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Supplement

Vitamin E and Macrophage Cyclooxygenase Regulation in the Aged^{1 ,2}

Dayong Wu^*,, Michael G. Hayek^** and Simin Nikbin Meydani^*3

^* Nutritional Immunology Laboratory, Jean Mayer Human Research Center on Aging at Tufts University, Boston, MA 02111; Department of Immunology, Norman Bethune University of Medical Sciences, Changchun, China; and ^** Iams Company, Lewisburg, OH 45338

³To whom correspondence should be addressed. E-mail: SMeydani{at}hnrc.tufts.edu.

Aging is associated with increased evidence of cardiovascular disease (CVD). Atherosclerosis, a major cause of CVD, is an inflammatory process whose development is influenced by several proinflammatory mediators. Products of arachidonic acid metabolism, in particular, prostaglandin (PG) E₂ and thromboxane (TX) A₂, play an important role in the development of atherosclerosis. We showed previously that the aged have higher PGE₂ production compared with their young counterparts. This age-associated increase in PGE₂ production is mainly a consequence of increased cyclooxygenase (COX) activity. We demonstrated further that increased COX activity in old mice is due to the increased expression of mRNA and protein for the inducible form of COX, COX-2. Vitamin E has been shown to reduce PGE₂ production and risk of CVD. In aged mice, we showed that a vitamin E–induced decrease in PGE₂ production is due to decreased COX activity. However, vitamin E had no effect on COX mRNA and protein levels, indicating a post-translational regulation of COX by vitamin E. Further experiments indicated that vitamin E decreases COX activity through reducing formation of peroxynitrite, a hydroperoxide shown to be involved in the activation of COX-2. Other homologues of tocopherols were also effective in inhibiting COX activity, but their degree of inhibition varied. The varied potency to inhibit COX activity was not explained totally by differences in their antioxidant capacity. Vitamin E–induced inhibition of COX activity might contribute to its effect of reducing CVD risk.

KEY WORDS: • vitamin E • cardiovascular disease • atherosclerosis • prostaglandin

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