, 2001; 70(3): 359 - 362. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Schuelke, B. Finckh, E. A. Sistermans, M. G. E. M. Ausems, C. Hubner, and A. von Moers Ataxia with vitamin E deficiency: Biochemical effects of malcompliance with vitamin E therapy Neurology, November 28, 2000; 55(10): 1584 - 1586. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 S. H. Audi, L. E. Olson, R. D. Bongard, D. L. Roerig, M. L. Schulte, and C. A. Dawson Toluidine blue O and methylene blue as endothelial redox probes in the intact lung Am J Physiol Heart Circ Physiol, January 1, 2000; 278(1): H137 - H150. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. C. Chan, C. K. Chow, and D. Chiu Interaction of Antioxidants and Their Implication in Genetic Anemia Experimental Biology and Medicine, December 1, 1999; 222(3): 274 - 282. [Abstract] [Full Text]
|
|
|
|
 |
|
 W.-H. CHENG, Y. X. FU, J. M. PORRES, D. A. ROSS, and X. G. LEI Selenium-dependent cellular glutathione peroxidase protects mice against a pro-oxidant-induced oxidation of NADPH, NADH, lipids, and protein FASEB J, August 1, 1999; 13(11): 1467 - 1475. [Abstract] [Full Text]
|
|
|
|
|
|
R. I. Bello, C. Gomez-Diaz, F. Navarro, F. J. Alcain, and J. M. Villalba Expression of NAD(P)H:Quinone Oxidoreductase 1 in HeLa Cells. ROLE OF HYDROGEN PEROXIDE AND GROWTH PHASE J. Biol. Chem., November 21, 2001; 276(48): 44379 - 44384. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
