Factors influencing the antitumorigenic properties of selenium in mice.

TLDR: The data suggest that some intermediate in the normal pathway for selenium detoxification is probably responsible for this trace element's antitumorigenic properties.

Abstract: Sodium selenite (Na2SeO3) was administered at 2.0 micrograms 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 micrograms 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 Na2(75)SeO3, 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.