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Fish Oil and Tocopherol-Induced Changes in Natural Killer Cell-Mediated Cytotoxicity and PGE₂ Synthesis in Young and Old Mice^1,2,

United States Department of Agriculture Human Nutrition Research Center on Aging at Tufts University, Boston, MA 02111

Natural killer cell (NK) activity decreases and prostaglandin E₂ (PGE₂) level increases in aged mice. Because PGE₂ is involved in control of NK activity this study was conducted to investigate whether or not decreasing PGE₂ level by changing the type of dietary fat or increasing the level of vitamin E (vit. E) modulates NK activity of young and old mice. Mice were fed either a corn oil (CO) or a fish oil (FO) diet supplemented with 30 or 500 mg/kg diet of vit. E for 6 wk. To study the effect of vit. E during active immune response and oxidative stress, groups of old mice fed CO and either 30 or 500 mg/kg diet of vit. E were injected with sheep red blood cells (SRBC) prior to assessment of their NK activity. As reported by others regarding mice fed a nonpurified diet, the old mice in all dietary groups had significantly less NK activity and tended to synthesize more PGE₂ than young mice. FO-fed mice synthesized less PGE₂ than CO-fed mice; however, their NK activity was not higher than that of CO-fed mice. By contrast young mice fed FO had a moderately lower NK activity than those fed CO. Vit. E supplementation did not change NK activity in nonimmunized mice but was effective in preventing SRBC-induced decrease in NK activity of old mice.

KEY WORDS: • natural killer cells • fish oil • vitamin E • prostaglandin E₂ • aging • immune system

¹ This work was supported in part by National Institute on Aging Grant No. 1R23AG05791-02 and Tufts University National Institutes of Health Biomedical Research Grant No. NNS2S07RR0719-09 to S.N.M., National Cancer Institute Grant No. CA41925 to G.Y. and United States Department of Agriculture Contract No. 53-3K065-10.

² Presented in part at the 1987 American Oil Chemists Society short course on polysaturated fatty acids and eicosanoids in Biloxi, MI.

³ Present address: Department of Pathology, School of Medicine, Tufts University, Boston, MA 02111.

Manuscript received 2 November 1987. Revision accepted 14 June 1988.