Antitumor activity of astaxanthin and its mode of action

Harumi Jyonouchi, Sining Sun, Koji Iijima, Myron D. Gross

Research output: Contribution to journalArticlepeer-review

189 Scopus citations

Abstract

Astaxanthin, a carotenoid without vitamin A activity, may exert antitumor activity through the enhancement of immune responses. Here, we determined the effects of dietary astaxanthin on tumor growth and tumor immunity against transplantable methylcholanthrene-induced fibrosarcoma (Meth-A tumor) cells. These tumor cells express a tumor antigen that induces T cell-mediated immune responses in syngenic mice. BALB/c mice were fed astaxanthin (0.02%, 40 μg/kg body wt/day in a beadlet form) mixed in a chemically defined diet starting zero, one, and three weeks before subcutaneous inoculation with tumor cells (3 x 105 cells, 2 times the minimal tumorigenic dose). Three weeks after inoculation, tumor size and weight were determined. We also determined cytotoxic T lymphocyte (CTL) activity and interferon-γ (IFN-γ) production by tumor-draining lymph node (TDLN) and spleen cells by restimulating cells with Meth-A tumor cells in culture. The astaxanthin-fed mice had significantly lower tumor size and weight than controls when supplementation was started one and three weeks before tumor inoculation. This antitumor activity was paralleled with higher CTL activity and IFN-γ production by TDLN and spleen cells in the astaxanthin-fed mice. CTL activity by TDLN cells was highest in mice fed astaxanthin for three weeks before inoculation. When the astaxanthin- supplemented diet was started at the same time as tumor inoculation, none of these parameters were altered by dietary astaxanthin, except IFN-γ production by spleen cells. Total serum astaxanthin concentrations were approximately 1.2 μmol/l when mice were fed astaxanthin (0.02%) for four weeks and appeared to increase in correlation with the length of astaxanthin supplementation. Our results indicate that dietary astaxanthin suppressed Meth-A tumor cell growth and stimulated immunity against Meth-A tumor antigen.

Original languageEnglish (US)
Pages (from-to)59-65
Number of pages7
JournalNutrition and Cancer
Volume36
Issue number1
DOIs
StatePublished - 2000

Bibliographical note

Funding Information:
This study was partly supported by grants funded through the Minnesota Medical Foundation (Minneapolis, MN) and the Tsumura Corp. (Tokyo, Japan). Address reprint requests to Harumi Jyonouchi, M.D., Dept. of Pediatrics, University of Minnesota, Box 610, UMHC, 420 Delaware St. SE, Minneapolis, MN 55455. Phone: (612) 626-3412. FAX: (612) 624-9188. E-mail: jyono001@jyono001.email.umn.edu.

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