Journal of Nutrition

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Journal of Nutrition Vol. 113 No. 11 November 1983, pp. 2147-2154
Copyright © 1983 by American Society for Nutrition
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Factors Influencing the Antitumorigenic Properties of Selenium in Mice1

Kenneth A. Poirier2 and John A. Milner3

Department of Food Science/Division of Nutritional Sciences, University of Illinois, 567 Bevier Hall, 905 S. Goodwin Avenue, Urbana, IL 61801

Sodium selenite (Na2SeO3) was administered at 2.0 µg selenium (Se) to Swiss ICR mice six times over a 9-day period by intraperitoneal (i.p.) injection or by gastric gavage. Survival time was significantly increased in Ehrlich ascites tumor (EAT)-bearing mice by 170 and 20%, respectively, compared to controls. In two separate studies, 5.0 µg Se as Na2SeO3 or selenodiglutathione (GSSeSG) administered i.p. was more effective in inhibiting EAT propagation in mice than either untreated (control) mice or mice receiving sodium selenide, dimethyl selenide [(CH3)2Se] or seleno-DL-cystine. In another study, EAT cells were preincubated with either 1 or 3 ppm Se as GSSeSG, Na2SeO3, or (CH3)2Se, washed, and reinoculated into mice. Only in mice inoculated with cells pretreated with GSSeSG was a significant increase in survival observed. The observed tumor inhibition was not limited to ascitic tumors since growth of solid Ehrlich tumors was also significantly inhibited by i.p. treatment of Na2SeO3. Following i.p. administration of Na275SeO3, the solid tumors retained more selenium-75 than did blood, lung, kidney, or liver. Supplementation of a torula yeast diet with 2.5 or 5.0 ppm Se as Na2SeO3 also significantly increased the survival time of EAT-bearing mice. These data show that the form and mode of administration of selenium influence the antitumorigenic properties of this trace element. In addition, the data suggest that some intermediate in the normal pathway for selenium detoxification is probably responsible for this trace element's antitumorigenic properties.


KEY WORDS: • Ehrlich ascites tumors • sodium selenite • selenodiglutathione • dimethylselenide

1 Supported in part by US Department of Agriculture, Science and Education Administration 5901-0410-9-0243 and US Public Health Service 5 T32 CA 090807. Presented in part at the 85th Annual Meeting for the Federation of American Societies of Experimental Biology (1) and the Fourth Triennial Joint Meeting of the American Institute of Nutrition, American Society for Clinical Nutrition, and the Canadian Society for Nutritional Sciences (2).

2 Part of data were taken from a thesis submitted for the Ph.D. degree in the Division of Nutritional Sciences, University of Illinois.

3 To whom all correspondence should be sent.

Manuscript received 28 March 1983.





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