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

Erin E. Reich, Kathleen S. Montine, Myron D. Gross, L. Jackson Roberts, Larry L. Swift, Jason D. Morrow, Thomas J. Montine

Research output: Contribution to journalArticlepeer-review

27 Scopus citations

Abstract

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 α-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 α-tocopherol-deficient, normal, or -supplemented diet had undetectable, 4486 ± 215, or 6406 ± 254 ng of α-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 α-tocopherol, combined to increase cerebral DHA oxidation by 81%. α-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 α-tocopherol contributed differently to oxidative damage to cerebral AA and DHA in aged mice.

Original languageEnglish (US)
Pages (from-to)5993-5999
Number of pages7
JournalJournal of Neuroscience
Volume21
Issue number16
DOIs
StatePublished - Aug 15 2001

Keywords

  • Aging
  • Apolipoprotein E
  • Brain
  • Isoprostanes
  • Mouse
  • Neuroprostanes
  • Oxidative damage
  • α-tocopherol

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