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Long-Term Vitamin E Deficiency in Mice Decreases Superoxide Radical Production in Brain
aDepartment of Neurology, Washington University School of Medicine, St. Louis, Missouri 63112, USA bDepartment of Medicine and Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232, USA
Address for correspondence: Laura L. Dugan, Department of Neurology, Campus Box 8111, Washington University School of Medicine, 660 South Euclid Avenue, St. Louis, MO 63110. Voice: 314-747-0467; fax: 314-362-9462. duganl{at}neuro.wustl.edu
We investigated the effect of long-term vitamin E deficiency (38 weeks) on free radical (superoxide) production and free radical products (neuroprostanes and isoprostanes) and on mitochondrial function (oxygraph and electron transport chain activities) in C57B6J mice. We found that after 38 weeks, while liver was approximately 95% deficient, the brain had retained approximately 50% of its
 -tocopherol. We also found that superoxide production was lowered in multiple brain regions of male vitamin E-deficient mice, as were neuroprostanes. Oxygraph studies showed higher respiratory control ratios (RCRs) in liver and lower RCRs in brain, which did not appear to be due to changes in electron transport chain activities. We conclude that vitamin E can function in vivo in both its traditional role as a lipid-soluble antioxidant as well as in non-traditional roles in the mitochondria.
Key Words: -tocopherol • vitamin E-deficient diet • superoxide • mitochondria
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