Abstract
Abnormal function of apolipoprotein E (apoE) has been implicated in the incidence
of some neurological disorders including dementia. Our recent experiments have shown
that apoE deficiency alters the dynamics of alpha tocopherol (vitamin E) handling
by brain. In the current investigation, we examined the uptake and retention of tritium-labeled
alpha tocopherol that was injected into the lateral cerebral ventricles of apoE-deficient
and wild type mice that were fed vitamin E-deficient diet. Eighteen weeks-old, male
mice were fed vitamin E-deficient diets for 28 weeks. Labeled cholesterol was injected
with the radioactive tocopherol and the cholesterol counts were used as internal standard.
After an equilibration time of 48 h, radioactive alpha tocopherol levels in most brain
regions were higher in apoE deficient animals when compared with the wild type. Along
with our other data, this suggests that the clearance of vitamin E is slower in apoE-deficient
brains. Nearly all of the injected alpha tocopherol was unchanged in the brains of
both apoE-deficient and wild type animals (even with the additional dietary stress
of vitamin E deficiency) suggesting low turnover rate of tocopherol in brain. The
data strongly suggest that apoE is a key protein involved with the transport and/or
retention of alpha tocopherol in brain.
Keywords
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Article info
Publication history
Published online: May 15, 2009
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Published by Elsevier Inc.
