Interactions between apolipoprotein E gene and dietary alpha-tocopherol influence cerebral oxidative damage in aged mice.

Reich EE, Montine KS, Gross MD, Roberts LJ, Swift LL, Morrow JD, Montine TJ
J Neurosci. 2001 21 (16): 5993-9

PMID: 11487622 · PMCID: PMC6763161

Cerebral oxidative damage is a feature of aging and is increased in a number of neurodegenerative diseases. We pursued the gene-environment interaction of lack of apolipoprotein E (apoE) and modulation of dietary alpha-tocopherol on cerebral oxidative damage in aged male and female mice by quantifying the major isomers of cerebral isoprostanes, derived from arachidonic acid (AA) oxidation, and neuroprostanes, derived from docosahexaenoic acid (DHA) oxidation. Mice fed alpha-tocopherol-deficient, normal, or -supplemented diet had undetectable, 4486 +/- 215, or 6406 +/- 254 ng of alpha-tocopherol per gram of brain tissue (p < 0.0001), respectively. Two factors, male gender and lack of apoE, combined to increase cerebral AA oxidation by 28%, whereas three factors, male gender, lack of apoE, and deficiency in alpha-tocopherol, combined to increase cerebral DHA oxidation by 81%. alpha-Tocopherol supplementation decreased cerebral isoprostanes but not neuroprostanes and enhanced DHA, but not AA, endoperoxide reduction in vivo and in vitro. These results demonstrated that the interaction of gender, inherited susceptibilities, and dietary alpha-tocopherol contributed differently to oxidative damage to cerebral AA and DHA in aged mice.

MeSH Terms (23)

Administration, Oral Aging Amidines Animals Apolipoproteins E Arachidonic Acid Body Weight Docosahexaenoic Acids Female Food, Formulated Male Mice Mice, Inbred C57BL Mice, Knockout Oxidants Oxidation-Reduction Oxidative Stress Prostaglandins Sex Factors Synaptosomes Telencephalon Vitamin E Vitamin E Deficiency

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