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Organoselenium (Sel-Plex diet) decreases amyloid burden and RNA and DNA oxidative damage in APP/PS1 mice. | LitMetric

AI Article Synopsis

  • A study evaluated the antioxidant effects of organic selenium (Se) in transgenic mice that mimic Alzheimer's disease by expressing specific human gene mutations.
  • Mice fed a Se-enriched diet had significantly lower levels of amyloid beta-peptide plaques and reduced DNA and RNA oxidation compared to those on a control or Se-deficient diet.
  • The Se-enriched diet also modestly increased brain antioxidant enzyme glutathione peroxidase activity, suggesting organic Se may have therapeutic potential for neurological disorders linked to oxidative stress.

Article Abstract

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 (Abeta) plaques were quantified. APP/PS1 mice provided Sel-Plex showed significantly (P<0.05) lower levels of Abeta 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 Abeta 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2683469PMC
http://dx.doi.org/10.1016/j.freeradbiomed.2009.03.008DOI Listing

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