Dietary Lutein Inhibits Mammary Tumor Growth And Normalizes Immune Balance In Tumor-Bearing Mice

Washington, DC, April 18, 1999 -- The carotenoid antioxidant lutein can normalize immune system balance in mammary tumor-bearing mice, effectively slowing tumor growth, according to a study presented today at the Federation of American Societies for Experimental Biology 1999 annual meeting.

"Tumor-bearing mice that were fed chow containing lutein had significantly smaller tumor growth than the mice on regular chow," said Boon Chew, Ph.D., Department of Animal Science, Washington State University. "Lutein normalized their immune response, enabling them to better fight the tumors."

Chew and his colleagues investigated the role of lutein in tumor immunity by examining hoe lutein stimulates the numbers and functionality of immune cells that suppress tumor development. Mice were fed a diet containing zero (control), 0.002, or 0.2 percent lutein (by weight) from marigold extract. After two weeks, half the mice were inoculated with mammary tumors. Researchers then assessed the blood and tissue lutein intake, tumor growth, changes in immune cell populations and the production of cytokines (soluble mediators).

After six weeks, mice that were fed chow with lutein had significantly smaller tumors than the mice on regular chow. While tumor progression suppressed the number of immune cells lutein prevented this suppression. Also, lutein increased the production of interferon gamma (IFNg) and interleukin-2. Researchers concluded that lutein normalized the immune balance in the tumor-bearing mice and increased the production of IFN, thereby maintaining an effective anti-tumor response.

Dr. Chew's previous research established that dietary lutein from marigold extract inhibited the growth of mammary tumors in mice. In addition, they showed that lutein can regulate gene activity in immune cells. Further research is needed to confirm speculation that lutein may exert its anti-tumor activity through its immuno-stimulatory action.

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Contact: Anne Tramer
Selz/Seabolt Communications

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