Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 46, Issue 11, Pages 1527-1533Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2009.03.008
Keywords
Alzheimer disease; DNA oxidation; RNA oxidation; Organoselenium; Antioxidants; Free radicals
Funding
- NIH [5-P01-AG05119, 5-P30-AG028383]
- Abercrombie Foundation
- Healey Family Foundation
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To evaluate potential antioxidant characteristics of organic selenium (Se), double knock-in transgenic mice expressing human mutations in the amyloid precursor protein (APP) and human presenilin-1 (PS1) were provided a Se-deficient diet, a Se-enriched diet (Sel-Plex), or a control diet from 4 to 9 months of age followed by a control diet until 12 months of age. Levels of DNA, RNA, and protein oxidation as well as lipid peroxidation markers were determined in all mice and amyloid beta-peptide (A beta) plaques were quantified. APP/PS1 mice provided Sel-Plex showed significantly (P<0.05) lower levels of A beta plaque deposition and significantly decreased levels of DNA and RNA oxidation. Sel-Plex-treated mice showed no significant differences in levels of lipid peroxidation or protein oxidation compared to APP/PS1 mice on a control diet. To determine if diminished oxidative damage was associated with increased antioxidant enzyme activities, brain glutathione peroxidase (GSH-Px), glutathione reductase, and glutathione transferase activities were measured. Sel-Plex-treated mice showed a modest but significant increase in GSH-Px activity compared to mice on a normal diet (P<0.5). Overall, these data suggest that organic Se can reduce A beta burden and minimize DNA and RNA oxidation and support a role for it as a potential therapeutic agent in neurologic disorders with increased oxidative stress. (C) 2009 Elsevier Inc. All rights reserved.
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