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ARS Home » Northeast Area » Boston, Massachusetts » Jean Mayer Human Nutrition Research Center On Aging » Research » Publications at this Location » Publication #223993

Title: Alpha- and gamma- tocopherol prevent age-related transcriptional alterations in the heart and brain of mice

Author
item PARK, SANG-KYU - UNIV OF WISCONSIN
item PAGE, GRIER - UNIV OF ALABAMA
item KIM, KYOUNGMI - UNIV OF ALABAMA
item ALLISON, DAVID - UNIV OF ALABAMA
item Meydani, Mohsen
item WEINDRUCH, RICHARD - UNIV OF WISCONSIN
item PROLLA, TOMAS - UNIV OF WISCONSIN

Submitted to: Journal of Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/14/2008
Publication Date: 5/1/2008
Citation: Park, S., Page, G.P., Kim, K., Allison, D.B., Meydani, M., Weindruch, R., Prolla, T.A. 2008. Alpha- and gamma- tocopherol prevent age-related transcriptional alterations in the heart and brain of mice. Journal of Nutrition. 138:1010-1018.

Interpretive Summary: This study investigated broad effects of vitamin E (alpha- and gamma- tocopherol) supplementation on aging, specifically heart and brain tissue using 30 month old B6C3F1 mice. In the heart, both E supplemented diets were effective in inhibiting the expression of genes previously associated with some heart disease. In the brain, some deterioration found in aging was somewhat prevented by the mixture of alpha- and gamma- forms of E, but not by alpha- alone. Vitamin E has been shown to boost some cells of the immune system. High dose vitamin E supplementation is also associated with increased life span and improved brain function in male mice from a short-lived strain. Cell damage occurs in normal aging of tissues. This damage can be reduced by vitamin E, vitamin C and other supplements. Although the mechanisms leading to age-related heart diseases are not well understood, it is thought that increased cell damage from oxidation contributes to heart disease with age. Aging of the brain is associated with subtle changes in nervous system. When the brain function is impaired, it increases the chance of common brain disorders. Although there may be several mechanisms involved in brain aging, damage from oxidation may contribute to dysfunction in the aged brain. Further, the brain is more susceptible to this kind of damage due to its high oxygen consumption and minimal defense against this damage. Brain dysfunction associated with aging can be prevented by vitamin E supplementation in rats and dogs. These results demonstrate that middle age-onset dietary supplementation with vitamin E-specifically alpha- and gamma-forms of E can partially prevent age-associated changes in heart and brain tissue and indicate possible preventive treatments for two important areas of disease in the elderly—the heart and the brain.

Technical Abstract: To investigate the global effects of vitamin E supplementation on aging, we used high density oligonucleotide arrays to measure transcriptional alterations in the heart and brain (neocortex) of 30-month-old B6C3F1 mice supplemented with alpha- and gamma-tocopherol since middle age (15 months). Gene expression profiles were obtained from 5- and 30-monthold controls and 30-month-old mice supplemented with alpha-tocopherol (1g/kg), or a mixture of alpha- and gamma-tocopherol (500mg/kg of each tocopherol). In the heart, both tocopherol supplemented diets were effective in inhibiting the expression of genes previously associated with cardiomyocyte hypertrophy and increased innate immunity, while having a moderate effect on age-related transcriptional alterations linked to the stress response and protein synthesis. In the brain, induction of genes encoding ribosomal proteins and proteins involved in ATP biosynthesis was observed with aging and was markedly prevented by the mixture of alpha- and gamma-tocopherol supplementation, but not by alpha-tocopherol alone. These results demonstrate that middle age-onset dietary supplementation with alpha- and gamma-tocopherol can partially prevent age-associated transcriptional changes and that these effects are tissue-and tocopherol-specific.